N-methylaspartate: an effective tool for lesioning basal forebrain cholinergic neurons of the rat

Gregory R. Stewart; Price Madelon; John W. Olney; Boyd K. Hartman; Constantino Cozzari

doi:10.1016/0006-8993(86)90555-X

N-methylaspartate: an effective tool for lesioning basal forebrain cholinergic neurons of the rat

Gregory R. Stewart, Price Madelon, John W. Olney, Boyd K. Hartman, Constantino Cozzari

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Abstract

The ability of the excitotoxin, N-methyl-d,l-aspartic acid (NMA), to destroy basal forebrain cholinergic (BFC) neurons was evaluated. NMA (100 nmol) was directly injected into the peripallidum, a region containing a proportionately large number of cortically-projecting BFC neurons. Cholineacetyltransferase (ChAT) activity 10 days later was markedly and significantly reduced (up to 62%) in the cortex ipsilateral to the lesion. NMA induced a focal lesion affecting BFC neurons without damaging axons of passage or causing lesions distant from the site of injection. ChAT immunohistochemistry (IHC) was used to directly demonstrate loss of ChAT-positive neurons from the lesion site. This loss persisted at all survival times examined, from 2 days to 7.5 months post-injection.

Original language	English (US)
Pages (from-to)	377-382
Number of pages	6
Journal	Brain Research
Volume	369
Issue number	1-2
DOIs	https://doi.org/10.1016/0006-8993(86)90555-X
State	Published - Mar 26 1986
Externally published	Yes

Bibliographical note

Funding Information:
Supported in part by NIH Grants MH37967. NS12311 and AG05681. Research Scientist Award MH38894 (J.W.O.) and a Lichtenstein grant. We thank Sandra Kalmbach and Sophia Goodman, respectively, for excellent assistance in immunohistochemical procedures and preparation of the manuscript.

Keywords

N-methyl-d,l-aspartic acid
basal forebrain
cholineacetyltransferase
excitoxin
immunohistochemistry
lesion
rat

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title = "N-methylaspartate: an effective tool for lesioning basal forebrain cholinergic neurons of the rat",

abstract = "The ability of the excitotoxin, N-methyl-d,l-aspartic acid (NMA), to destroy basal forebrain cholinergic (BFC) neurons was evaluated. NMA (100 nmol) was directly injected into the peripallidum, a region containing a proportionately large number of cortically-projecting BFC neurons. Cholineacetyltransferase (ChAT) activity 10 days later was markedly and significantly reduced (up to 62%) in the cortex ipsilateral to the lesion. NMA induced a focal lesion affecting BFC neurons without damaging axons of passage or causing lesions distant from the site of injection. ChAT immunohistochemistry (IHC) was used to directly demonstrate loss of ChAT-positive neurons from the lesion site. This loss persisted at all survival times examined, from 2 days to 7.5 months post-injection.",

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note = "Funding Information: Supported in part by NIH Grants MH37967. NS12311 and AG05681. Research Scientist Award MH38894 (J.W.O.) and a Lichtenstein grant. We thank Sandra Kalmbach and Sophia Goodman, respectively, for excellent assistance in immunohistochemical procedures and preparation of the manuscript.",

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AU - Olney, John W.

AU - Hartman, Boyd K.

AU - Cozzari, Constantino

N1 - Funding Information: Supported in part by NIH Grants MH37967. NS12311 and AG05681. Research Scientist Award MH38894 (J.W.O.) and a Lichtenstein grant. We thank Sandra Kalmbach and Sophia Goodman, respectively, for excellent assistance in immunohistochemical procedures and preparation of the manuscript.

PY - 1986/3/26

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N2 - The ability of the excitotoxin, N-methyl-d,l-aspartic acid (NMA), to destroy basal forebrain cholinergic (BFC) neurons was evaluated. NMA (100 nmol) was directly injected into the peripallidum, a region containing a proportionately large number of cortically-projecting BFC neurons. Cholineacetyltransferase (ChAT) activity 10 days later was markedly and significantly reduced (up to 62%) in the cortex ipsilateral to the lesion. NMA induced a focal lesion affecting BFC neurons without damaging axons of passage or causing lesions distant from the site of injection. ChAT immunohistochemistry (IHC) was used to directly demonstrate loss of ChAT-positive neurons from the lesion site. This loss persisted at all survival times examined, from 2 days to 7.5 months post-injection.

AB - The ability of the excitotoxin, N-methyl-d,l-aspartic acid (NMA), to destroy basal forebrain cholinergic (BFC) neurons was evaluated. NMA (100 nmol) was directly injected into the peripallidum, a region containing a proportionately large number of cortically-projecting BFC neurons. Cholineacetyltransferase (ChAT) activity 10 days later was markedly and significantly reduced (up to 62%) in the cortex ipsilateral to the lesion. NMA induced a focal lesion affecting BFC neurons without damaging axons of passage or causing lesions distant from the site of injection. ChAT immunohistochemistry (IHC) was used to directly demonstrate loss of ChAT-positive neurons from the lesion site. This loss persisted at all survival times examined, from 2 days to 7.5 months post-injection.

KW - N-methyl-d,l-aspartic acid

KW - basal forebrain

KW - cholineacetyltransferase

KW - excitoxin

KW - immunohistochemistry

KW - lesion

KW - rat

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N-methylaspartate: an effective tool for lesioning basal forebrain cholinergic neurons of the rat

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