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A General Method for Evaluating Deep Brain Stimulation Effects on Intravenous Methamphetamine Self-Administration
Published on: January 22, 2016
Involvement of glucocorticoid receptor on hyperpyrexia induced by methamphetamine administration
S Yoshida1, H Kinoshita, T Tatara
1Department of Anesthesia, Hyogo College of Medicine, Nishinomiya, Japan.
Soudni Lekarstvi
|November 6, 2012
Summary
Glucocorticoids contribute to methamphetamine-induced hyperpyrexia in rats. Blocking the glucocorticoid receptor or adrenalectomy significantly reduced the increase in body temperature, suggesting a key role for this pathway.
Area of Science:
- Pharmacology
- Neuroscience
- Endocrinology
Background:
- Methamphetamine (MA) is a psychostimulant drug with significant abuse potential.
- Hyperpyrexia, a dangerous elevation of body temperature, is a known adverse effect of MA.
- Glucocorticoids, like corticosterone, are stress hormones that play various physiological roles.
Purpose of the Study:
- To investigate the role of glucocorticoids in methamphetamine-induced hyperpyrexia.
- To determine if blocking glucocorticoid receptors affects MA-induced temperature increases.
Main Methods:
- Utilized a bio-telemetric system for continuous body temperature monitoring in rats.
- Administered methamphetamine to induce hyperpyrexia.
- Performed adrenalectomy or administered RU-486 (a glucocorticoid receptor antagonist).
Main Results:
- Methamphetamine administration led to a significant increase in rat body temperature (hyperpyrexia).
- Adrenalectomy, which removes the source of glucocorticoids, suppressed the hyperpyrexic response.
- Administration of RU-486 also significantly inhibited the MA-induced rise in body temperature.
Conclusions:
- Glucocorticoid signaling is implicated in the development of methamphetamine-induced hyperpyrexia.
- The glucocorticoid receptor plays a crucial role in mediating this adverse effect of MA.
- Targeting the glucocorticoid pathway may offer a strategy to manage MA-induced hyperthermia.
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