What's wrong with Hebbian synapse models?
dhe at eden.rutgers.edu
Wed Apr 5 01:03:43 EST 1995
rising at crl.com (Hawley K Rising) writes:
>I am trying to get through a book on large scale neuronal theories (Koch
>and Davis, Large Scale Neuronal Theories of the Brain,1994 MIT Press).
>In the introduction they say that although they've had a pervasive effect
>on models, most theories about brain function don't last a decade. An
>example they give is the Hebbian synapse (synapse strength grows in
>proportion to correlated activity of the pre and post synaptic neurons).
>What was wrong with this theory and can I get a source to read about
>whatever replaced it as acceptable?
As far as I know, the Hebbian synapse is alive and well and embodied
in LTP. A quick search through Medline revealed only a couple of
(REFERENCE 1 OF 3)
Liu Y Fields RD Fitzgerald S Festoff BW Nelson PG
Proteolytic activity, synapse elimination, and the Hebb synapse.
In: J Neurobiol (1994 Mar) 25(3):325-35
The Hebb synapse has been postulated to serve as a mechanism
subserving both regulation of synaptic strength in the adult nervous
system (long-term potentiation and depression) and developmental
activity-dependent plasticity. According to this model, pre- and
postsynaptic temporal concordance of activity results in
strengthening of connections, while discordant activity results in
synapse weakening. Evidence is presented that proteases and protease
inhibitors may be involved in modification of synaptic strength. This
leads to a modification of the Hebb assumptions, namely that
postsynaptic activity results in protease elaboration with a
consequent general reduction of synaptic connections to the active
postsynaptic element. Further, presynaptic activity, if strong
enough, induces local release of a protease inhibitor, such as
protease nexin I, which neutralizes proteolytic activity and produces
a relative preservation of the active input. This formulation
produces many of the effects of the classical Hebbian construction,
but the protease/inhibitor model suggests additional specific
mechanistic features for activity-dependent plasticity.
(REFERENCE 2 OF 3)
Nelson PG Fields RD Yu C Liu Y
Synapse elimination from the mouse neuromuscular junction in vitro: a
non-Hebbian activity-dependent process.
In: J Neurobiol (1993 Nov) 24(11):1517-30
The effect of action potentials on elimination of mouse neuromuscular
junctions (NMJ) was studied in a three-compartment cell culture
preparation. Axons from superior cervical ganglion or ventral spinal
cord neurons in two lateral compartments formed multiple
neuromuscular junctions with muscle cells in a central compartment.
The loss of synapses over a 2-7-day period was determined by serial
electrophysiological recording and a functional assay. Electrical
stimulation of axons from one side compartment during this period,
using 30-Hz bursts of 2-s duration, repeated at 10-s intervals,
caused a significant increase in synapse elimination compared to
unstimulated cultures (p < 0.001). The extent of homosynaptic and
heterosynaptic elimination was comparable, i.e., of the 226
functional synapses of each type studied, 111 (49%) of the synapses
that had been stimulated were eliminated, and 87 (39%) of
unstimulated synapses on the same muscle cells were eliminated. Also,
simultaneous bilateral stimulation caused significantly greater
elimination of synapses than unilateral stimulation (p < 0.005).
These observations are contrary to the Hebbian hypothesis of synaptic
plasticity. A spatial effect of stimulus-induced synapse elimination
was also evident following simultaneous bilateral stimulation. Prior
to stimulation, most muscle cells were innervated by axons from both
side compartments, but after bilateral stimulation, muscle cells were
predominantly unilaterally innervated by axons from the closer
compartment. These experiments suggest that synapse elimination at
the NMJ is an activity-dependent process, but it does not follow
Hebbian or anti-Hebbian rules of synaptic plasticity. Rather,
elimination is a consequence of postsynaptic activation and a
function of location of the muscle cell relative to the neuron. An
interaction between spatial and activity-dependent effects on synapse
elimination could help produce optimal refinement of synaptic
connections during postnatal development.
(REFERENCE 3 OF 3)
Granger R Whitson J Larson J Lynch G
Non-Hebbian properties of long-term potentiation enable high-capacity
encoding of temporal sequences.
In: Proc Natl Acad Sci U S A (1994 Oct 11) 91(21):10104-8
A hypothesis commonly found in biological and computational studies
of synaptic plasticity embodies a version of the 1949 postulate of
Hebb that coactivity of pre- and postsynaptic elements results in
increased efficacy of their synaptic contacts. This general proposal
presaged the identification of the first and still only known long-
lasting synaptic plasticity mechanism, long-term potentiation (LTP).
Yet the detailed physiology of LTP induction and expression differs
in many specifics from Hebb's rule. Incorporation of these
physiological LTP constraints into a simple non-Hebbian network model
enabled development of "sequence detectors" that respond
preferentially to the sequences on which they were trained. The
network was found to have unexpected capacity (e.g., 50 x 10(6)
random sequences in a network of 10(5) cells), which scales linearly
with network size, thereby addressing the question of memory capacity
in brain circuitry of realistic size.
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