Linked Life Data

6206401

Source:http://linkedlifedata.com/resource/pubmed/id/6206401

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1984-10-3
pubmed:abstractText
The effect of intranigral injections of stable substance P analogs with antagonist properties, namely [D-Pro2, D-Trp7,9]-substance P and [D-Pro2, D-Phe7, D-Trp9]-substance P, on the activity of the nigrostriatal dopaminergic pathway was studied. Dopaminergic neural activity was evaluated by measuring changes in striatal tyrosine hydroxylase activity in response to systemic treatment with haloperidol. When injected into the substantia nigra of normal rats, neither of the two substance P analogs influenced the Vmax of striatal tyrosine hydroxylase or the affinity of the enzyme for its pteridine cofactor. However, when applied into the substantia nigra 10 min before systemic haloperidol, 20 micrograms of either substance P analog was able to prevent the haloperidol-induced activation of striatal tyrosine hydroxylase. The effect was not altered by concurrent microinjection of the GABA-antagonist bicuculline. These results suggests that nigral substance P plays an important role in the activation of nigrostriatal dopamine neurons produced by haloperidol. Thus, both substance P and GABA may reciprocally and independently regulate the activity of nigrostriatal dopamine neurons in response to changes in dopamine receptor activity.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0028-1298
pubmed:author
pubmed:issnType
Print
pubmed:volume
326
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
83-6
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1984
pubmed:articleTitle
Intranigral application of substance P antagonists prevents the haloperidol-induced activation of striatal tyrosine hydroxylase.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.