The effect of quisqualic acid-induced lesions of the nucleus basalis magnocellularis on latent inhibition

• Published in: Brain research bulletin 1996, Vol.41 (5), p.313-317
• Main Authors: ROCHFORD, J, SEN, A. P, ROUSSE, I, WELNER, S. A
• Format: Article
• Language: English
• Subjects: Acetylcholinesterase - metabolism; Anatomical correlates of behavior; Animals; Basal Ganglia - drug effects; Basal Ganglia - enzymology; Basal Ganglia - pathology; Behavioral psychophysiology; Biological and medical sciences; Cerebral Cortex - enzymology; Cerebral Cortex - pathology; Choline O-Acetyltransferase - metabolism; Conditioning, Classical - drug effects; Conditioning, Operant - physiology; Excitatory Amino Acid Agonists - toxicity; Fundamental and applied biological sciences. Psychology; Histocytochemistry; Male; Psychology. Psychoanalysis. Psychiatry; Psychology. Psychophysiology; Quisqualic Acid - toxicity; Rats; Rats, Sprague-Dawley
• ISSN: 0361-9230; 1873-2747
• DOI: 10.1016/S0361-9230(96)00191-8

Latent inhibition (LI) is a reduction in the rate of acquisition of a Pavlovian conditioned response that results from prior nonreinforced preexposure to a conditioned stimulus (CS). LI has been suggested to reflect the operation of mechanisms involved in stimulus selection for subsequent cognitive processing. The present experiment was conducted to assess the effect of bilateral lesions of the nucleus basalis magnocellularis (NBM) on LI employing a conditioned emotional response paradigm. Bilateral lesions of the NBM were produced by administration of 0.12 M quisqualic acid and resulted in decreased cortical acetylcholinesterase staining, as well as a 40% reduction in cortical choline acetyltransferase activity. Following lever press training, preexposed animals received 40 presentations of a 60-s tone CS. Nonpreexposed animals received no tone presentations. Acquisition of conditioned suppression was then assessed over the course of 4 tone-shock (0.6 mA, 0.5 s) pairings. Control, preexposed animals displayed a retarded rate of acquisition in comparison to nonpreexposed controls, thereby demonstrating that the parameters used in the present experiment produced LI. In contrast, lesioned animals preexposed to the CS acquired conditioned suppression as readily as nonpreexposed lesioned animals. However, the acquisition of conditioned suppression in both lesioned groups was found to be similar to that displayed in the preexposed control group. This pattern of results was interpreted as being attributable to a lesion-induced impairment in the ability to maintain stimulus processing, rather than a deficit in the ability to filter a stimulus.