A Synaptic Plasticity Twofer: Synaptic distance and Glutamatergic exclusivity

1) In synaptic plasticity is there will be any change in the synaptic distance ?
2) I read many papers stating that AMPA receptors essential for synaptic plasticity. So does it mean synaptic plasticity is restricted only to the neurons which have glutamate as neurotransmitter?
— Venkatesh (NBRC, India)

Thank you for your questions! For those of you reading along, synaptic plasticity refers primarily to the ability of neural circuits, specifically the synaptic connections between them, to change with experience and/or neural activity. Usually, these changes involve alterations in the number of postsynaptic receptors trafficked to a synapse, the probability of releasing neurotransmitter at the presynaptic terminal when an action potential comes along, or larger structural/functional changes in the density of synaptic connections. I don't recall ever seeing any studies showing that the distance between synapses changes in synaptic plasticity. However, your intuition is correct about the importance of spatial factors: the volume of a postsynaptic dendritic spine, for example, is often thought of as a correlate of synaptic strength and maturity, and can change with experience and activity. So the answer is that, to the best of my knowledge, synaptic distance doesn't change, but other spatial factors like volume, or density of synaptic connections certainly do.

As to your second question, synaptic plasticity comes in several varieties, and AMPA receptors and glutamate are just one that happens to be relatively extensively characterized. One of the most well-studied model systems for synaptic plasticity is long term potentiation (LTP) and depression (LTD) at CA3->CA1 synapse of the hippocampus, which is glutamatergic and involves trafficking AMPA receptors to and from the synapse to change synaptic strength. However, this is far from the only form of synaptic plasticity. Even some glutamatergic neurons in the cerebral cortex don't use AMPA receptors for LTD, instead changing their synaptic strength by altering the probability of presynaptic neurotransmitter release. Plasticity occurs all over the brain, in neurons with a variety of different transmitters. Synapses from GABA-ergic cells can undergo their own version of LTD in the cortex and cerebellum, and there are synaptic learning mechanisms that are influenced or predominated by dopamine, acetylcholine, and other neurotransmitters. So not everything in the brain involves AMPA receptors and glutamate, they just happen to be part of the system we know the most about.