Time-dependent effects of prazosin on the development of methamphetamine conditioned hyperactivity and context-specific sensitization in mice

White, André O.; Rauhut, Anthony S.

doi:10.1016/j.bbr.2014.01.032

Cited by 9 publications

(3 citation statements)

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“…Thus, propranolol in the present experiment may have blocked the unconditioned and conditioned locomotor effects of methamphetamine by interacting in the BNST to modulate dopaminergic VTA activity. These results, viewed in conjunction with previous studies (White and Rauhut, 2014), suggest that both the α-adrenergic, especially the α 1 -adrenergic, and β-adrenergic receptors interact with the mesocorticolimbic dopaminergic system to modulate the unconditioned and conditioned hyperactive effects of methamphetamine. Propranolol also interacts with 5-HT 1A /5-HT 1B receptors; thus, the contribution of the serotonergic system cannot be excluded (Middlemiss, 1984).…”

Section: Discussionsupporting

confidence: 85%

Propranolol blocks the unconditioned and conditioned hyperactive effects of methamphetamine in CD-1 mice

Rauhut

2023

Behavioural Pharmacology

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The present experiment examined the contribution of the β-adrenergic receptor system in mediating the unconditioned (i.e. pharmacological) and conditioned (i.e. learned) hyperactive effects of methamphetamine. To this end, mice underwent an 8-day conditioning procedure involving two different, alternating session types (chamber and home-cage days). On chamber days (1, 3, 5, and 7), mice were injected (intraperitoneally) with vehicle (dH2O) or propranolol (16 or 32 mg/kg) and were injected (subcutaneously) 30 min (min) later by either vehicle (saline; unpaired) or methamphetamine (1.0 mg/kg; paired). On home-cage days (2, 4, 6, and 8), mice were injected (subcutaneously) with either vehicle (saline; paired) or methamphetamine (1.0 mg/kg; unpaired) in their home cages. The test day for conditioned hyperactivity occurred 48 h after the last chamber day. Propranolol dose-dependently blocked the unconditioned and conditioned hyperactive effects of methamphetamine, implicating a role for the β-adrenergic system in mediating these effects of methamphetamine.

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Section: Discussionsupporting

confidence: 85%

Propranolol blocks the unconditioned and conditioned hyperactive effects of methamphetamine in CD-1 mice

Rauhut

2023

Behavioural Pharmacology

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“…Genetic ablation of the alpha-1b adrenergic receptor also diminished cocaine consumption in an oral self-administration setting (Drouin et al, 2002a). Moreover, treatment with prazosin or with the longer acting alpha-1 adrenergic antagonist doxazosin attenuated sensitized locomotor response to d -amphetamine (Vanderschuren et al, 2003), methamphetamine (White and Rauhut, 2014), cocaine (Haile et al, 2012; Jimenez-Rivera et al, 2006), or (+/−)-3,4-methylenedioxymethamphetamine (MDMA) (Selken and Nichols, 2007). Pretreatment with prazosin also attenuated cocaine-induced reinstatement of extinguished drug-seeking behavior in rats (Zhang and Kosten, 2005; 2007).…”

Section: Introductionmentioning

confidence: 99%

Psychostimulants affect dopamine transmission through both dopamine transporter-dependent and independent mechanisms

Peña

Gevorkiana

Shi

2015

European Journal of Pharmacology

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The precise mechanisms by which cocaine and amphetamine-like psychostimulants exert their reinforcing effects are not yet fully defined. It is widely believed, however, that these drugs produce their effects by enhancing dopamine neurotransmission in the brain, especially in limbic areas such as the nucleus accumbens, by inducing dopamine transporter-mediated reverse transport and/or blocking dopamine reuptake though the dopamine transporter. Here, we present the evidence that aside from dopamine transporter, non-dopamine transporter-mediated mechanisms also participate in psychostimulant-induced dopamine release and contribute to the behavioral effects of these drugs, such as locomotor activation and reward. Accordingly, psychostimulants could increase norepinephrine release in the prefrontal cortex, the latter then alters the firing pattern of dopamine neurons resulting in changes in action potential-dependent dopamine release. These alterations would further affect the temporal pattern of dopamine release in the nucleus accumbens, thereby modifying information processing in that area. Hence, a synaptic input to a nucleus accumbens neuron may be enhanced or inhibited by dopamine depending on its temporal relationship to dopamine release. Specific temporal patterns of dopamine release may also be required for certain forms of synaptic plasticity in the nucleus accumbens. Together, these effects induced by psychostimulants, mediated through a non-dopamine transporter-mediated mechanism involving norepinephrine and the prefrontal cortex, may also contribute importantly to the reinforcing properties of these drugs.

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“…The selective α-1 adrenergic receptor antagonists decreased the locomotor activity of animals, doses between 0.5 and 2 mg/kg result in a decrease in mouse hyperactivity [19]. The groups of animals treated with doxazosin 1 mg/kg, or doxazosin plus AMY or AMY alone, had practically the same locomotor behavior profile, there being no differentiation between the groups (Figure 2c).…”

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confidence: 92%

Monoaminergic Involvement in Decreased Locomotor Activity of Mice Treated with α and β-amyrin from Protium heptaphyllum

Aragão

Filho

Bandeira

et al. 2018

Natural Product Communications

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A triterpenic mixture of α and β-amyrin (AMY) extracted from Protium heptaphyllum has demonstrated several pharmacological effects, including activity in the central nervous system. The aim of this study was to evaluate the effect of AMY administration on locomotor activity of mice by the open field test using some monoaminergic agonists and antagonists and the cerebral cortex levels of monoamines and their major metabolites by high-performance liquid chromatography. Mice were treated acutely with AMY at doses of 1, 2.5 and 5 mg/kg given intraperitoneally and with the pharmacological agents and placed in open field test, then the animals were sacrificed and the cerebral cortex extracted, and monoamines were assayed in tissue homogenates. AMY at 1, 2.5 and 5 mg/kg decreased locomotor activity of animals by 25, 31 and 39%, respectively in the open field test. Ondasentron, doxazosin, oxymetazoline and clonidine did not reverse the inhibitory effect of 5 mg/kg AMY. Venlafaxine and yohimbine reversed the inhibitory effect of 5 mg AMY. In the cortex, the 5-HT and 5-HIAA were significantly reduced by the administration of AMY. NE and HVA were also reduced with 2.5 and 5 mg/kg AMY, while Dopamine and DOPAC were not increased with AMY. In conclusion, AMY decreased locomotor activity of animals accompanied by a decrease in 5-HT and NE levels in the cerebral cortex, this locomotor effect is reversed by drug that blocker the α-2-adrenoreceptor.

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Time-dependent effects of prazosin on the development of methamphetamine conditioned hyperactivity and context-specific sensitization in mice

Cited by 9 publications

References 50 publications

Propranolol blocks the unconditioned and conditioned hyperactive effects of methamphetamine in CD-1 mice

Propranolol blocks the unconditioned and conditioned hyperactive effects of methamphetamine in CD-1 mice

Psychostimulants affect dopamine transmission through both dopamine transporter-dependent and independent mechanisms

Monoaminergic Involvement in Decreased Locomotor Activity of Mice Treated with α and β-amyrin from Protium heptaphyllum

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