Hello. It is already common knowledge that AMPA receptors, upon binding glutamate, become open to Na+ ions wich flow into the neuron, thus causing the membrane to depolarize. Nevertheless, I haven't found one paper clearly explaining what happens in the vicinity of AMPAR and how does this Na+ generated action potential travel across the neuron. Could anybody cast some light on the topic? Thanks in advance!
These 2 articles do a good job going in detail over the events of the action potential generation and propagation:
https://physoc.onlinelibrary.wiley.com/doi/full/10.1111/j.1469-7793.1997.617ba.x
Article Ionic mechanisms underlying human atrial action potential pr...
The AMPA receptors are gated by glutamate allowing sodium to flow that depolarizes the membrane. This generates a slow potential, a decaying depolarization as it travels to adjacent areas of membrane. If that slow potential travels to an area of the membrane where voltage gated Na channels exist, and if the depolarization activated by the AMPA receptor reaches about -55 mV at the volatage gated sodium channel, then the voltage gated sodium channel will activate. Once the voltage gated sodium channel is activated, the membrane depolarizes to about -70 mV. This depolarization to -70 mV will in turn activate surrounding voltage gated sodium channels, bringing the membrane to -70 mV in that region. This depolarization will then activate Na channels in their surrounding region - hence propagation.
Greg Maguire the resting membrane potential is about -70mV, the depolarization makes the cell less electronegative. At -55 sodium channels open, sodium comes in increasing the membrane potential and with action potential (AP) the membrane reaches about +30mV. Once the AP is past the membrane repolarizes, and actually hyperpolarizes (to -90 mV) due to potassium influx.
keeping resting membrane potential in any cell requires a symphony of channel activity regulation (Na/K pump, K-channels...ect). In the brain, there is an additional fine tuning orchestrated by AMPARs and GABARs. A balance of excitation (AMPA) and inhibition (GABA) that also helps to fine tune the firing of APs in the brain. Glutamate released at synaptic cleft might few AMPARs, their activity might sum up just enough to bring up the membrane potential close to an AP threshold in that neuron receiving that synaptic input and will trigger one or maybe a train of APs in that neuron. GABARs activation keeps the membrane voltage hyperpolarised, far from the AP threshold. that's the beautiful balance exerted by these two systems.
Some neurons also have an extra level of regulation involving HCN channels to generate rhythmic activity. You can find these and more in any textbook of cell physiology and neuroscience.
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