Stimulation of Endorphin Neurotransmission in the Nucleus Accumbens by Ethanol, Cocaine, and Amphetamine

Olive, M. Foster; Koenig, Heather N.; Nannini, Michelle; Hodge, Clyde W.

doi:10.1523/jneurosci.21-23-j0002.2001

Cited by 252 publications

(243 citation statements)

References 50 publications

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“…The sex-specific change in met-enkephalin levels may also explain why only ethanol-exposed female mice are less sensitive to the low-dose stimulant effect of ethanol [1]. Acute ethanol exposure increases the opioid peptide betaendorphin in NA [21,26]. Additionally, enkephalinase inhibitor, which potentiates the action of endogenous enkephalins, increases alcohol intake [8], while an opioid antagonist administered into the NA decreases the animal's response to alcohol [12].…”

Section: Discussionmentioning

confidence: 99%

Perinatal ethanol exposure alters met-enkephalin levels of male and female rats

Lugo¹,

Wilson²,

Kelly³

2006

Neurotoxicology and Teratology

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This study used a rat model of Fetal Alcohol Syndrome to investigate whether combined prenatal and postnatal ethanol exposure affects met-enkephalin levels in the brains of male and female Long-Evans adult rats. Intragastric ethanol was administered to a group of rats (ET) from gestational day (GD) 1 through 22 and from postnatal day (PD) 2 through 10. The control groups consisted of a nontreated control group (NTC) and an intubated control group (IC) that received the intragastric intubation procedure but no exposure to ethanol. We measured met-enkephalin levels in the prefrontal cortex, nucleus accumbens, hypothalamus, central and basolateral nucleus of amygdala and ventral tegmental area. Met-enkephalin levels in the hypothalamus of male and female ET animals were significantly higher than those in either the NTC or IC animals. Metenkephalin levels in the central nucleus of the amygdala of male and female ET animals were significantly lower than the levels in the NTC animals. Met-enkephalin levels in the nucleus accumbens of ET females were significantly greater than those in the IC females. These results demonstrate that the combination of prenatal and postnatal ethanol exposure affects basal metenkephalin levels in specific regions in a sex-specific manner. These changes in met-enkephalin levels may explain how early ethanol exposure affects opioid-regulated behaviors such as social play, sexual behavior, and other social behaviors.

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Section: Discussionmentioning

confidence: 99%

Perinatal ethanol exposure alters met-enkephalin levels of male and female rats

Lugo¹,

Wilson²,

Kelly³

2006

Neurotoxicology and Teratology

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“…To our understanding, however, the most convincing proposal to comprehend the neural mechanism by which these receptors participate in ethanol sensitization may be related to the actions of the mu opioid receptor endogenous ligand, b-endorphin. Ethanol administration produces an increase in b-endorphin release, as measured by in vivo microdialysis in the NAcb (Olive et al, 2001;Marinelli et al, 2003). Also, acute administration of ethanol increased b-endorphin neurotransmission in the ventral tegmental area (VTA) (Rasmussen et al, 1998).…”

Section: Discussionmentioning

confidence: 99%

The Role of Opioid Receptor Subtypes in the Development of Behavioral Sensitization to Ethanol

Pastor

Aragón

2005

Neuropsychopharmacol

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Nonspecific blockade of opioid receptors has been found to prevent development of behavioral sensitization to ethanol. Whether this effect is achieved through a specific opioid receptor subtype, however, is not clear. The present study investigated, for the first time, the role of specific opioid receptor subtypes in the development of ethanol-(2.5 g/kg/day; six sessions) induced locomotor sensitization in mice. We confirmed previous results showing that the nonspecific antagonism of opioid receptors (naltrexone; 0-2 mg/kg) prevented the development of behavioral sensitization to ethanol, an effect attained at doses presumed to occupy only mu opioid receptors. This was confirmed by using the selective mu opioid receptor antagonist CTOP (0-1.5 mg/kg), which also blocked sensitization to ethanol. The selective delta receptor antagonist, naltrindole (0-10 mg/kg), however, did not alter sensitization. We further assessed the role of mu opioid receptors in sensitization to ethanol by exploring the involvement of mu 1 , mu 1 + 2 , and mu 3 opioid receptor subtypes. Results of these experiments revealed that the blockade of mu 1 (naloxonazine; 0-30 mg/kg) or mu 3 opioid receptors (3-methoxynaltrexone; 0-6 mg/kg) did not prevent locomotor sensitization to ethanol. Using naloxonazine under treatment conditions that block mu 1 + 2 opioid receptor subtypes we observed a retarded sensitization. The present data suggest that the concurrent inactivation of all mu opioid receptor subtypes may be required to prevent the neural adaptations underlying the development of behavioral sensitization to ethanol. In addition, these results support previous data suggesting a putative role for the mu opioid receptor endogenous ligand, b-endorphin, and the hypothalamic arcuate nucleus in ethanol sensitization.

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“…Acute administration of AMPH or METH is known to increase endogenous opioid contents [35], and mesolimbic structures such as VTA and NAcc receive β-endorphin containing fibers [29]. Although opioid agonists had been known to increase the firing rate of dopamine neurons [31] and increase dopamine levels [20] in the VTA, the character of opioidergic system in chronic use of psychostimulants still remains unclear.…”

Section: Introductionmentioning

confidence: 99%

Attenuation of methamphetamine-induced behavioral sensitization in mice by systemic administration of naltrexone

Chiu

2005

Brain Research Bulletin

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Repeated intermittent exposure to psychostimulants was found to produce behavioral sensitization. The present study was designed to establish a mouse model and by which to investigate whether opioidergic system plays a role in methamphetamine-induced behavioral sensitization. Mice injected with 2.5 mg/kg of methamphetamine once a day for 7 consecutive days showed behavioral sensitization after challenge with 0.3125 mg/kg of the drug on day 11, whereas mice injected with a lower daily dose (1.25 mg/kg) did not. Mice received daily injections with either 1.25 or 2.5 mg/kg of methamphetamine showed behavioral sensitization after challenge with 1.25 mg/kg of the drug on days 11, 21, and 28. To investigate the role of opioidergic system in the induction and expression of behavioral sensitization, long-acting but non-selective opioid antagonist naltrexone was administrated prior to the daily injections of and challenge with methamphetamine, respectively. Our results show that the expressions of behavioral sensitization were attenuated by pretreatment with 10 or 20 mg/kg of naltrexone either during the induction period or before methamphetamine challenge when they were tested on days 11 and 21. These results indicate that repeated injection with methamphetamine dose-dependently induced behavioral sensitization in mice, and suggest the involvement of opioid receptors in the induction and expression of methamphetamine-induced behavioral sensitization.

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Stimulation of Endorphin Neurotransmission in the Nucleus Accumbens by Ethanol, Cocaine, and Amphetamine

Cited by 252 publications

References 50 publications

Perinatal ethanol exposure alters met-enkephalin levels of male and female rats

Perinatal ethanol exposure alters met-enkephalin levels of male and female rats

The Role of Opioid Receptor Subtypes in the Development of Behavioral Sensitization to Ethanol

Attenuation of methamphetamine-induced behavioral sensitization in mice by systemic administration of naltrexone

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