Stanford Neuro Peer-Reviewed Publications

Part shameless publicity, part proud bragging, part intra-program PSA, this post is all about articles, published in peer-reviewed scientific journals, featuring work by the students of the Stanford Neuroscience Ph.D program. Since last July, the current graduate researchers (and recently-minted alumni) have produced an admirable volume of scientific research, some of which has been published in the form of journal articles. As the authors in question tend not to go around bragging, I'll be doing so on their behalf.

To that end, what follows are two lists detailing the results of an afternoon spent spelunking through Pubmed. The first list contains the names of current (or recently graduated) Stanford Neuro students who are first authors on articles published since around June '11 (date arbitrarily chosen). The second list contains the names of Stanford Neuro students who are second through n-th authors on papers published within the same time period. Click on an individuals name to see the full paper title and abstract.

Congratulations to all the recently published authors in the Stanford Neuro program!

(Grad students: Apologies for any author/paper left off the list - let me know and I will gladly add you - Astra) First Author papers:

• Sergio Arroyo (Arroyo et al 2012 *co-first with Corbett)
• Corbett Bennett (Arroyo et al 2012 *co-first with Sergio)
• Poh Hui Chia (Chia et al 2012 )
• Lief Fenno (Tye et al 2011 *co-first with Kay Tye, Sung-yon Kim and Rohit Prakash)
• Emily Ferenczi (Mattis et al 2011 *co-first with Joanna Mattis and Kay Tye)
• Patrick House (House et al 2011)
• Mariko Howe (Howe and Barres 2012)
• David Kastner (Kastner and Baccus 2012)
• Sung-yon Kim (Tye et al 2011 *co-first with Kay Tye, Rohit Prakash and Lief Fenno)
• Joanna Mattis (Mattis et al 2011 *co-first with Joanna Mattis and Kay Tye)
• Rohit Prakash (Tye et al 2011 *co-first with Kay Tye, Sung-yon Kim and Lief Fenno)
• Andreas Rauschecker (Rauschecker et al 2011)
• Jana Schiach Borg (Schaich Borg et al 2012)
• Nicholas Steinmetz (Steinmetz and Moore 2012, review of Gregoriou et al 2012)
• Saul Villeda (Villeda et al 2011)
• Jack Wang (Wang et al 2012)

Second through n-th Author papers:

• Ron Alfa (Bader et al 2011)
• Astra Bryant (Paz et al 2011)
• Matt Carter (de Lecea et al 2012)
• Branden Cord (Pasca et al 2011, Byers et al 2011)
• Lief Fenno (Byers et al 2011, Mattis et al 2011, Paz et al 2011, Tye et al 2011, Yizhar et al 2011, Zhang et al 2011)
• Lisa Gunaydin (Mattis et al 2011, Anikeeva et al 2011)
• Logan Grosenick (Anikeeva et al 2011, Tye et al 2011)
• William Joo (Sweeney et al 2011)
• Li Li (Yoo et al 2011)
• Jana Lim (Greer et al 2011)
• Ivan Millan (Liu et al 2012)
• Kira Mosher (Villeda et al 2011)
• Daniel O'Shea (Mattis et al 2011, Yizhar et al 2011)
• Scott Owen (Bader et al 2011)
• Georgia Panagiotakos (Osterhout et al 2011)
• Rohit Prakash (Mattis et al 2011, Goshen et al 2011, Abilez et al 2011)
• Aslihan Selimbeyoglu (Rauschecker et al 2011)
• Sergey Stavisky (Sussillo et al 2012)
• Gabriela Suarez-Mier (Taniguchi et al 2011)
• Nathan Woodling (Liang et al 2011, Grabrucker et al 2011)
• Kelly Zalocusky (Witten et al 2011)

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First Author Papers

Arroyo et al (2012). Prolonged Disynaptic Inhibition in the Cortex Mediated by Slow, Non-α7 Nicotinic Excitation of a Specific Subset of Cortical Interneurons. J Neursci 32(11):3859-64.

Cholinergic activation of nicotinic receptors in the cortex plays a critical role in arousal, attention, and learning. Here we demonstrate that cholinergic axons from the basal forebrain of mice excite a specific subset of cortical interneurons via a remarkably slow, non-α7 nicotinic receptor-mediated conductance. In turn, these inhibitory cells generate a delayed and prolonged wave of disynaptic inhibition in neighboring cortical neurons, altering the spatiotemporal pattern of inhibition in cortical circuits.

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Chia et al (2012). NAB-1 instructs synapse assembly by linking adhesion molecules and F-actin to active zone proteins. Nat. Neurosci 15(2):234-42.

During synaptogenesis, macromolecular protein complexes assemble at the pre- and postsynaptic membrane. Extensive literature identifies many transmembrane molecules sufficient to induce synapse formation and several intracellular scaffolding molecules responsible for assembling active zones and recruiting synaptic vesicles. However, little is known about the molecular mechanisms coupling membrane receptors to active zone molecules during development. Using Caenorhabditis elegans, we identify an F-actin network present at nascent presynaptic terminals and required for presynaptic assembly. We unravel a sequence of events whereby specificity-determining adhesion molecules define the location of developing synapses and locally assemble F-actin. Next, the adaptor protein NAB-1 (neurabin) binds to F-actin and recruits active zone proteins SYD-1 and SYD-2 (liprin-α) by forming a tripartite complex. NAB-1 localizes transiently to synapses during development and is required for presynaptic assembly. Altogether, we identify a role for the actin cytoskeleton during presynaptic development and characterize a molecular pathway whereby NAB-1 links synaptic partner recognition to active zone assembly.

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House et al (2011). Predator cat odors activate sexual arousal pathways in brains of Toxoplasma gondii infected rats. PLoS One. 6(8):e23277

Cat odors induce rapid, innate and stereotyped defensive behaviors in rats at first exposure, a presumed response to the evolutionary pressures of predation. Bizarrely, rats infected with the brain parasite Toxoplasma gondii approach the cat odors they typically avoid. Since the protozoan Toxoplasma requires the cat to sexually reproduce, this change in host behavior is thought to be a remarkable example of a parasite manipulating a mammalian host for its own benefit. Toxoplasma does not influence host response to non-feline predator odor nor does it alter behavior on olfactory, social, fear or anxiety tests, arguing for specific manipulation in the processing of cat odor. We report that Toxoplasma infection alters neural activity in limbic brain areas necessary for innate defensive behavior in response to cat odor. Moreover, Toxoplasma increases activity in nearby limbic regions of sexual attraction when the rat is exposed to cat urine, compelling evidence that Toxoplasma overwhelms the innate fear response by causing, in its stead, a type of sexual attraction to the normally aversive cat odor.

