The influence of prolonged amphetamine treatment and amphetamine withdrawal on brain biogenic amine content and behaviour in the rat

Herman, Zbigniew S.; Trzeciak, Henryk I.; Chruściel, T. L.; Kmieciak-Kołada, K; Drybański, A; Sokola, A

doi:10.1007/bf00403998

Cited by 35 publications

(12 citation statements)

References 18 publications

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“…In agreement with the present results, early studies showed that withdrawal from chronic psychostimulant administration in animals is associated with deficits in spontaneous locomotor activity, as well as alterations in drug-influenced motor responses (e.g., Herman et al 1971;Tonge 1974;Lynch and Leonard 1978). More recently, measurement of motor function after termination of daily prolonged amphetamine self-administration sessions revealed decreased spontaneous locomotor activity and increased catalepsy in rats (Pulvirenti and Koob 1993).…”

Section: Discussionsupporting

confidence: 90%

Increased sensitivity to the locomotor depressant effect of a dopamine receptor antagonist during cocaine withdrawal in the rat

1999

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The effect of a dopamine receptor antagonist on locomotor activity was examined during withdrawal from either self-administered or experimenter-administered cocaine. In the self-administration experiment, the locomotor response to a challenge injection of cis-flupenthixol was assessed in photocell cages at 4 h after the cessation of a 12-h cocaine self-administration session. Rats which had self-administered cocaine, and were challenged with cis-flupenthixol (0.05 mg/kg), were found to be hypoactive relative to controls. In the experimenter-administered cocaine experiment, animals were given eight IP injections of 15 mg/kg cocaine over a 9.5-h period, for a total of 120 mg/kg. At 4, 8, and 24 h (tested in three separate groups of rats) after cessation of the eight injections, the locomotor response to a challenge injection of saline or cis-flupenthixol was tested. Cocaine-treated animals displayed a dose-dependent, heightened sensitivity to the locomotor depressant effects of 0.05 mg/kg and 0.2 mg/kg cis-flupenthixol 4 h post-cocaine, whereas they did not show increased sensitivity to 0.05 mg/kg cis-flupenthixol 8 or 24 h post-cocaine. However, cocaine-treated animals displayed a mild hypoactivity 8 h post-cocaine. In a separate group of animals, a dose-response experiment was performed which indicated that a dose of cis-flupenthixol as high as 0.2 mg/kg was required to produce locomotor depression in cocaine-naive rats. The results of this study support clinical observations of dopamine antagonist-precipitated motor dysfunction in abstinent cocaine abusers, and lend further support to the hypothesis that alterations in dopaminergic neurotransmission consequent to prolonged cocaine exposure are partly responsible for some of the symptoms of cocaine withdrawal.

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Section: Discussionsupporting

confidence: 90%

Increased sensitivity to the locomotor depressant effect of a dopamine receptor antagonist during cocaine withdrawal in the rat

1999

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“…Tissue levels of 5-HT significantly decreased in the cerebellum, striatum, cerebral cortex, and PFC after 12 h-3 days of AMPH/METH abstinence [80,83,93,94]. It is noted that the drug treatment regimens, except that of Persico et al [80], did not completely fit the proposed regimens promising behavioral changes associated with symptoms of AMPH withdrawal.…”

Section: Postmortem Brain Tissue Levels Of Dopamine and Metabolites Amentioning

confidence: 82%

“…route administration protocol [93,94]. Up-regulation of the MAO metabolic pathway after drug treatment could not account for this phenomenon, since MHPG levels also significantly decreased (Table 1; discussed below).…”

Section: Postmortem Brain Tissue Levels Of Dopamine and Metabolites Amentioning

confidence: 92%

Neurochemical Consequences of Dysphoric State During Amphetamine Withdrawal in Animal Models: A Review

