Linked Life Data

9772256

Source:http://linkedlifedata.com/resource/pubmed/id/9772256

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
1998-11-20
pubmed:abstractText
The effects of methionine-enkephalin (ME) on visualized bulbospinal neurons of the rostral ventrolateral medulla (RVL) were characterized in thin slices at 32 degrees C using the whole cell patch-clamp technique. Thirty-five percent of the recorded neurons were found to be tyrosine hydroxylase immunoreactive (C1 neurons). In voltage-clamp recordings, ME (3 microM) induced an outward current in 66% of RVL bulbospinal neurons. A similar percentage of C1 and non-C1 neurons were opioid sensitive. The current induced by ME was inwardly rectifying, reversed close to the potassium equilibrium potential, and was blocked by barium. Most spontaneous postsynaptic currents recorded in these neurons were tetrodotoxin (TTX)-resistant miniature postsynaptic currents (mPSCs). Approximately, 75% of mPSCs had rapid kinetics (decay time = 4.7 ms) and were glutamatergic [miniature excitatory postsynaptic currents (mEPSCs)] because they were blocked by 6-cyano-7-nitroquinoxaline-2,3-dione (10 microM). The remaining mPSCs had much slower kinetics (decay time = 19.6 ms) and were GABAergic [miniature inhibitory postsynaptic currents (mIPSCs)] as they were blocked by gabazine (3 microM) but not by strychnine (3-10 microM). ME decreased the frequency of mEPSCs and mIPSCs by 69 and 43%, respectively. The inhibitory effects of ME were mimicked by the selective mu-opioid receptor agonist endomorphin-1 (EM, 3 microM) and were blocked by naloxone (1 microM). In the absence of TTX, excitatory PSCs evoked by focal electrical stimulation were isolated by application of gabazine and strychnine. EM reduced the amplitude of the evoked EPSCs by 41% without changing their decay time. We conclude that opioids inhibit the majority of RVL C1 and non-C1 bulbospinal neurons by activating a potassium conductance postsynaptically and by decreasing the presynaptic release of glutamate. These cellular mechanisms could explain the depressive cardiovascular effects and the sympathoinhibition produced by opioid transmitters in the RVL, in particular during hypotensive hemorrhage.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0022-3077
pubmed:author
pubmed:issnType
Print
pubmed:volume
80
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2003-14
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1998
pubmed:articleTitle
Pre- and postsynaptic inhibitory actions of methionine-enkephalin on identified bulbospinal neurons of the rat RVL.
pubmed:affiliation
Department of Pharmacology, University of Virginia, Charlottesville, Virginia 22908, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.