Document Detail

Sensorimotor impairment and elevated levels of dopamine metabolites in the neostriatum occur rapidly after intranigral injection of 6-hydroxydopamine or gamma-hydroxybutyrate in awake rats.
MedLine Citation:
PMID:  6427648     Owner:  NLM     Status:  MEDLINE    
The unilateral injection of 6-hydroxydopamine (8 micrograms) into the ventral tegmental area of awake rats produced a rapidly developing and irreversible sensory neglect to contralateral tactile stimuli. This neglect developed in a caudal to rostral direction on the affected body surface and coincided with significant elevation in the concentrations of dopamine and two of its metabolites, dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) in the ipsilateral neostriatum. The unilateral injection of procaine or gamma-hydroxybutyric acid (GHB) into the substantia nigra of awake animals also produced a contralateral neglect that developed in a caudal to rostral direction, but the behavioral effect of these drugs diminished within 1 hr. Concentrations of dopamine, dihydroxyphenylacetic acid and homovanillic acid in the neostriatum were markedly elevated during continuous infusions of procaine or gamma-hydroxybutyric acid. The extent of sensory neglect and changes in dopamine metabolism in the neostriatum varied according to the amount of gamma-hydroxybutyric acid injected into the nigra and according to the proximity of injections of gamma-hydroxybutyric acid to the pars compacta. The rapid onset of sensory neglect following microinjections of 6-hydroxydopamine, procaine or gamma-hydroxybutyric acid is consistent with the ability of each of these drugs to block the conduction of impulses in mesostriatal neurons and suggests that concomitant increases in levels of dopamine, dihydroxyphenylacetic acid and homovanillic acid in the neostriatum resulted from decreases in the release of dopamine coupled with increased synthesis of dopamine. These findings also indicate that the catabolism of dopamine to dihydroxyphenylacetic acid or homovanillic acid may originate intraneuronally, without prior release of dopamine and its recapture by mesostriatal terminals, if the flow of impulses in this pathway has been blocked.
C A Altar; S O'Neil; J F Marshall
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Neuropharmacology     Volume:  23     ISSN:  0028-3908     ISO Abbreviation:  Neuropharmacology     Publication Date:  1984 Mar 
Date Detail:
Created Date:  1984-07-12     Completed Date:  1984-07-12     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  0236217     Medline TA:  Neuropharmacology     Country:  ENGLAND    
Other Details:
Languages:  eng     Pagination:  309-18     Citation Subset:  IM    
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MeSH Terms
3,4-Dihydroxyphenylacetic Acid / metabolism
4-Butyrolactone / administration & dosage,  pharmacology
Corpus Striatum / metabolism*
Dopamine / metabolism*
Homovanillic Acid / metabolism
Hydroxybutyrates / pharmacology*
Hydroxydopamines / administration & dosage,  pharmacology*
Procaine / administration & dosage
Psychomotor Performance / drug effects*
Rats, Inbred Strains
Sodium Oxybate / administration & dosage,  pharmacology*
Substantia Nigra / drug effects,  physiology*
Grant Support
Reg. No./Substance:
0/Hydroxybutyrates; 0/Hydroxydopamines; 102-32-9/3,4-Dihydroxyphenylacetic Acid; 1199-18-4/Oxidopamine; 306-08-1/Homovanillic Acid; 502-85-2/Sodium Oxybate; 59-46-1/Procaine; 96-48-0/4-Butyrolactone

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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