GABAergic inhibitory processes and hippocampal long-term potentiation

Long-term potentiation (LIP) is a widely studied form of activity-dependent synaptic plasticity, Hippocampal LIP evoked in the dentate and CA1 areas requires calcium influx through N-methyl-D-aspartate (NMDA) receptor-channel complexes, a process triggered during high-frequency stimulation by conjunctive presynaptic glutamate release and postsynaptic depolarization, It has been suggested that alterations in GABAergic recurrent and/or feedforward inhibitory synaptic transmission may accompany LTP induction in these hippocampal areas, To this end, possible LIP-related modifications in functional inhibition are addressed in the context of both paired-pulse depression and the excitatory postsynaptic potential-spike (E-S) relationship. Consideration is also given as to how GABAergic processes may contribute mechanistically to the induction of NMDA receptor-dependent LTP, It is concluded that although GABAergic disinhibition may contribute to the induction of LTP, it is not yet clear whether or not the induction of LIP has a lasting impact on inhibitory processes.