Redundant basal forebrain modulation in taste aversion memory formation

Gutierrez, Humberto and Gutiérrez, Ranier and Ramírez-Trejo, Luis and Silva-Gandarias, Ricardo and Ormsby, Christopher E. and Miranda, Maria Isabel and Bermúdez-Rattoni, Federico (1999) Redundant basal forebrain modulation in taste aversion memory formation. The Journal of Neuroscience : the Official Journal of the Society for Neuroscience, 19 (17). pp. 7661-7669. ISSN UNSPECIFIED

Full text not available from this repository.

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. It has been demonstrated that in spite of the strong cholinergic depletion after injections into the basal forebrain of the immunotoxin 192IgG-saporin, no detectable deficit can be found in the acquisition of several learning tasks, including conditioned taste aversion. Conversely, NMDA-induced lesions of the basal forebrain strongly impair taste aversion learning. In this study we show that 192IgG-saporin produces an efficient and selective cholinergic deafferentation of the rat neocortex but not the amygdala. Furthermore, a stronger relationship between severity of memory impairment after NMDA lesions and basoamygdaloid cholinergic deafferentation was found. Therefore, in a second experiment, we show that combining NMDA-induced lesions into the basolateral amygdala with 192IgG-saporin injections into the basal forebrain results in a strong disruption of taste aversion learning, whereas none of these treatments were by themselves capable of producing any detectable impairment in this learning task. The double lesion effect was only paralleled by simple NMDA lesions into the basal forebrain, suggesting that the learning deficits associated to excitotoxic lesions of the basal forebrain are the result of the simultaneous destruction of the corticopetal and basoamygdaloid interaction. A model is proposed, according to which the modulation of learning processes exerted by the basal forebrain can be redundantly performed by both the basocortical and basoamygdaloid pathway.

Keywords:Learning and memory
Subjects:C Biological Sciences > C120 Behavioural Biology
Divisions:College of Science > School of Life Sciences
ID Code:7865
Deposited On:21 Mar 2013 11:35

Repository Staff Only: item control page