Long-term effects of methamphetamine on the synthesis and metabolism of 5-hydroxytryptamine in various regions of the rat brain
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Neurotoxicity of methamphetamine: Main effects and mechanisms
2021, Experimental NeurologyCitation Excerpt :Large doses of METH also negatively impact serotonerigc systems in the dorsal striatum where striatal serotonin (5-HT) levels (Fukumura et al., 1998: Armstrong and Noguchi, 2004) and tryptophan hydroxylase (TPH) activity (Bakhit et al., 1981; Bakhit and Gibb, 1981) are reduced after injections of the drug. METH-induced abnormalities in 5-HT have also been reported in the nucleus accumbens (Nac), cortex, hippocampus, and hypothalamus (Hotchkiss and Gibb, 1980; Bakhit et al., 1981; Bakhit and Gibb, 1981; Baldwin et al., 1993; Armstrong and Noguchi, 2004). A very recent paper by Schweppe et al. (2020) reported that rats challenged with toxic doses of METH showed reduction in striatal and hippocampal DA, 5-HT, brain derived neurotrophic factor (BDNF), and TrkB even as long as 75 days after the drug injections.
Chronic methamphetamine self-administration disrupts cortical control of cognition
2016, Neuroscience and Biobehavioral ReviewsA dual-hit animal model for age-related parkinsonism
2010, Progress in NeurobiologyCitation Excerpt :METH is a powerfully addictive psychostimulant that causes major damage to monoamine-containing axon terminals in the striatum (Ricaurte et al., 1982; Sonsalla et al., 1992). High METH doses adversely affect monoaminergic systems of rodents and primates reducing brain levels of DA and serotonin (5-HT), as well as their synthesis controlling enzymes, tyrosine and tryptophan hydroxylase, respectively (Hotchkiss and Gibb, 1980; Wagner et al., 1980; Bakhit et al., 1981; Davidson et al., 2001). METH is a substrate for monoamine transporters and is transported into DAergic terminals, initially increasing cytosolic DA release and ultimately depleting DA (Kita et al., 2003).
Methamphetamine toxicity and messengers of death
2009, Brain Research ReviewsCitation Excerpt :The neurotoxic damage to striatal axonal terminals is accompanied by reactive astrocytosis (Bowyer et al., 1994; Cappon et al., 2000; Fukumura et al., 1998) and microglial activation (Pubill et al., 2002). In addition to the striatum, METH has been shown to cause decreases in 5-HT levels in medial prefrontal and somatosensory cortices, nucleus accumbens, hippocampus, hypothalamus and amygdala (Bakhit et al., 1981; Baldwin et al., 1993; Commins and Seiden, 1986; Friedman et al., 1998; Green et al., 1992; Ohmori et al., 1993; Ricaurte et al., 1980; Richards et al., 1993). There was also a significant decrease in 5-HTT binding in the anterior cingulate, nucleus accumbens, amygdala, hippocampus, somatosensory cortex, hypothalamus, thalamus and septum (Armstrong and Noguchi, 2004; Guilarte et al., 2003).
The methamphetamine experience: A NIDA partnership
2004, NeuropharmacologyElevation of fetal dopamine following exposure to methamphetamine in utero
2001, Developmental Brain Research