Abstract
Inhibitory synapses through GABAergic channels not only change spine's calcium dynamics but also modulate postsynaptic current mediated through glutamate receptors. However the mechanism and extent to which these inhibitory synapses can modulate postsynaptic potential is not clearly understood. We propose a mathematical model to explain this phenomenon which encompasses both presynaptic and postsynaptic mechanisms. Further this model also elaborates the effect of these channels in synaptic calcium dynamics and learning mechanism.
Highlights
One of the fundamental properties of nervous system is modifiable synaptic connections
When an action potential arrives at the presynaptic membrane, it produces an influx of calcium ions through voltage-dependent calcium channels
These calcium ions bind to these vesicles allowing them to fuse with the presynaptic membrane and release neurotransmitters into synaptic cleft through the fusion pores present on the membrane surface
Summary
One of the fundamental properties of nervous system is modifiable synaptic connections. Electrical synapse consists of a group of gap junctions occurring close together, while chemical synapse on the other hand, depends on the influx and efflux of specific types of proteins, called neurotransmitters These neurotransmitters are enclosed in small membrane bound spheres called synaptic vesicles inside the presynaptic cells. When an action potential arrives at the presynaptic membrane, it produces an influx of calcium ions through voltage-dependent calcium channels These calcium ions bind to these vesicles allowing them to fuse with the presynaptic membrane and release neurotransmitters into synaptic cleft through the fusion pores present on the membrane surface. These transmitters move freely through the cleft and eventually arrive at the postsynaptic membrane. These spines are femto-liter size protoplasmic protrusion and serve as the loci of synaptic plasticity [13, 29]
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