Nitric oxide and hippocampal synaptic plasticity

Abstract

The dependence of NMDA receptor-dependent LTP on postsynaptic depolarization and increases in postsynaptic calcium, coupled with evidence supporting presynaptically mediated increases in transmitter release accompanying LTP, suggest that a retrograde transsynaptic messenger participates in the synaptic enhancement. Although many questions remain unanswered, the available evidence suggests a role for NO as such a messenger in certain LTP paradigms. It is unclear, however, whether NO contributes to LTP under differing experimental conditions and whether other messengers, acting in concert with or independent of NO, contribute to a retrograde signalling system. Furthermore, the conditions under which NMDA receptor activation, postsynaptic calcium increases and NO contribute to synaptic enhancement, synaptic depression and excitotoxic neuronal injury need to be clarified. Furthermore, efforts aimed at clarifying the molecular targets of NO must remain a priority of this line of research.