Prolonged stimulation of presynaptic nicotinic acetylcholine receptors in the rat interpeduncular nucleus has differential effects on transmitter release.

Alterations in nicotinic acetylcholine (nAChR) receptor number can be induced by chronic exposure to nicotine possibly by stabilization of the desensitized state(s) of the receptor. Since within the central nervous system (CNS), many nAChRs are localized presynaptically, we have investigated the physiological consequences of prolonged nicotine applications on spontaneous transmitter release. In the presence of glutamate receptor antagonists, bicuculline-sensitive spontaneous GABA inhibitory synaptic currents (IPSCs) could be readily resolved in whole-cell recordings from neurons in the interpeduncular nucleus (IPN) maintained as brain slices.