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Howe and Barres (2012). A novel role for microglia in minimizing excitotoxicity. BMC Biol 10:7.

Microglia are the abundant, resident myeloid cells of the central nervous system (CNS) that become rapidly activated in response to injury or inflammation. While most studies of microglia focus on this phenomenon, little is known about the function of 'resting' microglia, which possess fine, branching cellular processes. Biber and colleagues, in a recent paper in Journal of Neuroinflammation, report that ramified microglia can limit excitotoxicity, an important insight for understanding mechanisms that limit neuron death in CNS disease.

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Kastner and Baccus (2011). Coordinated dynamic encoding in the retina using opposing forms of plasticity. Nat. Neursci 12(10):1317-22.

The range of natural inputs encoded by a neuron often exceeds its dynamic range. To overcome this limitation, neural populations divide their inputs among different cell classes, as with rod and cone photoreceptors, and adapt by shifting their dynamic range. We report that the dynamic behavior of retinal ganglion cells in salamanders, mice and rabbits is divided into two opposing forms of short-term plasticity in different cell classes. One population of cells exhibited sensitization-a persistent elevated sensitivity following a strong stimulus. This newly observed dynamic behavior compensates for the information loss caused by the known process of adaptation occurring in a separate cell population. The two populations divide the dynamic range of inputs, with sensitizing cells encoding weak signals and adapting cells encoding strong signals. In the two populations, the linear, threshold and adaptive properties are linked to preserve responsiveness when stimulus statistics change, with one population maintaining the ability to respond when the other fails.

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Mattis et al (2011). Principles for applying optogenetic tools derived from direct comparative analysis of microbial opsins. Nat. Methods 9(2):159-72.

Diverse optogenetic tools have allowed versatile control over neural activity. Many depolarizing and hyperpolarizing tools have now been developed in multiple laboratories and tested across different preparations, presenting opportunities but also making it difficult to draw direct comparisons. This challenge has been compounded by the dependence of performance on parameters such as vector, promoter, expression time, illumination, cell type and many other variables. As a result, it has become increasingly complicated for end users to select the optimal reagents for their experimental needs. For a rapidly growing field, critical figures of merit should be formalized both to establish a framework for further development and so that end users can readily understand how these standardized parameters translate into performance. Here we systematically compared microbial opsins under matched experimental conditions to extract essential principles and identify key parameters for the conduct, design and interpretation of experiments involving optogenetic techniques.

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Rauschecker et al (2011). Illusions of visual motion elicited by electrical stimulation of human MT complex. PLoS One. 6(7):e21798.

Human cortical area MT(+) (hMT(+)) is known to respond to visual motion stimuli, but its causal role in the conscious experience of motion remains largely unexplored. Studies in non-human primates demonstrate that altering activity in area MT can influence motion perception judgments, but animal studies are inherently limited in assessing subjective conscious experience. In the current study, we use functional magnetic resonance imaging (fMRI), intracranial electrocorticography (ECoG), and electrical brain stimulation (EBS) in three patients implanted with intracranial electrodes to address the role of area hMT(+) in conscious visual motion perception. We show that in conscious human subjects, reproducible illusory motion can be elicited by electrical stimulation of hMT(+). These visual motion percepts only occurred when the site of stimulation overlapped directly with the region of the brain that had increased fMRI and electrophysiological activity during moving compared to static visual stimuli in the same individual subjects. Electrical stimulation in neighboring regions failed to produce illusory motion. Our study provides evidence for the sufficient causal link between the hMT(+) network and the human conscious experience of visual motion. It also suggests a clear spatial relationship between fMRI signal and ECoG activity in the human brain.

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Schaich Borg et al (2011). Neural Basis of moral verdict and moral deliberation. Soc Neurosci 6(4):398-413.

How people judge something to be morally right or wrong is a fundamental question of both the sciences and the humanities. Here we aim to identify the neural processes that underlie the specific conclusion that something is morally wrong. To do this, we introduce a novel distinction between "moral deliberation," or the weighing of moral considerations, and the formation of a "moral verdict," or the commitment to one moral conclusion. We predict and identify hemodynamic activity in the bilateral anterior insula and basal ganglia that correlates with committing to the moral verdict "this is morally wrong" as opposed to "this is morally not-wrong," a finding that is consistent with research from economic decision-making. Using comparisons of deliberation-locked vs. verdict-locked analyses, we also demonstrate that hemodynamic activity in high-level cortical regions previously implicated in morality--including the ventromedial prefrontal cortex, posterior cingulate cortex, and temporoparietal junction--correlates primarily with moral deliberation as opposed to moral verdicts. These findings provide new insights into what types of processes comprise the enterprise of moral judgment, and in doing so point to a framework for resolving why some clinical patients, including psychopaths, may have intact moral judgment but impaired moral behavior.

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Steinmetz and Moore (2012). Lumping and splitting the neural circuitry of visual attention. Neuron 73(3):410-2.

Shifts of gaze and of covert attention rely on tightly linked yet divergent neural mechanisms. In this issue of Neuron, Gregoriou et al. (2012) provide interesting evidence that different functional classes of neurons within the frontal eye field contribute uniquely to these two functions.

Personal Note: Contains an excellent pun.

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Tye et al (2011). Amygdala circuitry mediating reversible and bidirectional control of anxiety. Nature 471: 358-362.

Anxiety—a sustained state of heightened apprehension in the absence of immediate threat—becomes severely debilitating in disease states¹. Anxiety disorders represent the most common of psychiatric diseases (28% lifetime prevalence)² and contribute to the aetiology of major depression and substance abuse^3, 4. Although it has been proposed that the amygdala, a brain region important for emotional processing^{5, 6, 7, 8}, has a role in anxiety^{9, 10, 11, 12, 13}, the neural mechanisms that control anxiety remain unclear. Here we explore the neural circuits underlying anxiety-related behaviours by using optogenetics with two-photon microscopy, anxiety assays in freely moving mice, and electrophysiology. With the capability of optogenetics^14, 15, 16 to control not only cell types but also specific connections between cells, we observed that temporally precise optogenetic stimulation of basolateral amygdala (BLA) terminals in the central nucleus of the amygdala (CeA)—achieved by viral transduction of the BLA with a codon-optimized channelrhodopsin followed by restricted illumination in the downstream CeA—exerted an acute, reversible anxiolytic effect. Conversely, selective optogenetic inhibition of the same projection with a third-generation halorhodopsin¹⁵(eNpHR3.0) increased anxiety-related behaviours. Importantly, these effects were not observed with direct optogenetic control of BLA somata, possibly owing to recruitment of antagonistic downstream structures. Together, these results implicate specific BLA–CeA projections as critical circuit elements for acute anxiety control in the mammalian brain, and demonstrate the importance of optogenetically targeting defined projections, beyond simply targeting cell types, in the study of circuit function relevant to neuropsychiatric disease.

