Galloping induced by pontine tegmentum damage in rats: A form of 'Parkinsonian festination' not blocked by haloperidol (akinesia/locomotion/nucleus reticularis tegmenti pontis/γ-aminobutyric acid/movement subsystems)

J. T. Cheng, T. Schallert, M. De Ryck, P. Teitelbaum

Research output: Contribution to journalArticle

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Abstract

Localized lesions or local applications of γ-aminobutyric acid (GABA) in the nucleus reticularis tegment pontis (NRTP) of rats cause rapidly accelerating forward locomotion. Such 'festination' can coexist with blockade of the dopamine system. We suggest that (i) the akinesia produced by dopamine deficiency results at least in part from release of excessive inhibition of locomotion by a neural system whose final common inhibitory path includes the region of the NRTP and (ii) when it occurs in addition to nigrostriatal damage, destruction in the region of the NRTP might be the cause of a form of festination seen in some patients suffering from Parkinsonism.

Original languageEnglish (US)
Pages (from-to)3279-3283
Number of pages5
JournalProceedings of the National Academy of Sciences of the United States of America
Volume78
Issue number5 I
DOIs
StatePublished - 1981

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