Morehead State University

Long-Term Learning Deficits and Neurochemical Changes Result

Institution

Morehead State University

Abstract

METH is known to produce neurotoxic effects in the central nervous system, affecting an array of behaviors. This study examined the effects of METH on spatial learning and correlative changes in neurochemistry. Rats were trained in a visuospatial task requiring a correct barpress opposite the stimulus location until they reached a criterion of acquisition (>85% correct, three sessions). Rats received four injections of METH (9.0 mg/kg) or saline at 12-hour interval. Two weeks following treatment, rats were retested on the same task to examine METH effects on retention. METH treatment displayed no significant effect on retention. Rats then began training on a reversal task requiring a correct barpress same as stimulus location to examine METH effects on new learning. METH treatment impaired performance on the reversal task, showing a delayed learning. The fact that learning prior to METH exposure remains intact suggests that learning METH-induced impairment is specific to new learning. Dopamine levels were measured using HPLC and compared between treatment conditions. Results indicated an upregulation of dopamine in the prefrontal cortex and the nucleus accumbens of METHtreated rats, suggesting the escalated levels of dopamine are responsible for learning deficits.

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Long-Term Learning Deficits and Neurochemical Changes Result

METH is known to produce neurotoxic effects in the central nervous system, affecting an array of behaviors. This study examined the effects of METH on spatial learning and correlative changes in neurochemistry. Rats were trained in a visuospatial task requiring a correct barpress opposite the stimulus location until they reached a criterion of acquisition (>85% correct, three sessions). Rats received four injections of METH (9.0 mg/kg) or saline at 12-hour interval. Two weeks following treatment, rats were retested on the same task to examine METH effects on retention. METH treatment displayed no significant effect on retention. Rats then began training on a reversal task requiring a correct barpress same as stimulus location to examine METH effects on new learning. METH treatment impaired performance on the reversal task, showing a delayed learning. The fact that learning prior to METH exposure remains intact suggests that learning METH-induced impairment is specific to new learning. Dopamine levels were measured using HPLC and compared between treatment conditions. Results indicated an upregulation of dopamine in the prefrontal cortex and the nucleus accumbens of METHtreated rats, suggesting the escalated levels of dopamine are responsible for learning deficits.