Kitanaka

Takemura

2007

Neurochem Res

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Chronic abuse of amphetamines, such as d-amphetamine (AMPH) and d-methamphetamine, results in psychological dependence, a condition in which the drug produces a feeling of satisfaction and a drive that requires periodic or continuous administration of the drug to produce overwhelming pleasure or to avoid discomfort such as dysphoria. The dysphoric state of AMPH withdrawal has been recognized as depressive syndromes, such as anhedonia, depression, anxiety, and social inhibition, in early drug abstinence. Medication for treatment of the dysphoric state is important for AMPH abusers to avoid impulsive self-injurious behavior or acts that are committed with unconscious or uncontrolled suicidal ideation. However, successful treatments for AMPH withdrawal remain elusive, since the exact molecular basis of the expression of dysphoria has not been fully elucidated. This review focuses on the molecular aspects of AMPH withdrawal as indexed by neurochemical parameters under a variety of injection regimens (for example, levels of brain monoamines and their metabolites, and gamma-aminobutyric acid, expression of genes and proteins involved in neuronal activity, and monoamine metabolism and availability) in rodent models which exhibit significant phenotypic features relevant to the syndromes of AMPH withdrawal in humans.

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“…The basal concentration of NE in dialysate was elevated in both the hypothalamus and hippocampus 1 day after the discontinuation of AMPH treatment, and remained elevated in the hippocampus even after 30 days of withdrawal. Although it is not clear how these changes in NE neurotransmission contribute to the AMPH withdrawal syndrome, they are consistent with the idea that AMPH exposure can produce alterations in NE systems that outlast the acute effects of the drug (Alloway and Rebec 1983;Bardsley and Bachelard 1981;Cassens et al 1979;Eichler et al 1980;Herman et al 1971;Tonge 1974;Short and Shuster 1976;Lynch et al 1977;Pearl and Seiden 1976;Segal et al 1980;Sorenson et al 1985). We previously reported, for example, that AMPH withdrawal is accompanied by a transient decrease in hypothalamic NE content (Paulson et al 1991), and the present study suggests this could be due to an increase in basal NE release.…”

Section: Discussionmentioning

confidence: 69%

“…In humans, the discontinuation of chronic AMPH use initially results in a withdrawal syndrome that is reported to include mood changes that resemble some symptoms of depression (Gawin and Ellinwood 1988;Jaffe 1990;Watson et al 1972). In rats, a post-AMPH withdrawal 'depression' in behavior has been described, and its major features include a decrease in nocturnal locomotor activity, a decrease in the efficacy of intracranial selfstimulation reward, and an insensitivity to external stimulation (Cassens et al 1981;Herman et al 1971;Kokkinidis and Zacharko 1980;Leith and Barrett 1976;Paulson et al 1991;Robinson and Camp, 1987;Schreiber et al 1976;Tonge 1974). These effects are relatively transient, usually lasting for only 1 to 10 days after the discontinuation of AMPH treatment (Cassens et al 1981; Leith and Barrett 1976;Paulson et al 1991).…”

mentioning

confidence: 99%

Time-Dependent Effects of Repeated Amphetamine Treatment on Norepinephrine in the Hypothalamus and Hippocampus Assessed with In Vivo Microdialysis

Camp

DeJonghe

Robinson

1997

Neuropsychopharmacology

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The influence of prolonged amphetamine treatment and amphetamine withdrawal on brain biogenic amine content and behaviour in the rat

Cited by 35 publications

References 18 publications

Increased sensitivity to the locomotor depressant effect of a dopamine receptor antagonist during cocaine withdrawal in the rat

Increased sensitivity to the locomotor depressant effect of a dopamine receptor antagonist during cocaine withdrawal in the rat

Neurochemical Consequences of Dysphoric State During Amphetamine Withdrawal in Animal Models: A Review

Time-Dependent Effects of Repeated Amphetamine Treatment on Norepinephrine in the Hypothalamus and Hippocampus Assessed with In Vivo Microdialysis

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