Abstract

The possible contribution of inadvertent damage of the thalamic reticular nucleus to memory impairment caused by lesion of nucleus basalis magnocellularis (NBM) was examined. Rats carrying chronically implanted cannulae received unilateral injection of 3 ng tetrodotoxin (TTX) into the reticular nucleus either 60 min before (PRE) or 2 min after (POST) acquisition of a combined passive avoidance (PAR)--active avoidance (AAR) task. Three days later retrieval was tested during unilateral TTX blockade of the reticular nucleus in the same (IPSI) or in the opposite (CONTRA) hemisphere. Unilateral inactivation of the reticular nucleus affected neither acquisition nor retrieval of PAR, but interfered with AAR acquisition under the PRE conditions. AAR reacquisition was impaired in the PRE-CONTRA but not in the other groups. The effects of reticular nucleus blockade (AAR disruption without PAR impairment) contrast with AAR facilitation and PAR disruption after NBM lesions. It is concluded that the consequences of NBM damage are not enhanced by unintentional thalamic encroachment.

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