Honors Theses

Date of Award


Document Type

Undergraduate Thesis



First Advisor

Karen Sabol

Relational Format



Rationale Methamphetamine (METH) induces hypothermia at cool (18°) ambient temperatures and hyperthermia at neutral (24°) and warm (30°) ambient temperatures. Our objective was to determine if pretreatment with raclopride (RAC), a dopamine D2 receptor antagonist would alter METH-induced core temperature changes. Methods Two experiments were conducted. In Experiment 1, RAC was administered alone, to determine its effects, if any, on core temperature. In Experiment 2, rats received pretreatment injections of 0.3, 0.6, or 1.2-mg/kg RAC or a saline control (sal) injection; rats then received injections of 10 mg/kg METH or sal injection. In both Experiment 1 and 2, core temperature measurements were made telemetrically in three different ambient temperatures (18,24, or 30° C) Results Experiment 1: Treatment with the 1.2 mg/kg dose of RAC at 18° C caused hypothermia at 30,45, and 75 minutes post- treatment. RAC had no effect on core temperature at either 24° or 30° C. Experiment 2: Treatment with METH at 18° C caused hypothermia. At 18° C, all three RAC (0.3, 0.6,1.2 mg/kg) treatments enhanced the METH-induced hypothermia at 60 minutes post-treatment. Treatment with METH at 24° C and 30° caused hyperthermia. At 24° C, the 1.2 mg/kg RAC dose attenuated the METH-induced hyperthermia, at 60 minutes post treatment. The 0.3 mg/kg dose and the 0.6 mg/kg dose had no effect on the METH-induced hyperthermia. At 30° C, the 0.6 mg/kg RAC dose attenuated the METH-induced hyperthermia at 60 minutes post-treatment. Neither the 0.3 mg/kg dose nor the 1.2 mg/kg doses of RAC had an effect on the METH-induced hyperthermia at 30° C. Conclusions Experiment 7.- At 18° C, the 1.2 mg/kg dose of RAC caused an unexpected decrease in core temperature. This result is inconsistent with literature findings. In the hterature, D2 agonists caused a decrease in core temperature at room temperature (24° C), and D2 antagonists attenuated these hypothermic effects. Our result of RAC-induced hypothermia suggests the D2 receptor is involved m heat production at cool (18° C) ambient temperatures. Experiment 2;Pre-treatment with RAC enhanced METH-induced hypothermia at 18° C, and lowered METH-induced hyperthermia at 24° C, which is inconsistent with the above mentioned D2 direct agonist literature that suggests a D2 antagonist should increase core temperature. While inconsistent with the direct agonist data, the attenuation of METHinduced hyperthermia at 24° C by 1.2 mg/kg RAC was consistent with D2 antagonist/METH literature. The enhanced METH-induced hypothermia at 18° C and attenuated METHinduced hyperthermia at 24° C may be due to the interaction of dopamine, serotonin, and norepinephrine following METH administration.

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