Cocaine-induced hypophagia and hyperlocomotion in rats are attenuated by prazosin

Wellman, Paul J.; Ho, Dao H.; Cepeda-Benito, Antonio; Bellinger, Larry L.; Nation, Jack R.

doi:10.1016/s0014-2999(02)02616-x

Cited by 52 publications

(49 citation statements)

References 44 publications

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“…The effect of prazosin observed here is similar to the effects reported in other studies examining the role of the α 1 -adrenergic receptor in the locomotor response to amphetamine or cocaine (Arnt 1995;Blanc et al 1994;Darracq et al 1998;Dickinson et al 1988;Drouin et al 2002a;Drouin et al 2002b;Snoddy et al 1985;Wellman et al 2002). In fact, our data indicate that MDMA-induced motor behavior is more sensitive to α 1 -adrenoceptor blockade than that produced by (+)-amphetamine.…”

Section: Discussionsupporting

confidence: 90%

“…Other studies have shown that systemic administration of prazosin can attenuate the locomotor response to cocaine, the NMDA receptor antagonist MK-801, and the DA reuptake inhibitor GBR 12783 (Arnt 1995;Dickinson et al 1988;Drouin et al 2002a;Harkin et al 2001;Mathe et al 1996;Snoddy and Tessel 1985;Svensson et al 1995;Wellman et al 2002). Thus, the experiments described herein tested the hypothesis that activation of α 1 -adrenoceptors in the prefrontal cortex and ventral tegmental area of the rat modulate the locomotor response to MDMA.…”

Section: Introductionmentioning

confidence: 79%

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α1-Adrenergic receptors mediate the locomotor response to systemic administration of (±)-3,4-methylenedioxymethamphetamine (MDMA) in rats

Selken

Nichols

2007

Pharmacology Biochemistry and Behavior

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The recreational drug 3,4-methylenedioxymethamphetamine (MDMA, ecstasy) increases locomotor activity when administered to rats. Although the published pharmacology of MDMA has focused almost exclusively on the roles of serotonin and dopamine, in vitro studies indicate that MDMA induces serotonin and norepinephrine release with equal potency. The present experiments tested the hypothesis that blockade of α 1 -adrenoceptors with systemic or local administration of the antagonist prazosin would attenuate the locomotor response to systemic administration of (±)-MDMA. Pretreatment with systemic prazosin (0.5 mg/kg) or microinjections into either the prefrontal cortex or ventral tegmental area completely blocked the locomotor stimulant effects of 5 mg/kg (±)-MDMA, assessed using a computerized Behavioral Pattern Monitor. Prazosin was more potent in blocking the locomotor stimulant effects of (±)-MDMA than a 2 mg/kg dose of (+)-amphetamine that produced a similar locomotor activity increase. These results indicate that activation of α 1 -adrenoceptors in both the prefrontal cortex and ventral tegmental areas modulate the locomotor response to MDMA.

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Section: Discussionsupporting

confidence: 90%

Section: Introductionmentioning

confidence: 79%

α1-Adrenergic receptors mediate the locomotor response to systemic administration of (±)-3,4-methylenedioxymethamphetamine (MDMA) in rats

Selken

Nichols

2007

Pharmacology Biochemistry and Behavior

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“…For example, LC lesions attenuate amphetamine-induced locomotion (Mohammed et al, 1986). Also, administration of the a1AR antagonist prazosin, either systemically or directly into the prefrontal cortex (PFC), reduces both amphetamine-and cocaine-induced locomotion and sensitization (Snoddy and Tessel, 1985;Dickenson et al, 1988;Blanc et al, 1994;Darracq et al, 1998;Drouin et al, 2002;Weinshenker et al, 2002a;Wellman et al, 2002;Auclair et al, 2004;Salomon et al, 2006). Furthermore, a1bAR knockout mice are refractory to psychostimulant-induced locomotor activity and sensitization (Drouin et al, 2002;Auclair et al, 2004;Salomon et al, 2006).…”

