Molecular mechanisms contributing to long-lasting synaptic plasticity at the temporoammonic-CA1 synapse

The hippocampus and the nearby medial temporal lobe structures are required for the formation, consolidation, and retrieval of episodic memories. Sensory information enters the hippocampus via two inputs from entorhinal cortex (EC): One input (perforant path) makes synapses on the dendrites of dentate granule cells as the first set of synapses in the trisynaptic circuit, the other (temporoammonic; TA) makes synapses on the distal dendrites of CAl neurons. Here we demonstrate that TA-CAl synapses undergo both early- and late-phase long-term potentiation (LTP) in rat hippocampal slices. LTP at TA-CAl synapses requires both NMDA receptor and voltage-gated Ca2+ channel activity. Furthermore, TA-CAl LTP is insensitive to the blockade of fast inhibitory transmission (GABA(A)-mediated) and, interestingly, is dependent on GABA(B)-dependent slow inhibitory transmission. These findings indicate that the TA-CAl synapses may rely on a refined modulation of inhibition to exhibit LTP.