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Villeda et al (2011). The ageing systemic milieu negatively regulates neurogenesis and cognitive function. Nature 477(7362):90-4.

In the central nervous system, ageing results in a precipitous decline in adult neural stem/progenitor cells and neurogenesis, with concomitant impairments in cognitive functions. Interestingly, such impairments can be ameliorated through systemic perturbations such as exercise. Here, using heterochronic parabiosis we show that blood-borne factors present in the systemic milieu can inhibit or promote adult neurogenesis in an age-dependent fashion in mice. Accordingly, exposing a young mouse to an old systemic environment or to plasma from old mice decreased synaptic plasticity, and impaired contextual fear conditioning and spatial learning and memory. We identify chemokines--including CCL11 (also known as eotaxin)--the plasma levels of which correlate with reduced neurogenesis in heterochronic parabionts and aged mice, and the levels of which are increased in the plasma and cerebrospinal fluid of healthy ageing humans. Lastly, increasing peripheral CCL11 chemokine levels in vivo in young mice decreased adult neurogenesis and impaired learning and memory. Together our data indicate that the decline in neurogenesis and cognitive impairments observed during ageing can be in part attributed to changes in blood-borne factors.

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Wang et al (2012). Axon degeneration: molecular mechanisms of a self-destructive pathway. J Cell Biol 196(1):7-18.

Axon degeneration is a characteristic event in many neurodegenerative conditions including stroke, glaucoma, and motor neuropathies. However, the molecular pathways that regulate this process remain unclear. Axon loss in chronic neurodegenerative diseases share many morphological features with those in acute injuries, and expression of the Wallerian degeneration slow (WldS) transgene delays nerve degeneration in both events, indicating a common mechanism of axonal self-destruction in traumatic injuries and degenerative diseases. A proposed model of axon degeneration is that nerve insults lead to impaired delivery or expression of a local axonal survival factor, which results in increased intra-axonal calcium levels and calcium-dependent cytoskeletal breakdown.

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Non-First Author Papers

Abilez et al (2011). Multiscale computations models for optogenetic control of cardiac function. Biophys J 101(6):1326-34.

The ability to stimulate mammalian cells with light has significantly changed our understanding of electrically excitable tissues in health and disease, paving the way toward various novel therapeutic applications. Here, we demonstrate the potential of optogenetic control in cardiac cells using a hybrid experimental/computational technique. Experimentally, we introduced channelrhodopsin-2 into undifferentiated human embryonic stem cells via a lentiviral vector, and sorted and expanded the genetically engineered cells. Via directed differentiation, we created channelrhodopsin-expressing cardiomyocytes, which we subjected to optical stimulation. To quantify the impact of photostimulation, we assessed electrical, biochemical, and mechanical signals using patch-clamping, multielectrode array recordings, and video microscopy. Computationally, we introduced channelrhodopsin-2 into a classic autorhythmic cardiac cell model via an additional photocurrent governed by a light-sensitive gating variable. Upon optical stimulation, the channel opens and allows sodium ions to enter the cell, inducing a fast upstroke of the transmembrane potential. We calibrated the channelrhodopsin-expressing cell model using single action potential readings for different photostimulation amplitudes, pulse widths, and frequencies. To illustrate the potential of the proposed approach, we virtually injected channelrhodopsin-expressing cells into different locations of a human heart, and explored its activation sequences upon optical stimulation. Our experimentally calibrated computational toolbox allows us to virtually probe landscapes of process parameters, and identify optimal photostimulation sequences toward pacing hearts with light.

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Anikeeva et al (2011). Optetrode: a multichannel readout for optogenetic control in freely moving mice. Nat. Neurosci  15(1): 163-70.

Recent advances in optogenetics have improved the precision with which defined circuit elements can be controlled optically in freely moving mammals; in particular, recombinase-dependent opsin viruses, used with a growing pool of transgenic mice expressing recombinases, allow manipulation of specific cell types. However, although optogenetic control has allowed neural circuits to be manipulated in increasingly powerful ways, combining optogenetic stimulation with simultaneous multichannel electrophysiological readout of isolated units in freely moving mice remains a challenge. We designed and validated the optetrode, a device that allows for colocalized multi-tetrode electrophysiological recording and optical stimulation in freely moving mice. Optetrode manufacture employs a unique optical fiber-centric coaxial design approach that yields a lightweight (2 g), compact and robust device that is suitable for behaving mice. This low-cost device is easy to construct (2.5 h to build without specialized equipment). We found that the drive design produced stable high-quality recordings and continued to do so for at least 6 weeks following implantation. We validated the optetrode by quantifying, for the first time, the response of cells in the medial prefrontal cortex to local optical excitation and inhibition, probing multiple different genetically defined classes of cells in the mouse during open field exploration.

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Bader et al (2011). Mouse model of Timothy syndrome recapitulates triad of autistic traits. PNAS 108(37):15432-7.

Autism and autism spectrum disorder (ASD) typically arise from a mixture of environmental influences and multiple genetic alterations. In some rare cases, such as Timothy syndrome (TS), a specific mutation in a single gene can be sufficient to generate autism or ASD in most patients, potentially offering insights into the etiology of autism in general. Both variants of TS (the milder TS1 and the more severe TS2) arise from missense mutations in alternatively spliced exons that cause the same G406R replacement in the Ca(V)1.2 L-type calcium channel. We generated a TS2-like mouse but found that heterozygous (and homozygous) animals were not viable. However, heterozygous TS2 mice that were allowed to keep an inverted neomycin cassette (TS2-neo) survived through adulthood. We attribute the survival to lowering of expression of the G406R L-type channel via transcriptional interference, blunting deleterious effects of mutant L-type channel overactivity, and addressed potential effects of altered gene dosage by studying Ca(V)1.2 knockout heterozygotes. Here we present a thorough behavioral phenotyping of the TS2-neo mouse, capitalizing on this unique opportunity to use the TS mutation to model ASD in mice. Along with normal general health, activity, and anxiety level, TS2-neo mice showed markedly restricted, repetitive, and perseverative behavior, altered social behavior, altered ultrasonic vocalization, and enhanced tone-cued and contextual memory following fear conditioning. Our results suggest that when TS mutant channels are expressed at levels low enough to avoid fatality, they are sufficient to cause multiple, distinct behavioral abnormalities, in line with the core aspects of ASD.

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Byers et al (2011). SNCA triplication Parkinson's patient's iPSC-derived DA neurons accumulate α-synuclein and are susceptible to oxidative stress. PLoS One 6(11):e26159.

