Linked Life Data

20203187

Source:http://linkedlifedata.com/resource/pubmed/id/20203187

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
9
pubmed:dateCreated
2010-3-5
pubmed:abstractText
Chronic morphine drives adaptations in synaptic transmission thought to underlie opiate dependence. Here we examine the role of micro-opioid receptor (MOR) trafficking in one of these adaptations, specifically, changes in GABA transmission in the ventral tegmental area (VTA). To address this question, we used a knock-in mouse, RMOR (for recycling MOR), in which genetic change in the MOR promotes morphine-induced receptor desensitization and endocytosis in GABA interneurons of the VTA. In wild-type mice (postnatal days 23-28) chronic morphine (10 mg/kg, s.c., twice daily for 5 d), induced a cAMP-dependent increase in the probability of GABA release onto VTA dopamine neurons. The increased GABA release frequency correlated with physical dependence on morphine measured by counting somatic signs of morphine withdrawal, such as, tremors, jumps, rears, wet-dog shakes, and grooming behavior precipitated by subcutaneous administration of naloxone (NLX) (2 mg/kg). This adaptation in GABA release was prevented in RMOR mice given the same morphine treatment, implicating MOR trafficking in this morphine-induced change in plasticity. Importantly, treatment with the cAMP activity inhibitor rp-cAMPS [(R)-adenosine, cyclic 3',5'-(hydrogenphosphorothioate) triethylammonium] (50 ng/0.5 microl), directly to the VTA, attenuated somatic withdrawal signs to systemic morphine produced by intra-VTA NLX (500 ng/0.5 microl), directly tying enhanced cAMP-driven GABA release to naloxone-precipitated morphine withdrawal in the VTA.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
1529-2401
pubmed:author
pubmed:issnType
Electronic
pubmed:day
3
pubmed:volume
30
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
3276-86
pubmed:dateRevised
2011-9-26
pubmed:meshHeading
pubmed-meshheading:20203187-Adaptation, Physiological, pubmed-meshheading:20203187-Animals, pubmed-meshheading:20203187-Chimera, pubmed-meshheading:20203187-Cyclic AMP, pubmed-meshheading:20203187-Disease Models, Animal, pubmed-meshheading:20203187-Endocytosis, pubmed-meshheading:20203187-Gene Knock-In Techniques, pubmed-meshheading:20203187-Interneurons, pubmed-meshheading:20203187-Male, pubmed-meshheading:20203187-Mice, pubmed-meshheading:20203187-Mice, Inbred C57BL, pubmed-meshheading:20203187-Mice, Transgenic, pubmed-meshheading:20203187-Morphine, pubmed-meshheading:20203187-Morphine Dependence, pubmed-meshheading:20203187-Naloxone, pubmed-meshheading:20203187-Narcotic Antagonists, pubmed-meshheading:20203187-Narcotics, pubmed-meshheading:20203187-Neural Inhibition, pubmed-meshheading:20203187-Receptors, Opioid, mu, pubmed-meshheading:20203187-Substance Withdrawal Syndrome, pubmed-meshheading:20203187-Synaptic Transmission, pubmed-meshheading:20203187-Thionucleotides, pubmed-meshheading:20203187-Ventral Tegmental Area, pubmed-meshheading:20203187-gamma-Aminobutyric Acid
pubmed:year
2010
pubmed:articleTitle
micro-Opioid receptor endocytosis prevents adaptations in ventral tegmental area GABA transmission induced during naloxone-precipitated morphine withdrawal.
pubmed:affiliation
Ernest Gallo Clinic and Research Center, Emeryville, California 94608, USA.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural