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Acetylcholine (ACh) regulates network operation in the hippocampus by controlling excitation and inhibition in rat CA1 pyramidal neurons (PCs), the latter through gamma-aminobutyric acid type-A receptors (GABA  A  Rs). Although, the enhancing effects of ACh on GABA  A  Rs have been reported ( Dominguez et al., 2014 ,  2015 ), its role in regulating tonic GABA A  inhibition has not been explored in depth. Therefore, we aimed at determining the effects of the activation of ACh receptors on responses mediated by synaptic and extrasynaptic GABA A Rs. Here, we show that under blockade of ionotropic glutamate receptors ACh, acting through muscarinic type 1 receptors, paired with post-synaptic depolarization induced a long-term enhancement of tonic GABA  A   currents (  t  GABA  A  ) and puff-evoked GABA  A   currents (  p  GABA A ). ACh combined with depolarization also potentiated IPSCs (i.e., phasic inhibition) in the same PCs, without signs of interactions of synaptic responses with   p  GABA A  and   t  GABA A , suggesting the contribution of two different GABA A  receptor pools. The long-term enhancement of GABA A  currents and IPSCs reduced the excitability of PCs, possibly regulating plasticity and learning in behaving animals.

Muscarinic Long-Term Enhancement of Tonic and Phasic GABAA Inhibition in Rat CA1 Pyramidal Neurons