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Intracellular studies of heterosynaptic long-term depression (LTD) in CA1 of hippocampal slices

โœ Scribed by Michael F. Barry; R.M. Vickery; S.R. Bolsover; Lynn J. Bindman


Publisher
John Wiley and Sons
Year
1996
Tongue
English
Weight
602 KB
Volume
6
Category
Article
ISSN
1050-9631

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โœฆ Synopsis


Heterosynaptic LTD is a persisting, activity-dependent decrease in synaptic efficacy that occurs at inactive synapses when postsynaptic depolarization and firing are initiated via another afferent pathway. The induction of heterosynaptic LTD is therefore non-associative, in contrast to the Hebbian induction of long-term potentiation (LTP).

Several ideas about the functional importance of heterosynaptic LTD have been proposed. LTD was envisaged by Dunwiddie and Lynch (1978) to be a counterbalance to LTP by preventing maximal potentiation of every synapse, and also to amplify the effect of LTP in some inputs by reducing the potency of others. The latter concept is analogous to surround inhibition in the sensory system, but at the level of the single cell rather than involving interneurons, and having an important temporal dimension. The functional implications of LTD have been further elaborated to include limiting postsynaptic excitation to prevent neurological disorders such as epilepsy, and forming a substrate for forgetting at previously potentiated synapses (Christie et al., 1994). In addition, models of learning in neural networks (see Brown et al., 1990) have made use of heterosynaptic LTD a5 well as LTP to regulate the changes in synaptic weight.

Evidence of a convincingly large heterosynaptic LTD exists for the dentate and CA3 regions of the hippocampus, while in CA1 heterosynaptic LTD has been an elusive, and sometimes a seemingly illusory, phenomenon to study in vitro. A number of laboratories failed to record heterosynaptic LTD of field excitatory postsynaptic potentials (fepsps) in CA1, observing at most transient decreases lasting up to 15 min in transmission at unstimulated stratum radiatum synapses after tetanic stimulation of an independent pathway (see Paulsen et al., 1993;Debanne et al., 1994; Christie et al., 1994, for references).


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