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Effects of repeated high-dose methamphetamine and ceftriaxone post-treatments on tissue content of dopamine and serotonin as well as glutamate and glutamine
2016, Neuroscience LettersCitation Excerpt :Importantly, repeated exposure to high doses of METH has been found to cause depletion of dopamine and serotonin (5-HT) at the nerve terminals [1–5] and promote a delayed increase in extracellular glutamate concentration in different brain regions [6–8]. Importantly, blockade of NMDA receptors prevented METH effects on dopamine depletion, which suggests the critical role of glutamatergic neurotransmission in METH-induced neurotoxicity [9]. It is well known that excessive glutamate is excitotoxic [10,11].
Methamphetamine neurotoxicity: Necrotic and apoptotic mechanisms and relevance to human abuse and treatment
2001, Brain Research ReviewsThe effect of (R)-HA966 or ACEA 1021 on dexfenfluramine or (5)-MDMA-induced changes in temperature, activity, and neurotoxicity
2001, Pharmacology Biochemistry and BehaviorDifferential effects of agents acting at various sites of the NMDA receptor complex in a place preference conditionig model
1996, European Journal of Pharmacology7-Chlorokynurenic acid prevents in vitro epileptiform and neurotoxic effects due to kainic acid
1996, General PharmacologyNmda antagonists: Antiepileptic-neuroprotective drugs with diversified neuropharmacological profiles
1995, Pharmacological Research
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