Calcium receptor antagonists modify cocaine effects in the central nervous system differently
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Cited by (90)
Usage of L-type calcium channel blockers to suppress drug reward and memory driving addiction: Past, present, and future
2022, NeuropharmacologyCitation Excerpt :In the next section, preclinical studies implicating LTCCs in the dopaminergic system in drug action and drug-associated learning and memory will be discussed. The first animal studies reporting the potential involvement of LTCCs in the dopaminergic system in the action of addictive drugs came from studies demonstrating that dihydropyridine LTCC blockers (nimodipine and isradipine) suppress cocaine-induced DA release in the ventral striatum and locomotor stimulation in rats, while other types of LTCC blockers (verapamil and diltiazem) were ineffective (Pani et al., 1990a, 1990b). Subsequently, a number of studies have reported that systemic administration of LTCC blockers inhibits acquisition of drug-induced conditioned place preference (CPP) (Biala and Langwinski, 1996; Pani et al., 1991; Pucilowski et al., 1993, 1995), a form of Pavlovian learning where distinct contextual cues of the conditioning box are paired with drug exposure, and also suppresses acquisition of operant responding (self-administration) for cocaine and morphine (Kuzmin et al., 1992).
Psychostimulants, antidepressants and neurokinin-1 receptor antagonists ('motor disinhibitors') have overlapping, but distinct, effects on monoamine transmission: The involvement of L-type Ca<sup>2+</sup> channels and implications for the treatment of ADHD
2014, NeuropharmacologyCitation Excerpt :Since then, there have been remarkably few studies of how the response to psychostimulants might be influenced by LTCCs. There is one report that the dopamine response to cocaine is prevented by dihydropyridines, but not other classes of LTCC-blockers (Pani et al., 1990). There is no evidence that psychostimulants bind to these channels and so it was inferred that cocaine activates dihydropyridine-sensitive LTCCs indirectly.
Dantrolene blockade of ryanodine receptor impairs ethanol-induced behavioral stimulation, ethanol intake and loss of righting reflex
2012, Behavioural Brain ResearchCitation Excerpt :These authors additionally suggested that manipulations affecting cellular Ca2+ pool or flux have a more prominent role in the behavioral-stimulating effect of EtOH in comparison to that of other drugs with motor-stimulating properties. Thus, Ca2+ manipulations at doses that reduced EtOH-induced locomotor activity or ethanol intake did not prevent the behavioral activation produced by psychostimulants such amphetamine, caffeine or cocaine [61,67–69]. Data obtained in this study, also provided evidence that dantrolene and thereby intracellular Ca2+ may be involved in the sedative effects of EtOH since dantrolene pretreatment decreased the duration of the EtOH-induced sleeping time.
Intracellular calcium chelation with BAPTA-AM modulates ethanol-induced behavioral effects in mice
2012, Experimental NeurologyCitation Excerpt :Pretreatment with antagonists of L-type VDCC blockers resulted in a reduction in the stimulatory effects of ethanol (Baliño et al., 2010; Engel et al., 1988; White and Smith, 1992). Also, it has been previously found that amphetamine-, caffeine-, or cocaine-induced activation was not prevented by such VDCC blockers (Baliño et al., 2010; Mills et al., 2007; Pani et al., 1990; Rogério and Takahashi, 1990) at doses that reduced ethanol-induced locomotor activity. These data, therefore, suggest that Ca2+ flux as well as intracellular Ca2+ levels is critical for the stimulatory effects of ethanol, but this does not appear to be a general mechanism underlying drug-induced locomotor activation.
Calcium channel antagonists suppress cross-tolerance to the anxiogenic effects of d-amphetamine and nicotine in the mouse elevated plus maze test
2008, Progress in Neuro-Psychopharmacology and Biological Psychiatry
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Research Associate, Department of Pharmacology, Pavlov Institute, Leningrad, U.S.S.R.