Section: Ne and Ethanol Samentioning

confidence: 99%

There and Back Again: A Tale of Norepinephrine and Drug Addiction

Weinshenker

Schroeder

2006

Neuropsychopharmacol

317

277

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Fueled by anatomical, electrophysiological, and pharmacological analyses of endogenous brain reward systems, norepinephrine (NE) was identified as a key mediator of both natural and drug-induced reward in the late 1960s and early 1970s. However, reward experiments from the mid-1970s that could distinguish between the noradrenergic and dopaminergic systems resulted in the prevailing view that dopamine (DA) was the primary 'reward transmitter' (a belief holding some sway still today), thereby pushing NE into the background. Most damaging to the NE hypothesis of reward were studies demonstrating that NE receptor antagonists and NE reuptake inhibitors failed to impact drug self-administration. In recent years new tools, such as genetically engineered mice, and new experimental paradigms, such as reinstatement of drug seeking following withdrawal, have propelled NE back into the awareness of addiction researchers. Of particular interest is disulfiram, an inhibitor of the NE biosynthetic enzyme dopamine b-hydroxylase, which has demonstrated promising efficacy in the treatment of cocaine dependence in preliminary clinical trials. The purpose of this review is to synthesize the new data linking NE to critical aspects of DA signaling and drug addiction, with a focus on psychostimulants (eg, cocaine), opiates (eg, morphine), and alcohol.

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“…Sensitization to amphetamine, cocaine, and ephedrine can be induced by as few as 7−9 daily doses of cocaine (Horger et al, 1994;Jimenez-Rivera et al, 2006;Miller et al, 1999;Post and Rose, 1976) thus a 7 day pretreatment procedure was used here. With regard to cocaine doses, 7.5 mg/kg is above threshold for induction of locomotion in adult male rats, whereas 15 mg/kg does not induce a maximal locomotor response (Wellman et al, 2002). …”

mentioning

confidence: 94%

Systemic ghrelin sensitizes cocaine-induced hyperlocomotion in rats

Wellman

Hollas

Elliott

2008

Regulatory Peptides

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The feeding-relevant pathway by which food restriction (FR) augments cocaine action is unknown. Systemic administration of the 28-amino acid acylated peptide ghrelin (1−10 nMol) increases food intake in rats and circulating levels of rat ghrelin are up-regulated by FR. The present experiment examined the impact of repeated administration of ghrelin or vehicle on the subsequent capacity of cocaine to enhance locomotion in rats. Male Sprague-Dawley rats were pretreated daily for seven days with 0, 5 or 10 nMol rat ghrelin (i.p.) in the home cage. On the 8 th day, rats were transported to a testing room, placed in a locomotion chamber for 15 min, and then injected (i.p.) with 0, 7.5, or 15 mg/kg cocaine hydrochloride. Locomotor activity was monitored over a 45 min post-cocaine period. Pretreatment with 5 or 10 nMol ghrelin alone did not significantly increase basal locomotion relative to that of the 0 nMol ghrelin group. Rats pretreated with 5 nMol or 10 nMol ghrelin showed an enhanced locomotor response after treatment with 15 mg/kg cocaine relative to rats treated with 0 nMol ghrelin. These results indicate that acute injection of ghrelin, at a feeding-relevant dose, can augment the acute effects of cocaine on locomotion in rats. KeywordsFood deprivation; Locomotion; Growth Hormone Food restriction (FR) is known to augment the locomotor actions of psychostimulant drugs such as cocaine or amphetamine (Bell et al., 1997;Campbell and Carroll, 2001;Carr, 2002;Carroll and Meisch, 1980, 1981). Additionally, FR acts to facilitate the acquisition of cocaine or amphetamine self-administration (Carroll, 1985) and augments the acquisition of cocaineinduced conditioned place preference (Bell et al., 1997). When animals already trained to selfadminister cocaine are deprived of food, their daily drug intake increases and FR can facilitate the reinstatement of cocaine-seeking behavior (Carroll, 1985). Conversely, food satiation can delay the acquisition of cocaine self-administration (Carroll and Lac, 1998). These findings suggest that feeding and drug addiction may share common pathways (DiLeone et al., 2003).The neural substrate through which the hyperlocomotor and reinforcing actions of drugs such as cocaine or amphetamine are enhanced by FR remains unknown (Carr, 2002). The stomach peptide ghrelin is an endogenous ligand for the growth-hormone secretagogue receptor (Kojima et al., 1999;Tschop et al., 2000) and functions as an orexigen receptor (Ariyasu et al. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. Inui et al., 2004;Naleid et al., 2005;Wren et al., 2001a;Wren et al.,...

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Cocaine-induced hypophagia and hyperlocomotion in rats are attenuated by prazosin

Cited by 52 publications

References 44 publications

α1-Adrenergic receptors mediate the locomotor response to systemic administration of (±)-3,4-methylenedioxymethamphetamine (MDMA) in rats

α1-Adrenergic receptors mediate the locomotor response to systemic administration of (±)-3,4-methylenedioxymethamphetamine (MDMA) in rats

There and Back Again: A Tale of Norepinephrine and Drug Addiction

Systemic ghrelin sensitizes cocaine-induced hyperlocomotion in rats

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