Parkinson's disease (PD) is an incurable age-related neurodegenerative disorder affecting both the central and peripheral nervous systems. Although common, the etiology of PD remains poorly understood. Genetic studies infer that the disease results from a complex interaction between genetics and environment and there is growing evidence that PD may represent a constellation of diseases with overlapping yet distinct underlying mechanisms. Novel clinical approaches will require a better understanding of the mechanisms at work within an individual as well as methods to identify the specific array of mechanisms that have contributed to the disease. Induced pluripotent stem cell (iPSC) strategies provide an opportunity to directly study the affected neuronal subtypes in a given patient. Here we report the generation of iPSC-derived midbrain dopaminergic neurons from a patient with a triplication in the α-synuclein gene (SNCA). We observed that the iPSCs readily differentiated into functional neurons. Importantly, the PD-affected line exhibited disease-related phenotypes in culture: accumulation of α-synuclein, inherent overexpression of markers of oxidative stress, and sensitivity to peroxide induced oxidative stress. These findings show that the dominantly-acting PD mutation is intrinsically capable of perturbing normal cell function in culture and confirm that these features reflect, at least in part, a cell autonomous disease process that is independent of exposure to the entire complexity of the diseased brain.

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De Lecea et al (2012). Shining Light on Wakefulness and Arousal. Biol Psychiatry.

Alterations in arousal states are associated with multiple neuropsychiatric disorders, including generalized anxiety disorders, addiction, schizophrenia, and depression. Therefore, elucidating the neurobiological mechanisms controlling the boundaries between arousal, hyperarousal, and hypoarousal is a crucial endeavor in biological psychiatry. Substantial research over several decades has identified distinct arousal-promoting neural populations in the brain; however, how these nuclei act individually and collectively to promote and maintain wakefulness and various arousal states is unknown. We have recently applied optogenetic technology to the repertoire of techniques used to study arousal. Here, we discuss the recent results of these experiments and propose future use of this approach as a way to understand the complex dynamics of neural circuits controlling arousal and arousal-related behaviors.

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Goshen et al (2011). Dynamics of retrieval strategies for remote memories. Cell 147(3):678-89.

Prevailing theory suggests that long-term memories are encoded via a two-phase process requiring early involvement of the hippocampus followed by the neocortex. Contextual fear memories in rodents rely on the hippocampus immediately following training but are unaffected by hippocampal lesions or pharmacological inhibition weeks later. With fast optogenetic methods, we examine the real-time contribution of hippocampal CA1 excitatory neurons to remote memory and find that contextual fear memory recall, even weeks after training, can be reversibly abolished by temporally precise optogenetic inhibition of CA1. When this inhibition is extended to match the typical time course of pharmacological inhibition, remote hippocampus dependence converts to hippocampus independence, suggesting that long-term memory retrieval normally depends on the hippocampus but can adaptively shift to alternate structures. Further revealing the plasticity of mechanisms required for memory recall, we confirm the remote-timescale importance of the anterior cingulate cortex (ACC) and implicate CA1 in ACC recruitment for remote recall.

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Grabrucker et al (2011). Amyloid beta protein-induced zinc sequestration leads to synaptic loss via dysregulation of the ProSAP2/Shank3 scaffold. Mol Neurodegener 6:65.

BACKGROUND: Memory deficits in Alzheimer's disease (AD) manifest together with the loss of synapses caused by the disruption of the postsynaptic density (PSD), a network of scaffold proteins located in dendritic spines. However, the underlying molecular mechanisms remain elusive. Since it was shown that ProSAP2/Shank3 scaffold assembly within the PSD is Zn2+-dependent and that the amyloid beta protein (Aβ) is able to bind Zn2+, we hypothesize that sequestration of Zn2+ ions by Aβ contributes to ProSAP/Shank platform malformation.

RESULTS: To test this hypothesis, we designed multiple in vitro and in vivo assays demonstrating ProSAP/Shank dysregulation in rat hippocampal cultures following Aβ oligomer accumulation. These changes were independent from alterations on ProSAP/Shank transcriptional level. However, application of soluble Aβ prevented association of Zn2+ ions with ProSAP2/Shank3 in a cell-based assay and decreased the concentration of Zn2+ clusters within dendrites. Zn2+ supplementation or saturation of Aβ with Zn2+ ions prior to cell treatment was able to counter the effects induced by Aβ on synapse density and ProSAP2/Shank3 levels at the PSD. Interestingly, intracellular Zn2+ levels in APP-PS1 mice and human AD hippocampus are reduced along with a reduction in synapse density and synaptic ProSAP2/Shank3 and Shank1 protein levels.

CONCLUSIONS: We conclude that sequestration of Zn2+ ions by Aβ significantly contributes to changes in ProSAP2/Shank3 platforms. These changes in turn lead to less consolidated (mature) synapses reflected by a decrease in Shank1 protein levels at the PSD and decreased synapse density in hippocampal neurons.

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Greer et al (2011). Transgenerational epigenetic inheritance of longevity in Caenorhabditis elegans. Nature 479(7373):365-71.

Chromatin modifiers regulate lifespan in several organisms, raising the question of whether changes in chromatin states in the parental generation could be incompletely reprogrammed in the next generation and thereby affect the lifespan of descendants. The histone H3 lysine 4 trimethylation (H3K4me3) complex, composed of ASH-2, WDR-5 and the histone methyltransferase SET-2, regulates Caenorhabditis elegans lifespan. Here we show that deficiencies in the H3K4me3 chromatin modifiers ASH-2, WDR-5 or SET-2 in the parental generation extend the lifespan of descendants up until the third generation. The transgenerational inheritance of lifespan extension by members of the ASH-2 complex is dependent on the H3K4me3 demethylase RBR-2, and requires the presence of a functioning germline in the descendants. Transgenerational inheritance of lifespan is specific for the H3K4me3 methylation complex and is associated with epigenetic changes in gene expression. Thus, manipulation of specific chromatin modifiers only in parents can induce an epigenetic memory of longevity in descendants.

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Liang et al (2011). Signaling via the prostaglandin E₂ receptor EP4 exerts neuronal and vascular protection in a mouse model of cerebral ischemia. J Clin Invest. 121(11):4362-71.

Stroke is the third leading cause of death in the United States. Fewer than 5% of patients benefit from the only intervention approved to treat stroke. Thus, there is an enormous need to identify new therapeutic targets. The role of inducible cyclooxygenase (COX-2) activity in stroke and other neurologic diseases is complex, as both activation and sustained inhibition can engender cerebral injury. Whether COX-2 induces cerebroprotective or injurious effects is probably dependent on which downstream prostaglandin receptors are activated. Here, we investigated the function of the PGE2 receptor EP4 in a mouse model of cerebral ischemia. Systemic administration of a selective EP4 agonist after ischemia reduced infarct volume and ameliorated long-term behavioral deficits. Expression of EP4 was robust in neurons and markedly induced in endothelial cells after ischemia-reperfusion, suggesting that neuronal and/or endothelial EP4 signaling imparts cerebroprotection. Conditional genetic inactivation of neuronal EP4 worsened stroke outcome, consistent with an endogenous protective role of neuronal EP4 signaling in vivo. However, endothelial deletion of EP4 also worsened stroke injury and decreased cerebral reperfusion. Systemic administration of an EP4 agonist increased levels of activated eNOS in cerebral microvessels, an effect that was abolished with conditional deletion of endothelial EP4. Thus, our data support the concept of targeting protective prostaglandin receptors therapeutically after stroke.

