Abstract
Spike-timing-dependent plasticity (STDP) provides a cellular implementation of the Hebb postulate, which states that synapses, whose activity repeatedly drives action potential firing in target cells, are potentiated. At glutamatergic synapses onto hippocampal and neocortical pyramidal cells, synaptic activation followed by spike firing in the target cell causes long-term potentiation (LTP)—as predicted by Hebb—whereas excitatory postsynaptic potentials (EPSPs) evoked after a spike elicit long-term depression (LTD)—a phenomenon that was not specifically addressed by Hebb. In both instances the action potential in the postsynaptic target neuron is an instructive signal that is capable of supporting synaptic plasticity. STDP generally relies on the propagation of Na+ action potentials that are initiated in the axon hillhock back into the dendrite, where they cause depolarization and boost local calcium influx. However, recent studies in CA1 hippocampal pyramidal neurons have suggested that local calcium spikes might provide a more efficient trigger for LTP induction than backpropagating action potentials. Dendritic calcium spikes also play a role in an entirely different type of STDP that can be observed in cerebellar Purkinje cells. These neurons lack backpropagating Na+ spikes. Instead, plasticity at parallel fiber (PF) to Purkinje cell synapses depends on the relative timing of PF-EPSPs and activation of the glutamatergic climbing fiber (CF) input that causes dendritic calcium spikes. Thus, the instructive signal in this system is externalized. Importantly when EPSPs are elicited before CF activity, PF-LTD is induced rather than LTP. Thus, STDP in the cerebellum follows a timing rule that is opposite to its hippocampal/neocortical counterparts. Regardless, a common motif in plasticity is that LTD/LTP induction depends on the relative timing of synaptic activity and regenerative dendritic spikes which are driven by the instructive signal.
Highlights
We will present recent observations that in CA1 hippocampal pyramidal cells long-term potentiation (LTP) is more sensitive to local dendritic spikes than to backpropagating action potentials that originate in the axon hillhock (Golding et al, 2002)
We will suggest that backpropagating action potentials provide an instructive plasticity signal in the neocortex and hippocampus, and that a similar function is served by the temporal correlation between local dendritic calcium spikes and synaptic activity in Purkinje cells
This study looked at the timing of pre- and postsynaptic activity in more detail, and found that LTP is induced when Excitatory postsynaptic potentials (EPSPs) precede the action potentials by 10 ms, but that application of these stimuli in reverse order results in long-term depression (LTD)
Summary
Hebb’s postulate on synaptic modifications, which was formulated in 1949 in his book “The Organization of Behavior,” has laid the foundation for subsequent experimental work on memory storage by neuronal assemblies (Hebb, 1949):“When an axon of cell A is near enough to excite a cell B and repeatedly or persistently takes part in firing it, some growth process or metabolic change takes place in one or both cells such that A’s efficiency, as one of the cells firing B, is increased.”A more popular version of this rule—assigned to neurobiologist Carla Shatz—says “neurons that fire together wire together.” The discovery of long-term potentiation (LTP) in 1973 demonstrated that synaptic connections can be strengthened in a use-dependent way, reflecting a key prediction of the Hebb postulate (Bliss and Lømo, 1973). We will present recent observations that in CA1 hippocampal pyramidal cells LTP is more sensitive to local dendritic spikes than to backpropagating action potentials that originate in the axon hillhock (Golding et al, 2002).
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