Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2004-11-3
pubmed:abstractText
Repeated exposure to drugs of abuse causes persistent behavioral sensitization and associated adaptations of striatal neurotransmission, which is thought to play an important role in certain aspects of drug addiction. Microdialysis and neurochemical studies suggest that intermittent morphine treatment may lead to a long-term increase in both ACh and dopaminergic neurotransmission in the nucleus accumbens (NAc). This implies that both cholinergic modulation of GABA synapses and their sensitivity to dopaminergic transmission might be changed, ultimately leading to a modified NAc output. Here we investigate to what extent cholinergic modulation and sensitivity to amphetamine, causing endogenous dopamine efflux, of GABAergic transmission in the nucleus accumbens are affected 3 weeks after a period of daily morphine injections in adult rats. To this end, we recorded medium spiny neurons using whole cell voltage clamp and monitored the frequency and amplitude of spontaneous GABAergic synaptic currents. We observed that the effect of nicotine on the frequency of spontaneous inhibitory postsynaptic currents (sIPSCs) was suppressed in rats pretreated with morphine, whereas the effects of mecamylamine and tetrodotoxin (TTX) were increased. These results indicate that the probability of GABA release was increased and that this effect resulted from an upregulation of the endogenous activation of presynaptic nicotinic receptors. In addition, we observed an increased sensitivity to in vitro application of amphetamine. This suggests that the long-term increase in dopaminergic transmission caused by the morphine treatment affects GABA synapses in the NAc. Hence, there may be two parallel synaptic mechanisms by which drugs of abuse may affect processing and integration of NAc inputs.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/Acetylcholine, http://linkedlifedata.com/resource/pubmed/chemical/Amphetamine, http://linkedlifedata.com/resource/pubmed/chemical/Anesthetics, Local, http://linkedlifedata.com/resource/pubmed/chemical/Central Nervous System Stimulants, http://linkedlifedata.com/resource/pubmed/chemical/Mecamylamine, http://linkedlifedata.com/resource/pubmed/chemical/Morphine, http://linkedlifedata.com/resource/pubmed/chemical/Narcotics, http://linkedlifedata.com/resource/pubmed/chemical/Nicotine, http://linkedlifedata.com/resource/pubmed/chemical/Nicotinic Agonists, http://linkedlifedata.com/resource/pubmed/chemical/Nicotinic Antagonists, http://linkedlifedata.com/resource/pubmed/chemical/Tetrodotoxin, http://linkedlifedata.com/resource/pubmed/chemical/gamma-Aminobutyric Acid
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0887-4476
pubmed:author
pubmed:copyrightInfo
copyright (c) 2004 Wiley-Liss, Inc.
pubmed:issnType
Print
pubmed:volume
55
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
17-25
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:15499607-Acetylcholine, pubmed-meshheading:15499607-Amphetamine, pubmed-meshheading:15499607-Anesthetics, Local, pubmed-meshheading:15499607-Animals, pubmed-meshheading:15499607-Central Nervous System Stimulants, pubmed-meshheading:15499607-Drug Interactions, pubmed-meshheading:15499607-Male, pubmed-meshheading:15499607-Mecamylamine, pubmed-meshheading:15499607-Membrane Potentials, pubmed-meshheading:15499607-Morphine, pubmed-meshheading:15499607-Narcotics, pubmed-meshheading:15499607-Neural Inhibition, pubmed-meshheading:15499607-Nicotine, pubmed-meshheading:15499607-Nicotinic Agonists, pubmed-meshheading:15499607-Nicotinic Antagonists, pubmed-meshheading:15499607-Nucleus Accumbens, pubmed-meshheading:15499607-Rats, pubmed-meshheading:15499607-Rats, Wistar, pubmed-meshheading:15499607-Synapses, pubmed-meshheading:15499607-Tetrodotoxin, pubmed-meshheading:15499607-gamma-Aminobutyric Acid
pubmed:year
2005
pubmed:articleTitle
Intermittent morphine treatment induces a long-lasting increase in cholinergic modulation of GABAergic synapses in nucleus accumbens of adult rats.
pubmed:affiliation
Department of Experimental Neurophysiology, Centre for Neurogenomics and Cognitive Research (CNCR), Vrije Universiteit Amsterdam, 1081 HV Amsterdam, The Netherlands.
pubmed:publicationType
Journal Article, Comparative Study, In Vitro