Differential effects of 192IgG-saporin and NMDA-induced lesions into the basal forebrain on cholinergic activity and taste aversion memory formation

Gutierrez, Humberto and Gutiérrez, Ranier and Silva-Gandarias, Ricardo and Estrada, Jimena and Miranda, Maria Isabel and Bermúdez-Rattoni, Federico (1999) Differential effects of 192IgG-saporin and NMDA-induced lesions into the basal forebrain on cholinergic activity and taste aversion memory formation. Brain research, 834 (1-2). pp. 136-141. ISSN 0006-8993

Full content URL: http://dx.doi.org/10.1016/S0006-8993(99)01519-X

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Item Type:Article
Item Status:Live Archive

Abstract

Mnemonic deficits resulting from excitotoxic lesion of the basal forebrain have been classically attributed to the resulting depletion of cortical acetylcholine activity. In this study, we have performed a detailed analysis of the cholinergic status of the insular cortex (IC) following local injections of either 192IgG-saporin (192IgG-sap) or N-methyl-D-aspartate (NMDA) directly into the nucleus basalis magnocellularis (NBM). By means of in vivo microdialysis, we show that the immunotoxin lesion results in an almost complete lack of extracellular acetylcholine release, whereas NMDA-induced lesions result in a marginal reduction in cortical cholinergic activity. Choline-acetyltransferase activity in the IC further confirmed this differential pattern of cortical deafferentation. Surprisingly, however, only NMDA-induced lesions showed a strong disruptive effect upon taste aversion learning whereas no detectable deficits could be found following 192IgG-sap lesions. By combining intrabasal injections of 192IgG-sap with acute pre-training infusions of the cholinergic antagonist scopolamine into the IC, a strong disruption of taste aversion was attained. These results imply that residual cholinergic activity, following 192IgG-saporin lesions, might be still critical for normal cortical mediation of memory processing. They also support the role of basal forebrain in mediating learning and memory processes, and demonstrate that mnemonic deficits resulting from excitotoxic lesions of the basal forebrain are not the sole result of cortical acetylcholine activity hypofunction.

Keywords:Learning and memory
Subjects:C Biological Sciences > C120 Behavioural Biology
Divisions:College of Science > School of Life Sciences
ID Code:7867
Deposited On:23 Mar 2013 19:50

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