The N-methyl-d-aspartate antagonist MK-801 protects against serotonin depletions induced by methamphetamine 3,4-methylenedioxymethamphetamine and p-chloroamphetamine

Ammonia Mediates Methamphetamine-Induced Increases in Glutamate and Excitotoxicity

“…Calpain is a protease whose activity increases in response to increases in calcium and promotes excitotoxicity (Harris and Morrow, 1988;Siman et al, 1989). During and shortly after METH exposure, significant increases in extracellular glutamate activate calcium-permeable glutamate receptors, which have been implicated in METH-mediated monoaminergic terminal damage (Farfel et al, 1992;Sonsalla et al, 1991;Stephans and Yamamoto, 1994). Subsequent to calcium-permeable glutamate receptor activation, there is an influx of intracellular calcium, activation of calpain, and excitotoxicity (Staszewski and Yamamoto, 2006).…”

“…Blockade of METH-induced increases in glutamate, activation of AMPA or NMDA receptors, or NOS-derived peroxynitrite protect against the mitochondrial and neuronal damage produced by the drug and provide evidence for activation of calcium-dependent proteases such as calpain in mediating the long-term damage to dopamine and serotonin terminals elicited by METH (Farfel et al, 1992;Staszewski and Yamamoto, 2006;Tata and Yamamoto, 2007). Calpain is a calcium-activated protease that is activated in the context of excitotoxicity in response to significant increases in intracellular calcium.…”

Effects of chronic unpredictable stress and methamphetamine on hippocampal glutamate function

“…Specifically, both acute restraint stress and Meth increase extracellular glutamate in the dorsal and ventral hippocampus, respectively (Lowy et al, 1993;Rocher and Gardier 2001). Furthermore, stressinduced dendritic atrophy and Meth-induced decreases in 5HT in the hippocampus are attenuated by glutamate receptor antagonism (Farfel et al, 1992;. Despite these parallels, no studies have examined the effects of Meth alone on glutamate in the dorsal hippocampus and how prior stress exposure might modify the glutamate response to Meth.…”

Mechanisms of Action and Persistent Neuroplasticity by Drugs of Abuse

“…Excitotoxicity: glutamate receptor involvement and intracellular excitotoxic processes. Studies employing in vivo microdialysis have shown that METH increases glutamate release in the striatum (Mark et al, 2004;Nash and Yamamoto, 1992;Stephans and Yamamoto, 1994) and that blockade of glutamate receptors attenuates METH-induced depletion of striatal DA and other markers of toxicity (Farfel et al, 1992;Bowyer, 1995;Battaglia et al, 2002;Shah et al, 2012), indicating that glutamate receptor-mediated processes are involved in METH toxicity. Conversely, MDMA appears to reduce glutamate release in certain brain regions, and the importance of excitotoxicity in mediating MDMA-induced 5-HT toxicity is still unclear (Capela et al, 2009).…”

“…Hypophysectomy, Drug-Induced Neuroplasticity thyroparathyroidectomy, as well as treatment with high doses of haloperidol or diazepam that reduce body temperature during amphetamine treatments, also reduce the observed toxicity Sprague et al, 2003). A large number of neurotransmitter systems appears to be involved in producing the hyperthermic effect, because blockade of receptors, including the NMDAR; D 1 R, D 2 R, and D 3 R; a1-adrenoreceptors; 5-HT 2 receptors; as well as the s and OX 1 receptors, all prevent or reduce METH-induced hyperthermia while protecting against METH toxicity (Sonsalla et al, 1991;Farfel et al, 1992;Doyle and Yamamoto, 2010;Seminerio et al, 2011Seminerio et al, , 2012Rusyniak et al, 2012;Ares-Santos et al, 2012;Kikuchi-Utsumi et al, 2013;Robson et al, 2013a;Sabol et al, 2013;Baladi et al, 2014).…”