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Liu et al (2012). Parkinson's Disease-Associated Kinase PINK1 Regulates Miro Protein Level and Axonal Transport of Mitochondria. PLoS Genetics 8(3): e1002537.

Mutations in Pten-induced kinase 1 (PINK1) are linked to early-onset familial Parkinson's disease (FPD). PINK1 has previously been implicated in mitochondrial fission/fusion dynamics, quality control, and electron transport chain function. However, it is not clear how these processes are interconnected and whether they are sufficient to explain all aspects of PINK1 pathogenesis. Here we show that PINK1 also controls mitochondrial motility. In Drosophila, downregulation of dMiro or other components of the mitochondrial transport machinery rescued dPINK1 mutant phenotypes in the muscle and dopaminergic (DA) neurons, whereas dMiro overexpression alone caused DA neuron loss. dMiro protein level was increased in dPINK1 mutant but decreased in dPINK1 or dParkin overexpression conditions. In Drosophila larval motor neurons, overexpression of dPINK1 inhibited axonal mitochondria transport in both anterograde and retrograde directions, whereas dPINK1 knockdown promoted anterograde transport. In HeLa cells, overexpressed hPINK1 worked together with hParkin, another FPD gene, to regulate the ubiquitination and degradation of hMiro1 and hMiro2, apparently in a Ser-156 phosphorylation-independent manner. Also in HeLa cells, loss of hMiro promoted the perinuclear clustering of mitochondria and facilitated autophagy of damaged mitochondria, effects previously associated with activation of the PINK1/Parkin pathway. These newly identified functions of PINK1/Parkin and Miro in mitochondrial transport and mitophagy contribute to our understanding of the complex interplays in mitochondrial quality control that are critically involved in PD pathogenesis, and they may explain the peripheral neuropathy symptoms seen in some PD patients carrying particular PINK1 or Parkin mutations. Moreover, the different effects of loss of PINK1 function on Miro protein level in Drosophila and mouse cells may offer one explanation of the distinct phenotypic manifestations of PINK1 mutants in these two species.

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Osterhout et al (2011). Cadherin-6 mediates axon-target matching in a non-image-forming visual circuit. Neuron 71(4):632-9.

Neural circuits consist of highly precise connections among specific types of neurons that serve a common functional goal. How neurons distinguish among different synaptic targets to form functionally precise circuits remains largely unknown. Here, we show that during development, the adhesion molecule cadherin-6 (Cdh6) is expressed by a subset of retinal ganglion cells (RGCs) and also by their targets in the brain. All of the Cdh6-expressing retinorecipient nuclei mediate non-image-forming visual functions. A screen of mice expressing GFP in specific subsets of RGCs revealed that Cdh3-RGCs which also express Cdh6 selectively innervate Cdh6-expressing retinorecipient targets. Moreover, in Cdh6-deficient mice, the axons of Cdh3-RGCs fail to properly innervate their targets and instead project to other visual nuclei. These findings provide functional evidence that classical cadherins promote mammalian CNS circuit development by ensuring that axons of specific cell types connect to their appropriate synaptic targets.

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Pasca et al (2011). Using iPSC-derived neurons to uncover cellular phenotypes associated with Timothy syndrome. Nat. Med 17(12):1657-62.

Monogenic neurodevelopmental disorders provide key insights into the pathogenesis of disease and help us understand how specific genes control the development of the human brain. Timothy syndrome is caused by a missense mutation in the L-type calcium channel Ca(v)1.2 that is associated with developmental delay and autism. We generated cortical neuronal precursor cells and neurons from induced pluripotent stem cells derived from individuals with Timothy syndrome. Cells from these individuals have defects in calcium (Ca(2+)) signaling and activity-dependent gene expression. They also show abnormalities in differentiation, including decreased expression of genes that are expressed in lower cortical layers and in callosal projection neurons. In addition, neurons derived from individuals with Timothy syndrome show abnormal expression of tyrosine hydroxylase and increased production of norepinephrine and dopamine. This phenotype can be reversed by treatment with roscovitine, a cyclin-dependent kinase inhibitor and atypical L-type-channel blocker. These findings provide strong evidence that Ca(v)1.2 regulates the differentiation of cortical neurons in humans and offer new insights into the causes of autism in individuals with Timothy syndrome.

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Paz et al (2011). A new mode of corticothalamic transmission revealed in the Gria4(-/-) model of absence epilepsy. Nat. Neuro 14(9):1167-73.

Cortico-thalamo-cortical circuits mediate sensation and generate neural network oscillations associated with slow-wave sleep and various epilepsies. Cortical input to sensory thalamus is thought to mainly evoke feed-forward synaptic inhibition of thalamocortical (TC) cells via reticular thalamic nucleus (nRT) neurons, especially during oscillations. This relies on a stronger synaptic strength in the cortico-nRT pathway than in the cortico-TC pathway, allowing the feed-forward inhibition of TC cells to overcome direct cortico-TC excitation. We found a systemic and specific reduction in strength in GluA4-deficient (Gria4(-/-)) mice of one excitatory synapse of the rhythmogenic cortico-thalamo-cortical system, the cortico-nRT projection, and observed that the oscillations could still be initiated by cortical inputs via the cortico-TC-nRT-TC pathway. These results reveal a previously unknown mode of cortico-thalamo-cortical transmission, bypassing direct cortico-nRT excitation, and describe a mechanism for pathological oscillation generation. This mode could be active under other circumstances, representing a previously unknown channel of cortico-thalamo-cortical information processing.

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Sussillo et al (2012). A recurrent neural network for closed-loop intracortical brain-machine interface decoders. J Neural Eng. 19;9(2):026027.

