Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2005-2-16
pubmed:abstractText
The effects of pretreatment with endomorphin-1 (EM-1) and endomorphin-2 (EM-2) given into the ventral periaqueductal gray (vPAG) to induce antianalgesia against the tail-flick (TF) inhibition produced by morphine given into the vPAG were studied in rats. Pretreatment with EM-1 (3.5-28 nmol) given into vPAG for 45 min dose-dependently attenuated the TF inhibition produced by morphine (9 nmol) given into vPAG. Similarly, pretreatment with EM-2 (1.7-7.0 nmol) for 45 min also attenuated the TF inhibition induced by morphine; however, a high dose of EM-2 (14 nmol) did not attenuate the morphine-produced TF inhibition. The attenuation of morphine-produced TF inhibition induced by EM-2 or EM-1 pretreatment was blocked by pretreatment with mu-opioid antagonist (-)-naloxone (55 pmol) but not nonopioid (+)-naloxone (55 pmol). However, pretreatment with a morphine-6beta-glucuronide-sensitive mu-opioid receptor antagonist 3-methoxynaltrexone (6.4 pmol) selectively blocked EM-2- but not EM-1-induced antianalgesia. Pretreatment with dynorphin A(1-17) antiserum reversed only EM-2- but not EM-1-induced antianalgesia. Pretreatment with antiserum against beta-endorphin, [Met(5)]enkephalin, [Leu(5)]enkephalin, substance P or cholecystokinin, or with delta-opioid receptor antagonist naltrindole (2.2 nmol) or kappa-opioid receptor antagonist norbinaltorphimine (6.6 nmol) did not affect EM-2-induced antianalgesia. It is concluded that EM-2 selectively releases dynorphin A(1-17) by stimulation of a novel subtype of mu-opioid receptor, tentatively designated as mu(3) in the vPAG to induce antianalgesia, whereas the antianalgesia induced by EM-1 is mediated by the stimulation of another subtype of mu(1)- or mu(2)-opioid receptor.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/Cholecystokinin, http://linkedlifedata.com/resource/pubmed/chemical/Dynorphins, http://linkedlifedata.com/resource/pubmed/chemical/Enkephalin, Leucine, http://linkedlifedata.com/resource/pubmed/chemical/Enkephalin, Methionine, http://linkedlifedata.com/resource/pubmed/chemical/Morphine, http://linkedlifedata.com/resource/pubmed/chemical/Naloxone, http://linkedlifedata.com/resource/pubmed/chemical/Oligopeptides, http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Opioid, mu, http://linkedlifedata.com/resource/pubmed/chemical/Substance P, http://linkedlifedata.com/resource/pubmed/chemical/beta-Endorphin, http://linkedlifedata.com/resource/pubmed/chemical/endomorphin 1, http://linkedlifedata.com/resource/pubmed/chemical/endomorphin 2
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0022-3565
pubmed:author
pubmed:issnType
Print
pubmed:volume
312
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1257-65
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
2005
pubmed:articleTitle
Differential mechanisms of antianalgesia induced by endomorphin-1 and endomorphin-2 in the ventral periaqueductal gray of the rat.
pubmed:affiliation
Department of Anesthesiology, Medical College of Wisconsin, Medical Education Building, Room M4308, 8701 Watertown Plank Rd., Milwaukee, WI 53226, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.