ian@omega.theory.cs.psu.edu (Ian Parberry) (04/21/89)
At NIPS last year, one of the workshop attendees told me that, assuming one
models neurons as performing a discrete or analog thresholding operation on
weighted sums of its inputs, the summation appears to be done in the axons
and the thresholding in the soma. This interested me because typical neural
network models don't take into account the hardware separation of these
operations, and Berman, Schnitger and myself had discovered (without realizing
the biological connection) that a new neural network model which allows
separation appears to be much more fault-tolerant than the old ones.
It's now time to write up the fault-tolerance result. I'd like to include
some references to "accepted" neurobiological sources which back up the
attendee's observation. Trouble is, I am not a neurobiologist, and do not
know where to look. Can somebody knowledgeable please advise me?
Thanks,
Ian.
-------------------------------------------------------------------------------
Ian Parberry
"Bureaucracy is expanding to meet the needs of an expanding bureaucracy"
ian@theory.cs.psu.edu ian@psuvax1.BITNET ian@psuvax1.UUCP (814) 863-3600
Dept of Comp Sci, 333 Whitmore Lab, Penn State Univ, University Park, Pa 16802mmm@cup.portal.com (Mark Robert Thorson) (04/22/89)
I was taught, 10 years ago, that action potentials are believed to originate at the axon hillock, which might be considered the transition between the axon and the soma (cell body). See FROM NEURON TO BRAIN by Kuffler and Nichols (Sinauer 1976), page 349. I would expect synaptic weights to be proportional to the axon circumference where it joins the cell body, but I have no evidence to support that belief.
mmm@cup.portal.com (Mark Robert Thorson) (04/23/89)
> I would expect synaptic weights to be proportional to the axon circumference > where it joins the cell body, but I have no evidence to support that belief. Opps, I meant "dendrite circumference", of course. And now that I think about it, that's wrong too. I was taught that there are two kinds of conduction in nerves cells, "electrotonic" and "propagative". The former might be described as an electrolytic and resistive form of conduction, while the latter involves action potentials originating in the axon hillock. When the professor said this, I immediately asked, "Do you ever see propagative conduction in dendrites?" He said yes, and drew a diagram of a neuron with a long axon and several dendrites, one of which was as long as the axon. He then proceeded to shade in both the axon and the long dendrite with colored chalk to indicate where propagative conduction took place.
boothe@mathcs.emory.edu (Ronald Boothe {guest}) (04/23/89)
In article <17490@cup.portal.com> mmm@cup.portal.com (Mark Robert Thorson) writes: >> I would expect synaptic weights to be proportional to the axon circumference >> where it joins the cell body, but I have no evidence to support that belief. > >Opps, I meant "dendrite circumference", of course. And now that I think >about it, that's wrong too. I was taught that there are two kinds of >conduction in nerves cells, "electrotonic" and "propagative". The former >might be described as an electrolytic and resistive form of conduction, >while the latter involves action potentials originating in the axon hillock. > For most neurons in brain you can probably ignore propagative conduction by dendrites and just consider the effects of electrotonic conduction. This conduction will be dissipated by the space constant of the cell membrane and therefore the input of each synaptic input needs to be weighted by its distance from the axon hillock. In addition, many dendrites have branches and varicosities which can alter the resistance to current flow along the dendrite, so the geometry of the dendrites also must be taken into account. Finally, a majority of excitatory synapses onto dendrites contact specialized anatomical structures called spines. These spines are shaped like mushrooms with the thin stalk projecting from the dendrite, and the synaptic input coming onto the head of the spine. This long thin stalk provides resistance to current flow, so the weight of each synaptic input is also influenced by the length and diameter of the stalk (some think a good biological mechanism for altering the weights of specific inputs is to change the shapes of the spines). There is lots of recent work on this topic in the neuroscience literature. I don't recall specific references right now, but some of the influentual early work was done by W. Rall. A check of the citation index to see who is making reference to the old Rall papers should turn up current literature. -- Ronald Boothe {guest} Emory University, Atlanta, GA ARPA, CSNET: boothe@emory.ARPA BITNET: boothe@emory UUCP: { sun!sunatl, gatech }!emory!boothe
carter@sloth.gatech.edu (Carter Bullard) (04/24/89)
