Linked Life Data

11488956

Source:http://linkedlifedata.com/resource/pubmed/id/11488956

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2001-8-7
pubmed:abstractText
The aim of the present study was to investigate the effect of dopamine (DA) on the excitability of dorsal raphe nucleus (DRN) 5-hydroxytryptamine (5-HT) neurons using the patch-clamp technique in brain slices. Bath application of DA (1-300 microM) produced a concentration-dependent membrane depolarization in all 5-HT neurons examined. This effect persisted in the presence of tetrodotoxin (TTX; 1 microM) and low extracellular calcium. Moreover, blockade of ionotropic glutamate receptors with 6,7-dinitroquinoxaline-2,3-dione (DNQX) and 2-amino-5-phosphonopentanoic acid (AP5) did not prevent DA-induced depolarization, indicating that it was mediated by a direct effect of DA on 5-HT neurons. The DA-induced depolarization was not antagonized by selective alpha1-adrenergic receptor antagonists, prazosin and WB 4101, but by a nonselective DA receptor antagonist, haloperidol. In addition, the selective D2-like receptor agonist quinpirole and antagonist sulpiride mimicked and blocked DA-induced depolarization, respectively. These results indicate that DA-induced membrane depolarization in DRN 5-HT neurons is mediated by the activation of D2-like DA receptors. The DA-induced membrane depolarization and inward current were associated with an increase in membrane conductance. Examination of the current-voltage (I-V) relationship for the DA-induced inward current revealed that the amplitude of the current increased with membrane hyperpolarization and reversed polarity at a potential near -15 mV. These data suggest that DA-induced depolarization in DRN 5-HT neurons is not mediated by a decrease in potassium conductance, but most likely by the activation of a nonselective cation current.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0953-816X
pubmed:author
pubmed:issnType
Print
pubmed:volume
14
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
125-34
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:11488956-Action Potentials, pubmed-meshheading:11488956-Adrenergic alpha-Agonists, pubmed-meshheading:11488956-Adrenergic alpha-Antagonists, pubmed-meshheading:11488956-Animals, pubmed-meshheading:11488956-Dopamine, pubmed-meshheading:11488956-Dopamine Agonists, pubmed-meshheading:11488956-Dopamine Antagonists, pubmed-meshheading:11488956-Electric Stimulation, pubmed-meshheading:11488956-Ion Channels, pubmed-meshheading:11488956-Male, pubmed-meshheading:11488956-Neurons, pubmed-meshheading:11488956-Organ Culture Techniques, pubmed-meshheading:11488956-Patch-Clamp Techniques, pubmed-meshheading:11488956-Raphe Nuclei, pubmed-meshheading:11488956-Rats, pubmed-meshheading:11488956-Rats, Sprague-Dawley, pubmed-meshheading:11488956-Receptors, Dopamine D2, pubmed-meshheading:11488956-Serotonin, pubmed-meshheading:11488956-Tetrodotoxin
pubmed:year
2001
pubmed:articleTitle
D2-like dopamine receptor activation excites rat dorsal raphe 5-HT neurons in vitro.
pubmed:affiliation
Research Institute on Addictions, University at Buffalo, SUNY at Buffalo, 1021 Main Street, Buffalo, New York 14203, USA. dahmane@ria.buffalo.edu
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't