Fetal methylazoxymethanol acetate-induced lesions cause reductions in dopamine receptor-mediated catalepsy and stereotypy

P. R. Sanberg; J. Pevsner; P. G. Autuono; J. T. Coyle

doi:10.1016/0028-3908(85)90191-1

Fetal methylazoxymethanol acetate-induced lesions cause reductions in dopamine receptor-mediated catalepsy and stereotypy

P. R. Sanberg, J. Pevsner, P. G. Autuono, J. T. Coyle

Research output: Contribution to journal › Article › peer-review

6 Scopus citations

Abstract

Telencephalic hypoplasia induced by methylazoxymethanol acetate (MAM) resulted in increased activity of tyrosine hydroxylase in the striatum, indicative of a relative increase in the density of dopaminergic terminals in the remaining tissue. Administration of the dopamine receptor stimulant, apomorphine, or the receptor blocker, haloperidol, produced less stereotypy and catalepsy, respectively, in rats lesioned with methylazoxymethanol, compared to controls. These behavioral changes probably resulted from the loss of striatal perikarya and consequent decrease in nigrostriatal dopaminergic target sites caused by methylazoxymethanol.

Original language	English (US)
Pages (from-to)	1057-1062
Number of pages	6
Journal	Neuropharmacology
Volume	24
Issue number	11
DOIs	https://doi.org/10.1016/0028-3908(85)90191-1
State	Published - Nov 1985
Externally published	Yes

Keywords

apomorphine
catalepsy
haloperidol
methylazoxymethanol
stereotypy

ASJC Scopus subject areas

Pharmacology
Cellular and Molecular Neuroscience

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10.1016/0028-3908(85)90191-1

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title = "Fetal methylazoxymethanol acetate-induced lesions cause reductions in dopamine receptor-mediated catalepsy and stereotypy",

abstract = "Telencephalic hypoplasia induced by methylazoxymethanol acetate (MAM) resulted in increased activity of tyrosine hydroxylase in the striatum, indicative of a relative increase in the density of dopaminergic terminals in the remaining tissue. Administration of the dopamine receptor stimulant, apomorphine, or the receptor blocker, haloperidol, produced less stereotypy and catalepsy, respectively, in rats lesioned with methylazoxymethanol, compared to controls. These behavioral changes probably resulted from the loss of striatal perikarya and consequent decrease in nigrostriatal dopaminergic target sites caused by methylazoxymethanol.",

keywords = "apomorphine, catalepsy, haloperidol, methylazoxymethanol, stereotypy",

author = "Sanberg, {P. R.} and J. Pevsner and Autuono, {P. G.} and Coyle, {J. T.}",

note = "Funding Information: Acknowledgemenfs-This researchw as supportedb y U.S. Public Health ServicesG rant NS-18414,R SDA Tvne II MH00125,a nd a grant from the Surdna Founda& to J. T. Coyle, and by a Tourette Syndrome Association ResearchF ellowship,a Huntington{\textquoteright}sD iseaseG rant from the Pratt Family and Friends, and the Ohio University Research Council, the Hereditary Disease Foundation and the Huntington{\textquoteright}s Disease Foundation of America to P. R. Sanberg. We are grateful to Dr D. S. Olton for the use of facilities, and to Dr T. H. Moran for helpful comments.",

year = "1985",

month = nov,

doi = "10.1016/0028-3908(85)90191-1",

language = "English (US)",

volume = "24",

pages = "1057--1062",

journal = "Neuropharmacology",

issn = "0028-3908",

publisher = "Elsevier Limited",

number = "11",

}

TY - JOUR

T1 - Fetal methylazoxymethanol acetate-induced lesions cause reductions in dopamine receptor-mediated catalepsy and stereotypy

AU - Sanberg, P. R.

AU - Pevsner, J.

AU - Autuono, P. G.

AU - Coyle, J. T.

N1 - Funding Information: Acknowledgemenfs-This researchw as supportedb y U.S. Public Health ServicesG rant NS-18414,R SDA Tvne II MH00125,a nd a grant from the Surdna Founda& to J. T. Coyle, and by a Tourette Syndrome Association ResearchF ellowship,a Huntington’sD iseaseG rant from the Pratt Family and Friends, and the Ohio University Research Council, the Hereditary Disease Foundation and the Huntington’s Disease Foundation of America to P. R. Sanberg. We are grateful to Dr D. S. Olton for the use of facilities, and to Dr T. H. Moran for helpful comments.

PY - 1985/11

Y1 - 1985/11

N2 - Telencephalic hypoplasia induced by methylazoxymethanol acetate (MAM) resulted in increased activity of tyrosine hydroxylase in the striatum, indicative of a relative increase in the density of dopaminergic terminals in the remaining tissue. Administration of the dopamine receptor stimulant, apomorphine, or the receptor blocker, haloperidol, produced less stereotypy and catalepsy, respectively, in rats lesioned with methylazoxymethanol, compared to controls. These behavioral changes probably resulted from the loss of striatal perikarya and consequent decrease in nigrostriatal dopaminergic target sites caused by methylazoxymethanol.

AB - Telencephalic hypoplasia induced by methylazoxymethanol acetate (MAM) resulted in increased activity of tyrosine hydroxylase in the striatum, indicative of a relative increase in the density of dopaminergic terminals in the remaining tissue. Administration of the dopamine receptor stimulant, apomorphine, or the receptor blocker, haloperidol, produced less stereotypy and catalepsy, respectively, in rats lesioned with methylazoxymethanol, compared to controls. These behavioral changes probably resulted from the loss of striatal perikarya and consequent decrease in nigrostriatal dopaminergic target sites caused by methylazoxymethanol.

KW - apomorphine

KW - catalepsy

KW - haloperidol

KW - methylazoxymethanol

KW - stereotypy

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Fetal methylazoxymethanol acetate-induced lesions cause reductions in dopamine receptor-mediated catalepsy and stereotypy

Abstract

Keywords

ASJC Scopus subject areas

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