Brief communicationEnvironment-specific cross-sensitization between the locomotor activating effects of morphine and amphetamine
References (24)
- et al.
Persistence of chronic morphine effects upon activity in rats eight months after ceasing the treatment
Neuropharmacology
(1975) - et al.
Long-term sensitization to the excitatory effects of morphine
Neuropharmacology
(1983) - et al.
Locomotor activity in morphine-dependent and post-dependent rats
Pharmacol. Biochem. Behav.
(1981) - et al.
Akinesia after locally applied morphine near the nucleus raphe pontis of the rat
Neurosci. Lett.
(1984) - et al.
Lesions of ventral tegmental dopamine neurons delay the development of tolerance to morphine catalepsy
Neurosci. Lett.
(1985) - et al.
The effect of morphine applied locally to mesencephalic dopamine cell bodies on spontaneous motor activity in the rat
Neurosci. Lett.
(1979) - et al.
Sensitization to the hyperthermic and catecholamine-releasing effects of morphine
Life Sci.
(1981) - et al.
Enduring changes in brain and behavior produced by chronic amphetamine administration: A review and evaluation of animal models of amphetamine psychosis
Brain Res. Rev.
(1986) - et al.
Effects of naloxone on morphine induced sedation and hyperactivity in the hamster
Pharmacol. Biochem. Behav.
(1986) - et al.
Conditioned drug effects and absence of tolerance to d-amphetamine induced motor activity
Pharmacol. Biochem. Behav.
(1973)
Conditioning and place-specific sensitization of increases in activity induced by morphine in the VTA
Pharmacol. Biochem. Behav.
Time-dose relationships for locomotor activity effects of morphine after acute or repeated treatment
Br. J. Pharmacol.
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2017, Current Opinion in Behavioral SciencesCitation Excerpt :For example, when drug availability is explicitly paired with a particular context, behavioral activation [34,35] and DA cell reactivity [36–38] are both elevated in the drug-paired environment. When animals are tested in environments that have been paired with the absence of drug delivery, behavioral activation [34,35] and DA cell reactivity [36–38] are diminished. While the hypothesis awaits explicit testing in humans, the studies of striatal DA release reviewed here are at least not inconsistent.
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2015, Brain ResearchCitation Excerpt :On ‘Test day’, three days later, the rats are exposed to training- or extinction-related context and cues to assess whether inactivation of the previously activated β-gal-expressing neurons altered the ability of the cues and contexts to reactivate the same neurons and induce context-specific behavior. The first application of the Daun02 inactivation procedure was context-specific sensitization of cocaine-induced locomotor activity where the sensitized response is expressed in only the drug-paired environment (A) and not in a non-drug-paired environment (B) (Anagnostaras and Robinson, 1996; Badiani and Robinson, 2004; Crombag et al., 2002; Hope et al., 2006; Koya et al., 2009; Marin et al., 2009; Mattson et al., 2008; Robinson et al., 1998; Stewart et al., 1984; Stewart and Vezina, 1991; Uslaner et al., 2003; Vezina and Stewart, 1984; Vezina et al., 1989). We first found that context-specific cocaine-induced locomotion induced Fos in ~3% of nucleus accumbens neurons.
Role of context in neurotensin-induced sensitization to the locomotor stimulant effect of amphetamine
2014, PeptidesCitation Excerpt :Other studies have also reported a sensitization effect between different drugs of abuse. Repeated systemic injections of morphine or cocaine for instance sensitize to the locomotor stimulant effect of amphetamine [11,22] and this interaction has been explained by an action of these drugs on a common neural pathway. In effect, all these drugs increase mesolimbic dopaminergic neurotransmission; morphine stimulates dopamine impulse flow while cocaine and amphetamine increase synaptic dopamine levels.