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 propionic acid (AMPA) lesions of nucleus basalis magnocellularis, rats showed significant lateralised bias in spontaneous turning and in turning 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 increased responsiveness to pin-prick stimulation of the skin (somaesthesia), snout and whisker stimulation and ammonia olfaction. Arecoline (0.5 mg/kg), at a dose which did not affect responses to sensorimotor stimulation in sham-operated rats, corrected the lesion-induced biased turning 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 stimulation in sham-operated rats, switched the lesion-induced turning bias towards the contralateral side. Neither cholinoceptor agonist reduced the lesion-induced increased sensory responsiveness. The effects of nicotine were blocked by the centrally acting nicotinic antagonist, mecamylamine (1.0 mg/kg), but not by hexamethonium (1.0 mg/kg), or ondansetron (0.01 mg/kg). Amphetamine (up to 1.0 mg/kg) did not affect the lesion-induced motor asymmetry. The results confirm that the basal forebrain cholinergic system plays a role in sensorimotor cortical functions, but suggest different functional roles for muscarinic and nicotinic receptors.