The effect of clonidine and related substances on voluntary ethanol consumption in rats

Opitz, K

doi:10.1016/0376-8716(90)90139-6

Cited by 27 publications

(15 citation statements)

References 29 publications

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“…The present results are in agreement with those from a previous report of Opitz (1990). These investigators found that the alpha-2 adrenoceptor agonists, clonidine, guanfacine, and tiamedine decrease alcohol intake in a twobottle choice-test.…”

Section: Effects Of Lofexidine and Yohimbine On Reinstatement Of Alcosupporting

confidence: 96%

Role of alpha-2 adrenoceptors in stress-induced reinstatement of alcohol seeking and alcohol self-administration in rats

et al. 2004

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Section: Effects Of Lofexidine and Yohimbine On Reinstatement Of Alcosupporting

confidence: 96%

Role of alpha-2 adrenoceptors in stress-induced reinstatement of alcohol seeking and alcohol self-administration in rats

et al. 2004

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“…The fact that two different pharmacologic interventions that decrease noradrenergic signaling, but via different mechanisms, are both capable of suppressing alcohol drinking is consistent with evidence that activation of the noradrenergic system plays a key role in mediating voluntary alcohol drinking. These results are also consistent with reports that: a) the α 2 -adrenergic receptor agonist, lofexidine, reduces operant self-administration of alcohol by Wistar rats (Lé, Harding, Juzytsch, Funk, & Shaham, 2005), b) clonidine and another α 2 -adrenergic receptor agonist, guanfacine, decrease alcohol drinking by food-restricted rats selectively bred for alcohol drinking (descendants of the Finnish Alko Alcohol (AA) rats) (Opitz, 1990), c) depletion of brain norepinephrine decreases alcohol drinking (Amit, Brown, Levitan, & Ogren, 1977; Brown et al, 1977) and alcohol self-administration in unselected rats (Davis et al, 1978), and d) prazosin reduces acute withdrawal-induced operant self-administration of alcohol by alcohol-dependent Wistar rats (Walker, Rasmussen, Raskind, & Koob, 2008). …”

Section: Discussionsupporting

confidence: 91%

The α2-adrenergic receptor agonist, clonidine, reduces alcohol drinking in alcohol-preferring (P) rats

Rasmussen

Alexander

Malone

et al. 2014

Alcohol

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Evidence suggests that noradrenergic signaling may play a role in mediating alcohol-drinking behavior in both rodents and humans. We have investigated this possibility by administering clonidine to alcohol-drinking rats selectively bred for alcohol preference (P line). Clonidine is an α2-adrenergic receptor agonist which, at low doses, inhibits noradrenergic signaling by decreasing norepinephrine release from presynaptic noradrenergic neurons. Adult male P rats were given 24-h access to food and water and scheduled access to a 15% (v/v) alcohol solution for 2 h daily. Rats received intraperitoneal (IP) injections with clonidine (0, 10, 20, 40, or 80 µg/kg body weight [BW], 10–11 rats/treatment group) once/day at 30 min prior to onset of the daily 2-h alcohol access period for 2 consecutive days. Clonidine, in doses of 40 or 80 µg/kg BW, significantly reduced alcohol intake on both days of treatment (p < 0.001). Two weeks later, rats were treated with clonidine for 5 consecutive days and clonidine, in doses of 40 or 80 µg/kg BW, reduced alcohol intake on all 5 treatment days (p < 0.001). Clonidine did not alter water consumption during the daily 2-h free-choice between alcohol and water. In a separate group of male P rats, clonidine (40 µg/kg BW) suppressed intake of a saccharin solution (0.04 g/L). These results are consistent with and complement our previous findings that the α1-adrenergic receptor antagonist, prazosin, decreases voluntary alcohol drinking in alcohol-preferring rats, but suggests that effects of clonidine may not be specific for alcohol. The results suggest that although activation of the noradrenergic system plays an important role in mediating voluntary alcohol drinking, care is needed in selecting which drugs to use to suppress central noradrenergic signaling in order to maximize the selectivity of the drugs for treating alcohol-use disorders.

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“…Hence, yohimbine, which also contains alpha-2 ARs antagonism may reinstates alcohol seeking after extinction (Marinelli et al, 2007). On the other hand, alpha-2 AR agonists may reduce alcohol consumption or alcohol-withdrawal symptoms (Opitz, 1990; Muzyk et al, 2011; Rasmussen et al, 2014; Fredriksson et al, 2015; Giovanitti et al, 2015). However, it has also been reported that specific agonists or antagonists of alpha-2 ARs may produce only minor changes in the voluntary alcohol drinking in alcohol-preferring rats (Korpi 1990).…”

Section: Discussionmentioning

confidence: 99%

“…Hence, yohimbine, an alpha-2 AR antagonist can reinstate alcohol seeking after extinction (Funk et al, 2016; Marinelli et al, 2007). On the other hand, alpha-2 A AR agonists that may decrease availability of NE reduce alcohol consumption (Fredriksson et al, 2015; Opitz, 1990; Rasmussen et al, 2014). However, very few studies have investigated direct effects of alcohol on apha-2 ARs, particularly in relation to depressive-like characteristics.…”

Section: Introductionmentioning

confidence: 99%

Role of cortical alpha-2 adrenoceptors in alcohol withdrawal-induced depression and tricyclic antidepressants

Getachew

Hauser

Csóka

et al. 2017

Drug and Alcohol Dependence

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Introduction Although a role for alpha-2 adrenoceptors (alpha-2 ARs) in alcohol use disorder (AUD) and depression is suggested, very little information on a direct interaction between alcohol and these receptors is available. Methods In this study adult female Wistar and Wistar-Kyoto (WKY) rats, a putative animal model of depression, were exposed to alcohol vapor 3 h daily for 10 days (blood alcohol concentration ~150 mg%) followed by daily injection of 10 mg/kg of imipramine (IMP, a selective norepinephrine NE/serotonin reuptake inhibitor) or nomifensine (NOMI, a selective NE/dopamine reuptake inhibitor). On day 11 animals were tested for open field locomotor activity (OFLA) and forced swim test (FST) and were sacrificed 2 h later for measurement of alpha-2 ARs densities in the frontal cortex and hippocampus using [3H]RX 821002 as the specific ligand. Results Chronic alcohol treatment increased the immobility in the FST, without affecting OFLA in both Wistar and WKY rats, suggesting induction of depressive-like behavior in Wistar rats and an exacerbation of this behavior in WKY rats. Alcohol treatment also resulted in an increase in cortical but not hippocampal alpha-2 ARs densities in both Wistar and WKY rats. The behavioral effects of alcohol were completely blocked by IMP and NOMI and the neurochemical effects (increases in alpha-2 ARs) were significantly attenuated by both drugs in both strains. Conclusions The results suggest a role for cortical alpha-2 ARs in alcohol withdrawal-induced depression and that selective subtype antagonists of these receptors may be of adjunct therapeutic potential in AUD-depression co-morbidity.

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The effect of clonidine and related substances on voluntary ethanol consumption in rats

Cited by 27 publications

References 29 publications

Role of alpha-2 adrenoceptors in stress-induced reinstatement of alcohol seeking and alcohol self-administration in rats

Role of alpha-2 adrenoceptors in stress-induced reinstatement of alcohol seeking and alcohol self-administration in rats

The α2-adrenergic receptor agonist, clonidine, reduces alcohol drinking in alcohol-preferring (P) rats

Role of cortical alpha-2 adrenoceptors in alcohol withdrawal-induced depression and tricyclic antidepressants

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