ANOXIC LTP SHEDS LIGHT ON THE MULTIPLE FACETS OF NMDA RECEPTORS

Hippocampal neurones in the CA1 region have become a model system to s tudy the mechanisms of long-term potentiation (LTP) and memory process es. The CA1 region is also highly vulnerable to ischaemic or anoxic ep isodes which induce a selective and delayed degeneration of pyramidal neurones. In CA1 neurones, anoxic episodes generate a novel form of LT P to which we refer as anoxic LTP. In common with tetanic LTP, the ind uction of anoxic LTP is voltage- and NMDA receptor-dependent. However in contrast with tetanic LTP, the expression of anoxic LTP is mediated exclusively by NMDA receptors. These observations suggest that anoxic -ischaemic episodes trigger a switch in favour of NMDA receptor-operat ed synaptic transmission. We suggest that the multiple forms of NMDA r eceptor-dependent LTPs are determined by extracellular and intracellul ar modulatory sites of this receptor.