COMPARISON OF SITE-SPECIFIC INJECTIONS INTO THE BASAL FOREBRAIN ON WATER MAZE AND RADIAL-ARM MAZE PERFORMANCE IN THE MALE-RAT AFTER IMMUNOLESIONING WITH 192 IGG SAPORIN

Citation
Wa. Dornan et al., COMPARISON OF SITE-SPECIFIC INJECTIONS INTO THE BASAL FOREBRAIN ON WATER MAZE AND RADIAL-ARM MAZE PERFORMANCE IN THE MALE-RAT AFTER IMMUNOLESIONING WITH 192 IGG SAPORIN, Behavioural brain research, 82(1), 1996, pp. 93-101
Citations number
49
Categorie Soggetti
Neurosciences
Journal title
ISSN journal
01664328
Volume
82
Issue
1
Year of publication
1996
Pages
93 - 101
Database
ISI
SICI code
0166-4328(1996)82:1<93:COSIIT>2.0.ZU;2-6
Abstract
In this study, we investigated the effects of 192 IgG saporin injectio ns into the medial septal area (MSA), or nucleus basalis magnocellular is (NBM), and combined injections into the MSA and NBM, on water maze and radial arm maze performance in the male rat. The results of the pr esent study reveal a dissociation between the effects of 192 Ige sapor in injections into the basal forebrain on the performance of two tasks of spatial learning in the rat. Bilateral injections of 192 IgG sapor in into the NBM, MSA or combined MSA/NBM failed to disrupt water maze performance when compared to controls. In contrast, injections of 192 IgG saporin into the MSA, NBM or MSA/NBM induced mild impairments on a radial arm maze task. Overall, the disruption of spatial learning obs erved in this study was, however, relatively mild compared to deficits in spatial learning reported using less selective lesions of the chol inergic basal forebrain. Consequently, the results of this study sugge st that a selective reduction in cholinergic transmission in the basal forebrain is, by itself, insufficient to account for the functional i mpairments observed in spatial learning in the rat. Although our data do support the use of 192 IgG saporin as a selective cholinergic toxin in the basal forebrain, they further suggests that assessment of spat ial learning in the rat following 192 IgG saporin lesions of the basal forebrain in combination with lesions to other neurotransmitter syste ms, may be a more viable approach to the elucidation of the neuropatho logical mechanisms that are associated with the cognitive deficits see n in Alzheimer's disease.