Excitatory postsynaptic potential

better.

So the typical parameters you sort of then they had like between connections between say two layer four cells that included both sort of like the typical synaptic weights based on sort of like looking at this paired recordings of EPSPs or like this synaptic potentials and so on.

Okay.

And then also another key thing is sort of like the noise level, right? Because there are synapses, which are not obviously the inputs from the first model, 31,000 neurons.

The pathophysiology of NORSE can be broken into why the brain starts seizing and why it becomes self-perpetuating.

Recall that a normal neuron operates with the balance between inhibitory postsynaptic potentials, IPSPs, which are largely GABAergic, and excitatory postsynaptic potentials, EPSPs, which are largely glutamatergic.

Seizures occur essentially when runaway excitation overwhelms inhibition.

Interestingly, in just minutes, synaptic GABA receptors will get internalized, and M- NMDA receptors are trafficked up to the surface, ramping up glutamatergic excitation.

The neuron has to reach threshold, that minus fifty-five millivolt mark, before it fires.

So what happens is that multiple EPSPs and IPSPs arrive at the same neuron and their effects add up.

This is summation.

There are two types.

Temporal summation is when multiple signals from the same presynaptic neuron arrive in rapid succession and their effects accumulate over time.

Spatial summation is when signals from multiple different presynaptic neurons arrive simultaneously, and their combined effect pushes the postsynaptic neuron toward threshold.

If the net effect of all the EPSPs minus all the IPSPs is enough to reach minus fifty-five millivolts, an action potential fires.

If not, it doesn't.