Short communicationDevelopmental dissociation of methamphetamine-induced depletion of dopaminergic terminals and astrocyte reaction in rat striatum
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Cited by (112)
Peri-adolescent exposure to (meth)amphetamine in animal models
2022, International Review of NeurobiologyAstroglial correlates of neuropsychiatric disease: From astrocytopathy to astrogliosis
2018, Progress in Neuro-Psychopharmacology and Biological PsychiatryCitation Excerpt :However results from another study showed that after either amphetamine or methamphetamine treatment, GFAP mRNA and protein expression increased 6–72 h later in the mouse brain (O'Callaghan et al., 2014). Similarly, abstinence from methamphetamine, at the same time point of 72 hours, resulted in increased GFAP expression in the dorsal striatum of adult rats (O'Callaghan and Miller, 1994; Hess et al., 1990; Pu and Vorhees, 1993; Pu et al., 1994; Thomas et al., 2004). Moreover, 12 or 72 hours of abstinence following methamphetamine treatment resulted in a hypertrophy of astrocytes in the striatum (O'Callaghan et al., 2014), indicating that limited abstinence from methampetamine can induce astrogliosis, in agreement with measurements of GFAP expression.
Ontogeny of monoamine neurotransmitters
2018, Handbook of Developmental NeurotoxicologyFronto-temporal alterations and affect regulation in methamphetamine dependence with and without a history of psychosis
2016, Psychiatry Research - NeuroimagingCitation Excerpt :One possibility is that this represents a compensatory response to MA-induced ischemic or neurotoxic injury, thus pointing to inflammation or reactive microgliosis and astrocytosis (Sekine et al., 2008; Yamamoto et al., 2010). Prior preclinical studies have supported this explanation (Pu and Vorhees, 1993; Asanuma et al., 2004; LaVoie et al., 2004). Another potential response to MA neurotoxicity is an upregulation of brain-derived neurotrophic factor (BDNF) levels, as has been previously reported in humans (Kim et al., 2005) and rodents (Braun et al., 2011).
Prenatal methamphetamine exposure and neurodevelopmental outcomes in children from 1 to 3years
2014, Neurotoxicology and TeratologyCitation Excerpt :Additionally, neurotoxic effects could occur indirectly through maternal anorexic effects of MA, through vasoconstrictive effects resulting in reduced uteroplacental blood flow and fetal hypoxia or through a cascade of events that repeatedly challenge the stress-response systems during gestation leading to an alteration in the hypothalamic–pituitary–adrenal axis (Lester and Padbury, 2009; Salisbury et al., 2009; Stek et al., 1993). Evidence from animal studies have revealed that prenatal administration of MA is toxic to dopaminergic and serotonergic neurons (Fuller and Hemrick-Luecke, 1992; Pu and Voorhees, 1993); and results in motor and learning impairment (Itoh et al., 1991; Slamberova et al., 2005; Wallace et al., 1999). Prenatal exposure in mice has been found to enhance conceptual DNA oxidation and lead to long-term and possibly permanent postnatal neurodevelopmental deficits in motor coordination (Jeng et al., 2005).