Long-term synaptic plasticity in hippocampal interneurons

Hippocampal interneurons express at least two forms of activity-dependent long-term potentiation (LTP) at glutamatergic synapses.One form ('Hebbian' LTP) depends on N-methyl-D-aspartate (NMDA) receptors and has similar induction and expression mechanisms to the LTP that takes place in pyramidal cells.However, different Ca2+–calmodulin-dependent kinases (acting downstream from NMDA receptors) from those that mediate LTP induction in pryamidal cells mediate LTP induction in interneurons.The other form of LTP ('anti-Hebbian' LTP) depends on Ca2+-permeable AMPA receptors, but not NMDA receptors. The voltage-dependent conductance of these receptors allows Ca2+ flow during negative membrane potentials but not during depolarisation. Metabotropic glutamate receptors also contribute to the induction of NMDA receptor-independent LTP.Neither form of LTP spreads to afferent pathways that were inactive during induction. Because interneurons do not have profuse dendritic spines, this observation argues against an obligatory role for spines in preventing the spread of LTP.Both forms of LTP have their counterparts in two complementary forms of long-term depression (LTD).NMDA receptor-dependent LTP and LTD appear to be expressed postsynaptically. NMDA receptor-independent LTP and LTD appear to be expressed presynaptically.Different forms of plasticity occur at distinct synapses in the hippocampus and greatly expand the computational capacity of hippocampal networks.