UNILATERAL LESION OF DORSAL HIPPOCAMPUS ENHANCES REINFORCING LATERAL HYPOTHALAMIC-STIMULATION IN THE CONTRALATERAL HEMISPHERE

Citation
Pk. Zimmermann et al., UNILATERAL LESION OF DORSAL HIPPOCAMPUS ENHANCES REINFORCING LATERAL HYPOTHALAMIC-STIMULATION IN THE CONTRALATERAL HEMISPHERE, Brain research bulletin, 44(3), 1997, pp. 265-271
Citations number
72
Categorie Soggetti
Neurosciences
Journal title
ISSN journal
03619230
Volume
44
Issue
3
Year of publication
1997
Pages
265 - 271
Database
ISI
SICI code
0361-9230(1997)44:3<265:ULODHE>2.0.ZU;2-P
Abstract
Whereas convincing evidence exists for an important role of the hippoc ampus in mechanisms underlying memory and encoding of location in spac e, the contribution of the hippocampus to the system underlying centra l processes of reinforcement is less well established. Scattered data suggesting that hippocampal ablation increases the effectiveness of po sitive reinforcers have alternatively been interpretated in terms of g eneral and unspecific behavioral disinhibition, which results in highe r levels of activity and rates of responding. In the present experimen t, 22 Wistar rats were either given a neurotoxic or a sham lesion in t he CA, region of the hippocampus, and the effect on lateral hypothalam ic self-stimulation behavior was assessed. To control for nonspecific performance effects rates of lever pressing were assessed ipsi-and con tralateral to the lesioned hemisphere as well as under condition of ex tinction (current set to zero). Following the neurotoxic lesion the an imals displayed significant higher rates of self-stimulation at the el ectrode sites in the hypothalamus situated contralateral but not ipsil ateral to the hemisphere with the lesion compared with controls. The i ncrease in self-stimulation commenced on the third day postlesion and was maintained over the 8 days of testing, The lesion did not change t he animals' behavior under extinction. Thus, the hippocampal lesion le d to an amplification of rewarding lateral hypothalamic self-stimulati on behavior, indicative of a lesion induced disinhibition of the brain 's reinforcement system. (C) 1997 Elsevier Science Inc.