Recurrent neural networks (RNNs) are useful tools for learning nonlinear relationships in time series data with complex temporal dependences. In this paper, we explore the ability of a simplified type of RNN, one with limited modifications to the internal weights called an echostate network (ESN), to effectively and continuously decode monkey reaches during a standard center-out reach task using a cortical brain-machine interface (BMI) in a closed loop. We demonstrate that the RNN, an ESN implementation termed a FORCE decoder (from first order reduced and controlled error learning), learns the task quickly and significantly outperforms the current state-of-the-art method, the velocity Kalman filter (VKF), using the measure of target acquire time. We also demonstrate that the FORCE decoder generalizes to a more difficult task by successfully operating the BMI in a randomized point-to-point task. The FORCE decoder is also robust as measured by the success rate over extended sessions. Finally, we show that decoded cursor dynamics are more like naturalistic hand movements than those of the VKF. Taken together, these results suggest that RNNs in general, and the FORCE decoder in particular, are powerful tools for BMI decoder applications.

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Sweeney et al (2011). Secreted semaphorins from degenerating larval ORN axons direct adult projection neuron dendrite targeting. Neuron 72(5):734-47.

During assembly of the Drosophila olfactory circuit, projection neuron (PN) dendrites prepattern the developing antennal lobe before the arrival of axons from their presynaptic partners, the adult olfactory receptor neurons (ORNs). We previously found that levels of transmembrane Semaphorin-1a, which acts as a receptor, instruct PN dendrite targeting along the dorsolateral-ventromedial axis. Here we show that two secreted semaphorins, Sema-2a and Sema-2b, provide spatial cues for PN dendrite targeting. Sema-2a and Sema-2b proteins are distributed in gradients opposing the Sema-1a protein gradient, and Sema-1a binds to Sema-2a-expressing cells. In Sema-2a and Sema-2b double mutants, PN dendrites that normally target dorsolaterally in the antennal lobe mistarget ventromedially, phenocopying cell-autonomous Sema-1a removal from these PNs. Cell ablation, cell-specific knockdown, and rescue experiments indicate that secreted semaphorins from degenerating larval ORN axons direct dendrite targeting. Thus, a degenerating brain structure instructs the wiring of a developing circuit through the repulsive action of secreted semaphorins.

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Taniguchi et al (2011). Function of prostaglandin E2 EP receptors in the acute outcome of rodent hypoxic ischemic encephalopathy. Neurosci Lett 504(3):185-90.

Neonatal hypoxic-ischemic encephalopathy (HIE) is a leading cause of severe and permanent neurologic disability after birth. The inducible cyclooxygenase COX-2, which along with COX-1 catalyzes the first committed step in prostaglandin (PG) synthesis, elicits significant brain injury in models of cerebral ischemia; however its downstream PG receptor pathways trigger both toxic and paradoxically protective effects. Here, we investigated the function of PGE(2) E-prostanoid (EP) receptors in the acute outcome of hypoxic-ischemic (HI) injury in the neonatal rat. We determined the temporal and cellular expression patterns of the EP1-4 receptors before and after HIE and tested whether modulation of EP1-4 receptor function could protect against cerebral injury acutely after HIE. All four EP receptors were expressed in forebrain neurons and were induced in endothelial cells after HIE. Inhibition of EP1 signaling with the selective antagonist SC-51089 or co-activation of EP2-4 receptors with the agonist misoprostol significantly reduced HIE cerebral injury 24 h after injury. These receptor ligands also protected brain endothelial cells subjected to oxygen glucose deprivation, suggesting that activation of EP receptor signaling is directly cytoprotective. These data indicate that the G-protein coupled EP receptors may be amenable to pharmacologic targeting in the acute setting of neonatal HIE.

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Witten et al (2011). Recombinase-driver rat lines: tools, techniques, and optogenetic application to dopamine-mediated reinforcement. Neuron 72(5):721-33.

Currently there is no general approach for achieving specific optogenetic control of genetically defined cell types in rats, which provide a powerful experimental system for numerous established neurophysiological and behavioral paradigms. To overcome this challenge we have generated genetically restricted recombinase-driver rat lines suitable for driving gene expression in specific cell types, expressing Cre recombinase under the control of large genomic regulatory regions (200-300 kb). Multiple tyrosine hydroxylase (Th)::Cre and choline acetyltransferase (Chat)::Cre lines were produced that exhibited specific opsin expression in targeted cell types. We additionally developed methods for utilizing optogenetic tools in freely moving rats and leveraged these technologies to clarify the causal relationship between dopamine (DA) neuron firing and positive reinforcement, observing that optical stimulation of DA neurons in the ventral tegmental area (VTA) of Th::Cre rats is sufficient to support vigorous intracranial self-stimulation (ICSS). These studies complement existing targeting approaches by extending the generalizability of optogenetics to traditionally non-genetically-tractable but vital animal models.

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Yizhar et al (2011). Neocortical excitation/inhibition balance in information processing and social dysfunction. Nature 477(7363):171-8.

Severe behavioural deficits in psychiatric diseases such as autism and schizophrenia have been hypothesized to arise from elevations in the cellular balance of excitation and inhibition (E/I balance) within neural microcircuitry. This hypothesis could unify diverse streams of pathophysiological and genetic evidence, but has not been susceptible to direct testing. Here we design and use several novel optogenetic tools to causally investigate the cellular E/I balance hypothesis in freely moving mammals, and explore the associated circuit physiology. Elevation, but not reduction, of cellular E/I balance within the mouse medial prefrontal cortex was found to elicit a profound impairment in cellular information processing, associated with specific behavioural impairments and increased high-frequency power in the 30-80 Hz range, which have both been observed in clinical conditions in humans. Consistent with the E/I balance hypothesis, compensatory elevation of inhibitory cell excitability partially rescued social deficits caused by E/I balance elevation. These results provide support for the elevated cellular E/I balance hypothesis of severe neuropsychiatric disease-related symptoms.

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Yoo et al (2011). MicroRNA-mediated conversion of human fibroblasts to neurons. Nature 476(7359):228-31.

Neurogenic transcription factors and evolutionarily conserved signalling pathways have been found to be instrumental in the formation of neurons. However, the instructive role of microRNAs (miRNAs) in neurogenesis remains unexplored. We recently discovered that miR-9* and miR-124 instruct compositional changes of SWI/SNF-like BAF chromatin-remodelling complexes, a process important for neuronal differentiation and function. Nearing mitotic exit of neural progenitors, miR-9* and miR-124 repress the BAF53a subunit of the neural-progenitor (np)BAF chromatin-remodelling complex. After mitotic exit, BAF53a is replaced by BAF53b, and BAF45a by BAF45b and BAF45c, which are then incorporated into neuron-specific (n)BAF complexes essential for post-mitotic functions. Because miR-9/9* and miR-124 also control multiple genes regulating neuronal differentiation and function, we proposed that these miRNAs might contribute to neuronal fates. Here we show that expression of miR-9/9* and miR-124 (miR-9/9*-124) in human fibroblasts induces their conversion into neurons, a process facilitated by NEUROD2. Further addition of neurogenic transcription factors ASCL1 and MYT1L enhances the rate of conversion and the maturation of the converted neurons, whereas expression of these transcription factors alone without miR-9/9*-124 was ineffective. These studies indicate that the genetic circuitry involving miR-9/9*-124 can have an instructive role in neural fate determination.

