Neuronal nicotinic receptors modulate synaptic function in the hippocampus and are sensitive to blockade by the convulsant strychnine and by the anti-Parkinson drug amantadine

Evidence is provided that rapid application of nicotinic agonists to CA1 interneurons in hippocampal slices can trigger responses with at least one of three components: (i) whole-cell currents due to activation of nicotinic receptors (nAChRs) on the neuron under study; (ii) fast current transients representing back-propagating action potentials; and (iii) post-synaptic currents mediated by γ-aminobutyric acid (GABA) released from presynaptic neurons by activation of preterminal nAChRs. The use of the α7-nAChR-selective agonist choline and of nAChR-subtype-selective antagonists led to the conclusion that these responses can be mediated by α7 or α4β2 nAChRs. Experiments carried out in cultured hippocampal neurons demonstrated that the evoked GABA release can also be reduced by activation of these receptors, and showed that the convulsant strychnine is a competitive antagonist of α7 nAChRs and a non-competitive antagonist of α4β2 nAChRs, whereas the anti-Parkinson drug amantadine is a non-competitive antagonist of α7, α4β2, and α3β4 nAChRs. Copyright (C) 1998 Elsevier Science Ireland Ltd. All rights reserved.