Methamphetamine human brain effects

Dopaminergic activity. Smoke was administered intranasally to mice for 20 minutes twice daily for 3 days before methamphet-amine treatment. The treatment significantly attenuated the neurotoxicity as judged by a lesser depletion of dopamine, dihydrophenylacetic acid, and homovanillic acid. The lesser effect of methamphetamine on the content of serotonin level was unaltered by prior inhalation of smoke h Tobacco glycoside, administered to mice, increased behavior via dopamine 2 neuronal activity but not dopamine 1 activity in a dose-dependent manner. The results indicated that smoking can affect the human brain function via not only the nicotinic cholinergic neuron but also the dopamine 2 neuron . 

Suzuki and colleagues (1986, 1987) have tested the effects of altering methamphetamine p-hydroxylation in rats it appeared that inhibition enhanced the methamphetamine-induced stereotyped behavior. One might conjecture that an equivalent effect could occur in humans with inborn CYP2D6 deficiency if a toxic dose of methamphetamine were applied. Unfortunately, studies of animals do not necessarily help p-hydroxyamphetamine is the main metabolite of amphetamine in rats but not in human liver (see above), and most studies on brain metabolism have not been conducted in human tissue. 

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