Open AccessJournal Article
Long-term effects of multiple doses of methamphetamine on tryptophan hydroxylase and tyrosine hydroxylase activity in rat brain
A J Hotchkiss,J W Gibb +1 more
TLDR
Agents which prevent the METH-induced decrease of neostriatal tyrosine hydroxylase activity, i.e., haloperidol, alpha-methyl-p-tyrosine and gamma-aminobutyric acid transaminase inhibitors also prevented the decrease in TPH activity caused by METH.Abstract:
Tryptophan hydroxylase (TPH) activity was measured in various rat brain regions after administering large doses of methamphetamine (METH). After four sequential doses of METH (15 mg/kg), given every 6 hr, TPH activity was decreased (to approximately 10% of control) in both the neostriatum and hippocampus. The depression of enzyme activity persisted for at least 30 days. When compared with the depression of neostriatal tyrosine hydroxylase activity, the depression of neostriatal and hippocampal TPH activity occurred sooner and was more pronounced. The depression of TPH activity was dependent on the number of doses and the amount of drug administered. Five days after one to two doses of METH, a transient recovery was observed but when four doses were given, the enzyme was depressed. No decrease in TPH activity was observed in brain areas containing serotonergic cell bodies. Agents which prevent the METH-induced decrease of neostriatal tyrosine hydroxylase activity, i.e., haloperidol, alpha-methyl-p-tyrosine and gamma-aminobutyric acid transaminase inhibitors also prevented the decrease in TPH activity caused by METH. In addition, fluoxetine, an inhibitor of 5-hydroxytryptamine re-uptake, prevented the METH-induced decrease in neostriatal and hippocampal TPH activity but did not alter the decrease in nenostriatal tyrosine hydroxylase activity.read more
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Enduring changes in brain and behavior produced by chronic amphetamine administration: A review and evaluation of animal models of amphetamine psychosis
Terry E. Robinson,Jill B. Becker +1 more
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Dissociable Deficits in the Decision-Making Cognition of Chronic Amphetamine Abusers, Opiate Abusers, Patients with Focal Damage to Prefrontal Cortex, and Tryptophan-Depleted Normal Volunteers: Evidence for Monoaminergic Mechanisms
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TL;DR: It is suggested that chronic amphetamine abusers show similar decision-making deficits to those seen after focal damage to orbitofrontal PFC, which may reflect altered neuromodulation of the orbitof prefrontal PFC and interconnected limbic-striatal systems by both the ascending 5-HT and mesocortical dopamine projections.
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Neurocognitive Effects of Methamphetamine: A Critical Review and Meta-analysis
J. Cobb Scott,Steven Paul Woods,Steven Paul Woods,Georg E. Matt,Rachel Meyer,Robert K. Heaton,J. Hampton Atkinson,Igor Grant +7 more
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Reduced Striatal Dopamine Transporter Density in Abstinent Methamphetamine and Methcathinone Users: Evidence from Positron Emission Tomography Studies with [11C]WIN-35,428
Una D. McCann,Dean F. Wong,Fuji Yokoi,Victor L. Villemagne,Robert F. Dannals,George A. Ricaurte +5 more
TL;DR: Persistent reductions in DAT density in methamphetamine and methcathinone users are suggestive of loss of DAT or loss of DA terminals and raise the possibility that as these individuals age, they may be at increased risk for the development of parkinsonism or neuropsychiatric conditions in which brain DA neurons have been implicated.
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Methamphetamine toxicity and messengers of death
Irina N. Krasnova,Jean Lud Cadet +1 more
TL;DR: The accumulated evidence indicates that multiple events converge to mediate METH-induced terminal degeneration and neuronal apoptosis, and suggest that pharmacological strategies geared towards the prevention and treatment of the deleterious effects of this drug will need to attack the various pathways that form the substrates of METH toxicity.