What's wrong with Hebbian synapse models?

[David]

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
modern-day emendations:

(REFERENCE 1 OF 3)
94253824

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)
94110789

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)
95023993
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.