Fig. 2.
Model of the study hypothesis. Acetylcholine activates nAChRs on GABA interneurons in the hippocampus (A), which in turn leads to inhibition of primary hippocampal glutamate neurons. This situation would keep activation of glutamate neurons under check during normal nonlearning or nonremembering situations. Because α7 nAChRs rapidly desensitize, the acetylcholine input to GABA interneurons is reduced (B), and the normally robust GABA output (C) is dramatically reduced (D), thereby releasing the glutamate neuron from GABA inhibition. This disinhibition leads to enhanced glutamate release onto other hippocampal neurons involved in memory and the activation of long-term potentiation, which is an underlying substrate for memory.