Opposite effects of acute versus chronic naltrexone administration on ethanol-induced locomotion

Sanchis‐Segura, Carles; Pastor, Raúl; Aragón, Carlos M.G.

doi:10.1016/j.bbr.2003.11.003

Cited by 22 publications

(26 citation statements)

References 42 publications

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“…In addition, the basic neurochemical effects of ethanol leading to the induction of locomotion also remain uncertain. Ethanol has been shown to interact with several neurotransmitter systems (Imperato and Di Chiara, 1986;Givens and Breese, 1990;Dar, 2001;Phillips and Shen, 1996;Ericson et al, 2003;Rodd-Henricks et al, 2003;Sanchis-Segura et al, 2004). Based upon the data reviewed above, it is possible that ethanol facilitates GABAA receptor function on SNr output neurons (Diana et al, 1993;Criswell et al, 1993Criswell et al, , 1999.…”

Section: Effects Of Snr Infusions Of Ethanolmentioning

confidence: 99%

Motor Stimulant Effects of Ethanol Injected into the Substantia Nigra Pars Reticulata: Importance of Catalase-Mediated Metabolism and the Role of Acetaldehyde

Arizzi-LaFrance

Correa

Aragón

et al. 2005

Neuropsychopharmacol

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A series of experiments was conducted to investigate the locomotor effects of local injections of ethanol and the ethanol metabolite, acetaldehyde, into substantia nigra pars reticulata (SNr). Infusions of ethanol into SNr resulted in a dose-related increase in locomotor activity, with maximal effects at a dose of 1.4 mmol. Ethanol injected into a control site dorsal to substantia nigra failed to stimulate locomotion, and another inactive site was identified in brainstem areas posterior to substantia nigra. The locomotor effects of intranigral ethanol (1.4 mmol) were reduced by coadministration of 10 mg/kg sodium azide, a catalase inhibitor that acts to reduce the metabolism of ethanol into acetaldehyde in the brain. SNr infusions of acetaldehyde, which is the first metabolite of ethanol, also increased locomotion. Taken together, these results indicate that SNr is one of the sites at which ethanol and acetaldehyde may be acting to induce locomotor activity. These results are consistent with the hypothesis that acetaldehyde is a centrally active metabolite of ethanol, and provide further support for the idea that catalase activity is a critical step in the regulation of ethanol-induced motor activity. These studies have implications for understanding the brain mechanisms involved in mediating the ascending limb of the biphasic dose-response curve for the effect of ethanol on locomotor activity.

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Section: Effects Of Snr Infusions Of Ethanolmentioning

confidence: 99%

Motor Stimulant Effects of Ethanol Injected into the Substantia Nigra Pars Reticulata: Importance of Catalase-Mediated Metabolism and the Role of Acetaldehyde

Arizzi-LaFrance

Correa

Aragón

et al. 2005

Neuropsychopharmacol

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“…This concentration of ethanol was selected based on previous studies (Pastor et al, 2002;Sanchis-Segura et al, 2004) showing no signs of toxicity after intraperitoneal (i.p.) injections.…”

Section: Drug Sources and Preparationmentioning

confidence: 99%

“…3-Methoxynaltrexone (0, 3, or 6 mg/kg) was administered immediately before saline or ethanol. Doses of naltrexone, naltrindole, naloxonazine, and 3-methoxynatrexone were selected based on studies involving ethanolinduced behaviors in rodents, including acute ethanol stimulation (Ciccocioppo et al, 2002;Honkanen et al, 1996;Mhatre and Holloway, 2003;Pastor et al, 2005;Sanchis-Segura et al, 2004). As there were no previous data showing CTOP effects on ethanol-induced locomotor behaviors, we examined the effect of this compound on acute ethanol stimulation (experiment 2a).…”

Section: Behavioral Proceduresmentioning

confidence: 99%

“…Taken from this experiment, doses of CTOP tested for sensitization were 1 and 1.5 mg/kg. The same dose of ethanol (2.5 g/kg) was used for the treatment and the challenge phase; this dose was selected based on previous studies showing that it significantly increases horizontal locomotion in mice (Pastor et al, 2002;Sanchis-Segura et al, 2004). For all experiments, mice were moved from the colony room to the testing room and left undisturbed at least 30-45 min prior to experimentation to permit acclimation to the testing environment.…”

Section: Behavioral Proceduresmentioning

confidence: 99%

“…Recent data suggest that the acute locomotor stimulating effects of ethanol are mediated by mu, but not delta opioid receptors (Hall et al, 2001;Pastor et al, 2005;Sanchis-Segura et al, 2004). In addition, it has been proposed that acute ethanol stimulation may be selectively mediated by some of the subtypes of the mu opioid receptor.…”

Section: Introductionmentioning

confidence: 99%

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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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Naloxone does not attenuate the locomotor effects of ethanol in FAST, SLOW, or two heterogeneous stocks of mice

et al. 2005

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Opposite effects of acute versus chronic naltrexone administration on ethanol-induced locomotion

Cited by 22 publications

References 42 publications

Motor Stimulant Effects of Ethanol Injected into the Substantia Nigra Pars Reticulata: Importance of Catalase-Mediated Metabolism and the Role of Acetaldehyde

Motor Stimulant Effects of Ethanol Injected into the Substantia Nigra Pars Reticulata: Importance of Catalase-Mediated Metabolism and the Role of Acetaldehyde

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

Naloxone does not attenuate the locomotor effects of ethanol in FAST, SLOW, or two heterogeneous stocks of mice

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