In article <17450@cup.portal.com> mmm@cup.portal.com (Mark Robert Thorson) writes: >I was taught, 10 years ago, that action potentials are believed to originate >at the axon hillock, which might be considered the transition between the >axon and the soma (cell body). See FROM NEURON TO BRAIN by Kuffler >and Nichols (Sinauer 1976), page 349. > >I would expect synaptic weights to be proportional to the axon circumference >where it joins the cell body, but I have no evidence to support that belief. well, the idea of synaptic weights emerged principally from neuropharmacology. It attempted to explain such phenomenon as the changes in the way neurons responded to GABA (gama amino butyric acid) in the presence of valium, the dopaminergic theory of psychosis and why some antipsychotic drugs (chlorpromazine) seemed to work best during the morning, altered responses to visual stimuli, at the cerebellar level, in the presence of amphetamine, in cats, ..... the list goes on. the basic idea is that the transfer of information from one neuron to the next is chemically based. To summarize, as the nerve action potential reaches the "terminal bouton" (that is the collection of synapses that represent the "end" of a neuron), the electrical gradient changes on the membrane of the presynaptic neuron set off a set of reactions that result in the release of chemicals, "neurotransmitters", 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. But the ability for a MEPP to cause a change at the axon hillock is dependant on the distance between the loci of the chemical reaction to the neurotransmitter and the axon hillock, the strength of the MEPP, and the properties of the cell membrane that facilitate the propagation of the MEPP along the membranes surface. This is determined by many factors, but the topology of the neuron is, indeed, important. However, the principle contributors to synaptic weight are generally thought to be biochemically based. These include such properties as, the amount of neurotransmitter that is released from the presynaptic neuron, the number of receptors that are available on the postsynaptic neuron, the effectiveness of the transmitter to create a MEPP, the duration of the neurotransmitter/receptor association, and the effectiveness of the postsynaptic membrane to propagate the MEPP. The amount of neurotransmitter released with any given nerve action potential is not constant with time, as the transmitter pool that is available for release is limited. The history of excitation of a neuron is important, since neurotransmitters can be depleted with repeated excitation. This is transmitter exhaustion, and is a real phenomenon that can be demonstrated experimentally and clinically. The factors that determine presynaptic neurotransmitter availabilty are generally described with 4th or 5th order non-linear differential equations, depending on whether you consider the variations in diet or not. The number of receptors that are available on the postsynaptic neuron, their effectiveness to respond to chemical stimuli, and the rate of receptor turnover has been the subject of pharmacological study for over 50 years, and is rather complicated. The best models are 3rd and 4th order differential equations, where the history of excitation is a prominent factor. The ability for the postsynaptic nerve membrane to propagate the MEPPs to the axon hillock is also dependent on the history of excitation. Sooooooo, the number of historical dependants on synaptic weight can be considered to be rather high. The topology of the nerve is not that variable, but the biochemical aspects of nerve function are extremely variable. It is probably this and a great deal of other factors, such as the role of glial cells on neuronal functionality, that contribute the greatest to the "weights" of a particular neuronal event. Carter Bullard School of Information & Computer Science, Georgia Tech, Atlanta GA 30332 uucp: ...!{decvax,hplabs,ihnp4,linus,rutgers}!gatech!carter Internet: carter@gatech.edu
cs012133@brunix (Jonathan Stone) (04/25/89)
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.
g523116166ea@deneb.ucdavis.edu (0040;0000008388;0;327;142;) (04/26/89)
A useful review of electrotonic ("cable-core) models for neural
conduction is J. Jack, et al, _Electric Current Flow in Excitable
Cells_, Oxford U. Press, 1975. Only a little dated, and the clarity of
its presentation more than compensates.
A current review of the neural spine phenomenon and some of the
modelling is in R. Coss and D. Perkel, "The Function of Dendritic
Spines: A review of Theoretical Issues", Behavioral and Neural Biology
(44)151-185, 1985. Coss was my PhD advisor, and I did most of the
modelling in his lab. Major problem wasn't technical but interpretive,
I thought: we don't know a neural system in which the spine swelling
could be meaningful (analytically, that is- lots of qualitative
speculation). Spine swelling is suggestive and we did fascinating
natural history studes: e.g., we let young honeybees out of their hive
for the first time to conduct their first flight and to learn all the
cues for returning home safely. We recovered them and popped, freeze-
dried, and sliced their brains for neuromorphometry. The spine
population after this one-trial learning was significantly skewed to
more swollen shapes. Other studies have used cichlid fish and ground
squirrels. Marion Diamond (UCB) probably could comment on any human
data.
Hopefully helpfully...
====
R. Goldthwaite rogoldthwaite@{deneb.}ucdavis.edu
Psychology and Animal Behavior/evolution, U.California, Davis, 95616
"Genetic algorithms: designer genes make new niches"
new PhD: postdocs/job possibilities welcome!