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Zhang et al (2011). The Microbial Opsin Family of Optogenetic Tools. Cell  147(7): 1446-57.

The capture and utilization of light is an exquisitely evolved process. The single-component microbial opsins, although more limited than multicomponent cascades in processing, display unparalleled compactness and speed. Recent advances in understanding microbial opsins have been driven by molecular engineering for optogenetics and by comparative genomics. Here we provide a Primer on these light-activated ion channels and pumps, describe a group of opsins bridging prior categories, and explore the convergence of molecular engineering and genomic discovery for the utilization and understanding of these remarkable molecular machines.

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Rapid dynamics of hippocampal spatial representation in echolocating bats

For a recent neuroscience journal club, I presented several papers on echolocating bats. Under the premise that “bats are awesome” (F. Collman, personal communication), what follows are the major points from my presentation. The slideshow below contains parts of my presentation including figures from several relevant papers. A disclaimer – I will be vastly oversimplifying the research, and presenting only a fraction of what the authors discovered and discussed. For less concise descriptions of the research in question, interested persons should read the appropriate papers. The hippocampus is a region of the brain critically important for episodic and spatial memory. Patients without their hippocampi (like the famous patient H.M.) cannot form new episodic memories. Patient case studies such as H.M’s sparked a keen interest in the hippocampus amongst neuroscientists, and there have been great strides in elucidating the neural circuitry within the hippocampus. The question of exactly how that neural circuitry encodes episodic and spatial memory is a matter for many lines of ongoing research and much debate.

One well described phenomenon within the hippocampus, that may play a critical role in the spatial component of spatial memory formation, are hippocampal neurons termed “place cells”. These neurons are driven when the animal passes through a particular region of its environment. Earlier work in rodents demonstrated that when an animal is placed within a particular environment, its place cells tile the entire area, tracking the animal’s movements. The spatial region that any given place cell (called the “place field”) encodes is flexible – changes to the environment (i.e. moving landmarks, changing wall colors, altering odors) will alter the place field. Introducing an animal into a brand new environment will cause an individual place cell to generate a new place field, however returning that animal to the old environment will recall the original place field. Theoretically, the location information provided by place cells could be utilized in the generation of memories. Place cells fire as you move through the world, and the order in which the population fires could be stored as a memory of movement through space. Exactly how this storage could be achieved, and where in the brain it takes place, is the subject of many ongoing research projects. It’s also not what the rest of this post will be about.

Instead, we’ll turn to a slightly different question – one of how sensory information influences the structure of the place fields. Another persistent research question is what exact inputs generate the place field. It seems like common sense that sensory information would play some role in establishing and maintaining the place field, and in causing a place cell to fire as the animal moved through the appropriate place field. As I mentioned about, it is known that altering the sensory information within the environment will cause place cells to change their fields. However, these changes occurred over long time scales (the order of minutes to days). Researchers from the University of Maryland were interested in much quicker changes in place fields – namely, how place cells responded to newly arrived sensory information. Do place cells rapidly alter their fields based on temporally precise sensory events?

To answer this question, the researchers, Nachum Ulanovsky and Cynthia Moss turned to the big brown bat (Eptesicus fuscus). These echolocating bats, sized approximately 10 cm, produce echolocation calls on average once every 260 ms, which the bats preferentially use to provide sensory information about their environment. These calls, the authors reasoned, were the perfect sensory event with which they could investigate the possibility that the spatial precision of a place field is rapidly altered by sensory information. As a first step, the authors conclusively demonstrated place cells within the bat hippocampus; recording place fields while bats crawled along an angled wall, using echolocation to hunt for food (Ulanovsky and Moss, 2007). They then looked closely at the activity of place cells immediately after each echolocation call, and discovered that as time passed following a call, place fields got bigger (see Ulanovsky and Moss, 2011). In other words, after an echolocation call, place cell was pickier about the precise spatial region through which a bat had to move in order for that place cell to fire. This enhanced spatial precision lasted for ~ 300 ms after each call, demonstrating for the first time, rapid changes in hippocampal place fields tied to the influx of sensory information. The time constants of these changes (~300 ms) are much more rapid than those previously reported, which were on the order of seconds.

[slideshare id=11261716&doc=echolocationblogpresentation-120125174833-phpapp01]

Take home message:

Place cells can rapidly integrate incoming sensory information, tuning the spatial selectivity of their place cells to match the spatial acuity of the new information. The spatial selectivity decays between sonar calls as the animal has to rely on less accurate sensory information (or even do without any sensory information, depending on the availability of and preference for non-echolocation based sensory information).

What does this mean for non-bats? The research does make some interesting predictions for rodent or primate studies – namely that quickly providing visual information (perhaps by rapidly flashing on a strobe light) would lead to similar rapid place cell dynamics. However, whether the varying acuity of sensory information provides ongoing regulation of place fields in a more physiological context, is unclear. For example, animals with fovea (such as humans and non-human primates) can increase the acuity of visual information for a particular region of space by directing their fovea towards that region. Similarly, the process of attention is characterized by enhancements in the neural representations of sensory information. How these might influence the spatial selectivity of place fields remains an open question, as does the effect of rapid place field dynamics on the creation of spatial and episodic memory.

Ulanovsky and Moss (2007). Hippocampal cellular and network activity in freely moving echolocating bats. Nat. Neurosci 10(2): 224-233.

Ulanovsky and Moss (2011). Dynamics of hippocampal spatial representation in echolocating bats. Hippocampus 21:150-161.

An Open Letter to Michael Keller

Mr. Keller: As Publisher of both the Stanford University Press and HighWire Press (a division of the Stanford University Libraries), you understand the value of the free and broad dissemination of knowledge.

You must also appreciate the threat that the Research Works Act (HR 3699) poses to the open exchange of ideas. This exchange is central to scientific progress and is the most fundamental means the scientific community has to return the public investment on our research. In limiting access to publicly-funded research, this act stands against the stated mission of both Stanford University Press and HighWire Press, as well as the motto of Stanford University itself.

I therefore urge you to join other respected members of the Association of American Publishers, including AAAS, the MIT Press, and the University of California Press, in publicly stating their opposition to the Research Works Act.

Sincerely, Kelly Zalocusky

PhD Candidate Stanford University Neuroscience Program

-------------------------------------------------------------

In case Mr. Keller is not an avid NeuroBlog reader, I have also sent him the letter directly. I encourage my fellow NeuroBlog readers to do the same. Really, truly--feel free to copy, paste, and send this exact letter. Michael A. Keller can be reached at Michael.Keller@Stanford.edu

Admin Note:

As a colleague and fellow PhD Candidate at Stanford University, I whole-heartedly agree Ms. Zalocusky's sentiments, and I applaude her for speaking out against the Research Works Act (HR 3699). I hope that readers will join with us in contacting both members of the American Association of Publishers, as well as our elected representatives in national government, in protest of the Research Works Act.

