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, 86(2), 1997, pp. 181-189
Citations number
49
Categorie Soggetti
Neurosciences
Journal title
ISSN journal
01664328
Volume
86
Issue
2
Year of publication
1997
Pages
181 - 189
Database
ISI
SICI code
0166-4328(1997)86:2<181:COSIIT>2.0.ZU;2-T
Abstract
In this study we investigated the effects of 192 IgG saporin injection s into the medial septal area (MSA), or nucleus basalis magnocellulari s (NBM), and combined injections into the MSA and NBM, on the water ma ze and radial arm maze performance in the male rat. The results of the present study reveal a dissociation between the effects of 192 IgG sa porin injections into the basal forebrain on the performance of two ta sks of spatial learning in the rat. Bilateral injections of 192 IgG sa porin into the NBM, MSA or combined MSA/NBM failed to disrupt water ma ze performance when compared to controls. In contrast, injections of 1 92 IgG saporin into the MSA, NBM or MSA/NBM induced mild impairments o n a radial arm maze task. Overall, the disruption of spatial learning observed in this study however was relatively mild compared to deficit s in spatial learning reported using less selective lesions of the cho linergic basal forebrain. Consequently, the results of this study sugg est that a selective reduction in cholinergic transmission in the basa l forebrain is by itself, insufficient to account for the functional i mpairments observed in spatial learning in the rat. Although our data does support the use of 192 IgG saporin as a selective cholinergic tox in in the basal forebrain, it 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. (C) 1997 Elsevier Science B.V.