NICOTINIC CHOLINERGIC NORMALIZATION OF AMPHETAMINE-INDUCED LOSS OF AUDITORY GATING IN FREELY MOVING RATS

The impairment in normal sensory processing which is usually observed in schizophrenics has been demonstrated using a paired-stimulus paradi gm. Normal individuals show a diminished midlatency evoked potential r esponse to the second of a pair of clicks given at a 0.5-s interval. T his phenomenon is termed auditory ''gating''. Schizophrenics routinely fail to suppress their response to the second click in this paradigm; thus, they do not gate. Heavy tobacco use is common among schizophren ics and it has recently been shown that nicotine causes a transient no rmalization of auditory gating in these individuals. Our laboratory ha s been utilizing animal models to investigate the sensory deficit obse rved in schizophrenia. In the present study rats were administered amp hetamine to produce a schizophrenia-like loss of auditory gating. They were then given nicotine, which resulted in a dose-dependent normaliz ation of the amphetamine-induced loss of gating. This effect was block ed by concurrent central administration of d-tubocurarine. Neither nic otine nor d-tubocurarine had any effect on auditory gating when admini stered alone. These data are in agreement with the human studies showi ng normalization of auditory gating with nicotine administration and s uggest a possible role for the nicotinic cholinergic receptor in the m odulation of auditory gating in the rat model.