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From: cs012133@brunix (Jonathan Stone)
Newsgroups: comp.ai.neural-nets
Subject: Re: wanted: neurobiology references
Summary: EPSPs, not MEPPs
Message-ID: <4724@brunix.UUCP>
Date: 24 Apr 89 19:06:17 GMT
References: <4486@psuvax1.cs.psu.edu> <17450@cup.portal.com> <545@hydra.gatech.EDU>
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Reply-To: cs012133@cslab3a.UUCP (Jonathan Stone)
Organization: Brown University Department of Computer Science
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In article <545@hydra.gatech.EDU> carter@sloth.gatech.edu (Carter Bullard) writes:
>into the synaptic cleft.  Because the recipient (post synaptic) neuron
>has receptors on its outer membrane that respond to the neurotransmitter,
>small deformations in the electrical potential of the target neuron occur.
>These are called miniature excitatory (or inhibitory) postsynaptic
>potentials (MEPPs).  These electrical changes propagate along the membrane,
>similar to ripples on a waters surface.  The axon hillock, which is a
>specialized area on the surface of the cell body of a neuron, can act as a
>capacitor, of sorts, in that it can "summate" the potential changes over
>time.  It is thought that the threshold for excitation originates at the
>axon hillock, but this is not always the case, as the entire membrane of
>the neuron has the ability to start a nerve action potential.  The axon
>hillock is generally responsible for summating MEPPs.

I think there is a little confusion here. I learned that MEPP stands for Miniature End-Plate Potential, in reference to the variation in potential of the MEP (Motor End-Plate, where a neuron joins a muscle fiber) caused by the release of a packet of acetylcholine by a motor neuron.  What the writer meant to say is EPSP (and IPSP), which means what he said MEPP means, minus the miniature.

Also, the specialization necessary to initiate (or sustain) a self-propagating action potential is the presence of voltage-gated sodium channels, which I do not believe are located anywhere but along the axon (and at its start). To say that the hillock summates over time is inaccurate because I don't think it waits...it simply samples the potential as soon as it is able (a set time period after the previous AP) and fires whenever the potential rises above threshold.  The summation is done at the INPUT site





 in that if a second input arrives before the effect of the first has dissipated, the effect of the  second will be added to that of the first. It is obvious if you understand the underlying mechanisms.

As far as synaptic weight, there is presently much debate over the biochemical mechanism, with several recent advances. It will probably be solved when the mechanism is discovered for how weights are changed. Previously, the hot answer was change in shape of the dendritic spine, but now it seems that the NMDA receptor as well as the molecule CaM-Kinase are the mediating factors (though their effect may simply be to change the shape of the spine). The big debate now, though, is whether anti-Hebbian learning





 is pre-not-post or post-not-pre.

Hebbian learning occurs when the presynaptic neuron effectively causes the postsynaptic neuron to fire--both are depolarized (active) simultaneously: the connection between the two is strengthened. However, ANTI-Hebbian learning, or weakening of the synapse, occurs under uncertain conditions. Whether this occurs when the presynaptic cell fires but not the post, or when the postsynaptic cell fires but not the pre, is the topic that most interests my teacher, Mark Bear, who currently favors pre-not-post.  Cr





ap, I'm late for class--sorry, but I hope this much helps the discussion.