title: Unilateral AMPA lesions of nucleus basalis magnocellularis induce a sensorimotor deficit which is differentially altered by arecoline and nicotine.
abstract: 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.
authors.affiliation: Department of Psychology, Institute of Psychiatry, Denmark Hill, London, UK.
authors.forename: F A
authors.initials: FA
authors.lastname: Abdulla
authors.forename: M R
authors.initials: MR
authors.lastname: Calaminici
authors.forename: J D
authors.initials: JD
authors.lastname: Stephenson
authors.forename: J D
authors.initials: JD
authors.lastname: Sinden
mesh_terms: D000344:Afferent Pathways / Q000187:drug effects / Q000502:physiology; D000661:Amphetamine / Q000494:pharmacology; D000818:Animals; D001115:Arecoline / Q000494:pharmacology*; D001931:Brain Mapping; D002799:Cholinergic Fibers / Q000187:drug effects* / Q000502:physiology; D004292:Dominance, Cerebral / Q000187:drug effects* / Q000502:physiology; D008297:Male; D009538:Nicotine / Q000494:pharmacology*; D009949:Orientation / Q000187:drug effects / Q000502:physiology; D011597:Psychomotor Performance / Q000187:drug effects* / Q000502:physiology; D051381:Rats; D017207:Rats, Sprague-Dawley; D011950:Receptors, Cholinergic / Q000187:drug effects* / Q000502:physiology; D011984:Sensory Receptor Cells / Q000187:drug effects / Q000502:physiology; D012903:Smell / Q000187:drug effects / Q000502:physiology; D013239:Stereotyped Behavior / Q000187:drug effects / Q000502:physiology; D013377:Substantia Innominata / Q000187:drug effects* / Q000502:physiology; D018350:alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid / Q000494:pharmacology*
chemical_list: D011950:Receptors, Cholinergic; D001115:Arecoline; D009538:Nicotine; D018350:alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid; D000661:Amphetamine