Abstract
Methamphetamine (METH) abuse is a serious public health problem as evidenced by findings that high‐dose administration of this stimulant causes persistent dopaminergic deficits in both non‐human and human models. Noteworthy, adolescent (i.e., postnatal day (PND) 40) rats are less susceptible to this damage than young adult (PND90) rats. Further, bi‐weekly treatment with METH, beginning at PND40 and continuing throughout development, prevents the persistent dopaminergic deficits caused by a “challenge” high‐dose METH regimen when administered at PND90. Mechanisms underlying this “resistance” in rats treated with METH during development were thus investigated. Results revealed that METH treatment throughout development attenuated both acute and persistent effects on monoaminergic transporter function caused by a challenge METH treatment. METH treatment during development also attenuated the hyperthermic response caused by a “challenge” METH treatment. Mechanisms underlying these phenomena, including the role of pharmacokinetics, will be discussed. (Supported by: DA09407, 019447, 013367, 00869, 11389, 04222, 00378)
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