UNILATERAL AMPA LESIONS OF NUCLEUS BASALIS MAGNOCELLULARIS INDUCE A SENSORIMOTOR DEFICIT WHICH IS DIFFERENTIALLY ALTERED BY ARECOLINE AND NICOTINE

One week after unilateral alpha-amino-3-hydroxy-5-methyl-4-isoxazole p ropionic acid (AMPA) lesions of nucleus basalis magnocellularis, rats showed significant lateralised bias in spontaneous turning and in turn ing induced by tail pinch or by placing the rat on a 45 degrees grid. Turning was biased to the lesioned side and this side also showed incr eased responsiveness to pin-prick stimulation of the skin (somaesthesi a), snout and whisker stimulation and ammonia olfaction. Arecoline (0. 5 mg/kg), at a dose which did not affect responses to sensorimotor sti mulation in sham-operated rats, corrected the lesion-induced biased tu rning to tail pinch and the 45 degrees grid test and reduced the bias in the open field. In contrast, nicotine (0.05 mg/kg), at a dose which also did not substantially affect responses to sensorimotor stimulati on in sham-operated rats, switched the lesion-induced turning bias tow ards the contralateral side. Neither cholinoceptor agonist reduced the lesion-induced increased sensory responsiveness. The effects of nicot ine were blocked by the centrally acting nicotinic antagonist, mecamyl amine (1.0 mg/kg), but not by hexamethonium (1.0 mg/kg), or ondansetro n (0.01 mg/kg). Amphetamine (up to 1.0 mg/kg) did not affect the lesio n-induced motor asymmetry. The results confirm that the basal forebrai n cholinergic system plays a role in sensorimotor cortical functions, but suggest different functional roles for muscarinic and nicotinic re ceptors.