Astra Bryant

PhD Candidate Stanford University Neuroscience Program

Stanford At SfN11 - Wednesday Schedule

For those of you still at SfN11 on Wednesday, be sure to visit the final posters from Stanford Neuroscience.

The Stanford Neuroscience affiliates presenting their research on Wednesday, Nov 16 are:

Posters

2:00-3:00 pm: Helen Bronte-Stewart

Program#/Poster#: 888.06/AA34

Title: Evidence for alpha and beta band hypersynchrony at rest in the GPi in generalized dystonia and its attenuation during high frequency GPi DBS in DYT3+ dystonia

Location: Hall A-C

4:00-5:00 pm: Corrina Darian-Smith

Program#/Poster#: 917.04/SS4

Title: Alterations to corticospinal projections following dorsal rhizotomy in the macaque monkey

Location: Hall A-C

Stanford at SfN11 - Tuesday Schedule

What has the Stanford Neuroscience community been up to? Find out by visiting our presentations and posters at SfN2011!

The Stanford Neuroscience affiliates presenting their research on Tuesday, Nov 15 are:

Presentations

9:10-9:45 am: Rob Malenka

Title: Function and plasticity of distinct subtypes of dopamine neurons

Location: Ballroom A

Posters

8:00-9:00 am: Cora Ames (Shenoy Lab)

Program#/Poster#: 591.17/MM25

Title: Neural dynamics of movement execution following incomplete or incorrect planning

Location: Hall A-C

4:00-5:00 pm: Izumi Toyoda (Buckmaster Lab)

Program#/Poster#: 672.04/Y3

Title: Possible mini-seizures in a rat model of temporal lobe epilepsy

Location: Hall A-C

Stanford at SfN11 - Monday Schedule

What has the Stanford Neuroscience community been up to? Find out by visiting our presentations and posters at SfN2011!

The Stanford Neuroscience affiliates presenting their research on Monday, Nov 14 are:

Presentations

10:15-10:35 am: Marius Wernig

Title: Novel reprogramming methods and ways to bypass the pluripotent state by directly converting non-neuronal somatic cells into functional neurons

Location: Ballroom B

Posters

8:00-9:00 am: Brittany Burrows

Program#/Poster#: 405.13/YY63

Title: Effects of reward and FEF microstimulation on choice and visually guided saccades during a free-choice task

Location: Hall A-C

9:00-10:00 am: Lynette Foo (Barres Lab)

Program#/Poster#: 330.02/A32

Title: Development of a novel method to purify and culture rodent astrocytes

Location: Hall A-C

9:00-10:00 am: Nick Steinmetz (Moore and Boahen lab)

Program#/Poster#: 379.06/OO26

Title: Pattern of presaccadic modulation of visual responses in macaque V4 measured simultaneously across cortical layers

Location: Hall A-C

10:00-11:00 am: Gary Steinberg

Program#/Poster#: 362.19/EE19

Title: Functional engraftment of CHR2-expressing human neural stem cells in experimental model of stroke

Location: Hall A-C

1:00-2:00 pm: Andreas Rauschecker

Program#/Poster#: 486.01/OO11

Title: Position-sensitivity in the VWFA measured using fMRI pattern-classification and intracranial recordings in humans

Location: Hall A-C

2:00-3:00 pm: Josef Parvizi

Program#/Poster#: 486.02/OO12

Title: Ventral occipito-temporal circuits for word form recognition elucidated using subdural electrode recordings in humans

Location: Hall A-C

Stanford at SFN11: Sunday Schedule

What has the Stanford Neuroscience community been up to? Find out by visiting our presentations and posters at SFN2011! The Stanford Neuroscience affiliates presenting their research on Sunday, Nov 13 are:

Presentations

8:30-8:45 am: Matt Kaufman (Krishna Shenoy lab)

Title: Changes of mind in a decision-making maze task in monkey

Location: 146A

10:15-10:35 am : Sam McClure

Title: Behavioral implications of relative value coding in the human brain

Location: 207B

1:45-2:00 pm: David Kastner (Stephen Baccus lab)

Title: Mechanism and circuitry underlying retinal sensitization

Location: 152B

Posters

8:00-9:00 am: Mehrdad Shamloo

Program#/Poster#: 152.01/W7

Title: Xamoterol rescues memory deficit in mouse model of down syndrome by activation of beta-1 adrenergic receptor.

Location: Hall A-C

9:00-10:00 am: Jake Rinaldi (Jennifer Raymod lab)

Program#/Poster#: 183.14/QQ25

Title: Climbing fiber activity as an error signal for VOR motor learning

Location: Hall A-C

10:00-11:00 am: Paul Buckmaster

Program#/Poster#: 154.03/Y18

Title: Temporal lobe epilepsy in California sea lions.

Location: Hall A-C

1:00-2:00 pm: Lisa Gunaydin (Karl Deisseroth lab)

Program#/Poster#: 306.05/YY16

Title: Bidirectional modulation of social behavior by optogenetic tuning of mesolimbic dopamine circuitry

Location: Hall A-C

1:00-2:00 pm: Emily Ferenczi (Karl Deisseroth lab)

Program#/Poster#: 306.09/YY20

Title: Stability of optogenetic tool deactivation kinetics under varying stimulation conditions

Location: Hall A-C

2:00-3:00 pm: Kelsey Clark (Tirin Moore lab)

Program#/Poster#: 272.18/JJ23

Title: Role of dopamine-mediated activity in the frontal eye field in spatial working memory

Location: Hall A-C

2:00-3:00 pm: Rohit Prakash (Karl Deisseroth lab)

Program#/Poster#: 306.10/YY21

Title: Development of two-photon optogenetic control by integrating optics with molecular engineering

Location: Hall A-C

3:00-4:00 pm: Lief Fenno (Karl Deisseroth lab)

Program#/Poster#: 306.07/YY18

Title: Combinatorial optogenetics with integrated spectral and temporal control

Location: Hall A-C

3:00-4:00 pm: Dan O'Shea (Krishna Shenoy lab)

Program#/Poster#: 306.11/YY22

Title: Optogenetic control of excitatory neurons via a red-shifted opsin in primate premotor cortex

Location: Hall A-C

4:00-5:00 pm: Joanna Mattis (Karl Deisseroth lab)

Program#/Poster#: 306.12/YY23

Title: Principles for optogenetics derived from direct comparative analysis of microbial opsins

Location: Hall A-C