Effects of continuous naloxone administration on ventral tegmental self-stimulation

doi:10.1016/0006-8993(91)91250-5

Brain Research

Volume 560, Issues 1–2, 27 September 1991, Pages 315-320

https://doi.org/10.1016/0006-8993(91)91250-5 Get rights and content

Abstract

Continuous subcutaneous administration of naloxone (3 mg/kg/h), shifted ventral tegmental self-stimulation rate-frequency curves to the right, without suppressing behavioral performance. In addition this chronic blockade of opioid receptors altered μ binding parameters in the hippocampus and olfactory tubercle of naloxone-treated animals. These findings speak to the role opioid peptides play in the mediation of brain stimulation reward.

Reference (31)

BozarthM.A. et al.
Intracranial administration of morphine into the ventral tegmental area in rats
Life Sci.
(1981)
BroekkampC.L.E. et al.
Facilitation of self-stimulation behavior following intracerebral microinjections of opioids into the ventral tegmental area
Pharmacol. Biochem. Behav.
(1979)
EspositoR.U. et al.
Opiods and rewarding brain stimulation
Neurosci. Biobehav. Rev.
(1978)
EspositoR.U. et al.
Effects of morphine on intracranial self-stimulation to various brainstem loci
Brain Research
(1979)
GallistelC.R. et al.
Quantitative determination of the effects of catecholaminergic agonists and antagonists on the rewarding efficacy of brain stimulation
Pharmacol. Biochem. Behav.
(1987)
GyslingK. et al.
Morphine-induced activation of A10 dopamine neurons in the rat
Brain Research
(1983)
HandT.H. et al.
6-OHDA lesions of the ventral tegmental area block morphine-induced but not amphetamine-induced facilitation of self-stimulation
Brain Research
(1985)
JenckF. et al.
Opioid receptor subtypes associated with ventral tegmental facilitation of hypothalamic brain stimulation reward
Brain Research
(1987)
KornetskyC. et al.
The role of the olfactory tubercle in the effects of cocaine, morphine and brain-stimulation reward
Brain Research
(1991)
SchaeferG.J.
Opiate antagonists and rewarding brain stimulation
Neurosci. Biobehav. Rev.
(1988)

TeppermanF.S. et al.

Brain and serum levels of naloxone following peripheral administration

Life Sci.

(1983)

Van WolfswinkelL. et al.

Long-term changes in self-stimulation threshold by repeated morphine and naloxone treatment

Life Sci.

(1985)

WestT.E.G. et al.

Effects of naltrexone on nucleus accumbens, lateral hypothalamic and ventral tegmental self-stimulation rate-frequency functions

Brain Research

(1988)

BrownR.M. et al.

Opiate receptor subtypes and brain function

NIDA Res. Monogr.

(1986)

DiChiara G. et al.

Preferential stimulation of dopamine release in the nucleus accumbens by opiates, alcohol and barbiturates: studies with transcerebral dialysis in freely moving rats

Ann. New York Acad. Sci.

(1986)

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: This work was supported by NIDA Grant DA06485 to E.A.S.

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Effects of continuous naloxone administration on ventral tegmental self-stimulation

Abstract

Life Sci.

Pharmacol. Biochem. Behav.

Neurosci. Biobehav. Rev.

Brain Research

Pharmacol. Biochem. Behav.

Brain Research

Brain Research

Brain Research

Brain Research

Neurosci. Biobehav. Rev.

Life Sci.

Life Sci.

Brain Research

Opiate receptor subtypes and brain function

NIDA Res. Monogr.

Preferential stimulation of dopamine release in the nucleus accumbens by opiates, alcohol and barbiturates: studies with transcerebral dialysis in freely moving rats

Ann. New York Acad. Sci.