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Titolo:
Direct actions of cannabinoids on synaptic transmission in the nucleus accumbens: A comparison with opioids
Autore:
Hoffman, AF; Lupica, CR;
Indirizzi:
NIDA, Cellular Neurobiol Branch, Intramural Res Program, NIH, Baltimore, MD 21224 USA NIDA Baltimore MD USA 21224 ral Res Program, NIH, Baltimore, MD 21224 USA
Titolo Testata:
JOURNAL OF NEUROPHYSIOLOGY
fascicolo: 1, volume: 85, anno: 2001,
pagine: 72 - 83
SICI:
0022-3077(200101)85:1<72:DAOCOS>2.0.ZU;2-F
Fonte:
ISI
Lingua:
ENG
Soggetto:
RAT HIPPOCAMPAL-NEURONS; FREELY-MOVING RATS; GABA RELEASE; PRESYNAPTIC INHIBITION; RUTHENIUM RED; IN-VITRO; RECEPTOR ACTIVATION; PROJECTION NEURONS; IDENTIFIED NEURONS; GABAERGIC NEURONS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
71
Recensione:
Indirizzi per estratti:
Indirizzo: Lupica, CR Univ Arizona, Hlth Sci Ctr, Dept Pharmacol, 1501 N Campbell Ave, Tucson, AZ 85724 USA Univ Arizona 1501 N Campbell Ave Tucson AZ USA 85724 85724 USA
Citazione:
A.F. Hoffman e C.R. Lupica, "Direct actions of cannabinoids on synaptic transmission in the nucleus accumbens: A comparison with opioids", J NEUROPHYS, 85(1), 2001, pp. 72-83

Abstract

The nucleus accumbens (NAc) represents a critical site for the rewarding and addictive properties of several classes of abused drugs. The medium spiny GABAergic projection neurons (MSNs) in the NAc receive innervation from intrinsic GABAergic interneurons and glutamatergic innervation from extrinsic sources. Both GABA and glutamate release onto MSNs are inhibited by drugsof abuse, suggesting that this action may contribute to their rewarding properties. To investigate the actions of cannabinoids in the NAc, we performed whole cell recordings from MSNs located in the shell region in rat brainslices. The cannabinoid agonist WIN 55,212-2 (1 muM) had no effect on the resting membrane potential, input resistance, or whole cell conductance, suggesting no direct postsynaptic effects. Evoked glutamatergic excitatory postsynaptic currents (EPSCs) were inhibited to a much greater extent by [Tyr-D-Ala(2), N-CH3-Phe(4), Gly-ol-enkephalin] (DAMGO, similar to 35%) than byWIN 55,212-2 (<20%), and an analysis of miniature EPSCs suggested that theeffects of DAMGO were presynaptic, whereas those of WIN 55,212-2 were postsynaptic. However, electrically evoked GABAergic inhibitory postsynaptic currents (evIPSCs), were reduced by WIN 55,212-2 in every neuron tested (EC50= 123 nM; 60% maximal inhibition), and the inhibition of IPSCs by WIN 55,212-2 was completely antagonized by the CB1 receptor antagonist SR141716A (1<mu>M). In contrast evIPSCs were inhibited in similar to 50% of MSNs by the mu/delta opioid agonist D-Ala(2)-methionine(2)-enkephalin-amide and were completely unaffected by a selective mu -opioid receptor agonist (DAMGO). WIN 55,212-2 also increased paired-pulse facilitation of the evIPSCs and didnot alter the amplitudes of tetrodotoxin-resistant miniature IPSCs, suggesting a presynaptic action. Taken together, these data suggest that cannabinoids and opioids differentially modulate inhibitory and excitatory synaptictransmission in the NAc and that the abuse liability of marijuana may be related to the direct actions of cannabinoids in this structure.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 30/03/20 alle ore 11:36:16