Effects of Repeated High-Dose Methamphetamine on Local Cerebral Glucose Utilization in Rats

Huang, Yo-Ping

doi:10.1016/s0893-133x(99)00029-9

Cited by 24 publications

(16 citation statements)

References 27 publications

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“…It is unexpected that no significant functional changes within the NAc were seen under conditions of MA neurotoxicity. This finding, although not conclusive, is consistent with an earlier positron emission topographic study that failed to observe changes in cerebral glucose utilization, after MA administration, in the NAc (Huang et al 1999). …”

Section: Discussionsupporting

confidence: 85%

Neuronal dysfunction of a long projecting multisynaptic pathway in response to methamphetamine using manganese-enhanced MRI

Hsu¹,

Chen²,

Zechariah³

et al. 2007

Psychopharmacology

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Section: Discussionsupporting

confidence: 85%

Neuronal dysfunction of a long projecting multisynaptic pathway in response to methamphetamine using manganese-enhanced MRI

Hsu¹,

Chen²,

Zechariah³

et al. 2007

Psychopharmacology

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“…In particular, neuroimaging studies of mAMPH abusers reveal abnormal regional glucose metabolism in the anterior cingulate, orbital frontal and parietal cortices, as well as reductions of striatal dopamine transporters DAT; Kim et al, 2005, London et al, 2004; Volkow et al, 2001). These human studies are consistent with animal experiments showing persistent reductions in regional cerebral glucose metabolism and long-lasting decreases in several markers of striatal dopaminergic terminal integrity, such as dopamine (DA) content, tyrosine hydroxylase activity, and DAT (Huang et al, 1999; Pontieri et al, 1991; Hotchkiss et al, 1979; Ricaurte et al, 1982). …”

Section: Introductionsupporting

confidence: 80%

Cortical ionotropic glutamate receptor antagonism protects against methamphetamine-induced striatal neurotoxicity

2011

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Binge administration of the psychostimulant drug, methamphetamine (mAMPH), produces long-lasting structural and functional abnormalities in the striatum. mAMPH binges produce non-exocytotic release of dopamine (DA), and mAMPH-induced activation of excitatory afferent inputs to cortex and striatum is evidenced by elevated extracellular glutamate (GLU) in both regions. The mAMPH-induced increases in DA and GLU neurotransmission are thought to combine to injure striatal DA nerve terminals of mAMPH-exposed brains. Systemic pretreatment with either competitive or noncompetitive N-methyl-D-aspartic acid (NMDA) antagonists protects against mAMPH-induced striatal DA terminal damage, but the locus of these antagonists’ effects has not been determined. Here, we applied either the NMDA receptor antagonist, (DL)-amino-5-phosphonovaleric acid (AP5), or the alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor antagonist, dinitroquinoxaline-2,3-dione (DNQX), directly to the dura mater over frontoparietal cortex to assess their effects on mAMPH-induced cortical and striatal immediate-early gene (c-fos) expression. In a separate experiment we applied AP5 or DNQX epidurally in the same cortical location of rats during a binge regimen of mAMPH, and assessed mAMPH-induced striatal dopamine transporter (DAT) depletions one week later. Our results indicate that both ionotropic glutamate receptor antagonists reduced the mAMPH-induced Fos expression in cerebral cortex regions near the site of epidural application and reduced Fos immunoreactivity in striatal regions innervated by the affected cortical regions. Also, epidural application of the same concentration of either antagonist during a binge mAMPH regimen blunted the mAMPH-induced striatal DAT depletions with a topography similar to its effects on Fos expression. These findings demonstrate that mAMPH-induced dopaminergic injury depends upon cortical NMDA and AMPA receptor activation and suggest the involvement of the corticostriatal projections in mAMPH neurotoxicity.

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“…During exposure to Meth or MDMA, there is a high demand for energy and acute increases in energy metabolism in brain regions that exhibit increased activity produced by the drugs (Pontieri et al, 1990, Quate et al, 2004). Soon after the excessive increase in energy metabolism reported during drug exposure, there is evidence of compromised energy metabolism and depleted energy stores (Chan et al, 1994, Huang et al, 1999, Darvesh et al, 2002). These decreases in energy metabolism are further exacerbated by damage to mitochondria and specific complexes of the electron transport chain including complex II–III and IV (Burrows et al, 2000).…”

Section: Mechanisms Of Neurotoxicitymentioning

confidence: 99%

Neurotoxicity of methamphetamine and 3,4-methylenedioxymethamphetamine

2014

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Amphetamines are a class of psychostimulant drugs that are widely abused for their stimulant, euphoric, empathogenic and hallucinogenic properties. Many of these effects result from acute increases in dopamine and serotonin neurotransmission. Subsequent to these acute effects, methamphetamine and 3,4 methylenedioxymethamphetamine (MDMA) produce persistent damage to dopamine and serotonin nerve terminals. This review summarizes the numerous interdependent mechanisms including excitotoxicity, mitochondrial damage and oxidative stress that have been demonstrated to contribute to this damage. Emerging non-neuronal mechanisms by which the drugs may contribute to monoaminergic terminal damage, as well as the neuropsychiatric consequences of this terminal damage are also presented. Methamphetamine and 3,4-methylenedioxymethamphetamine (MDMA) have similar chemical structures and pharmacologic properties compared to other abused substances including cathinone (khat), as well as a relatively new class of novel synthetic amphetamines known as ‘bath salts’ that have gained popularity amongst drug abusers.

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Effects of Repeated High-Dose Methamphetamine on Local Cerebral Glucose Utilization in Rats

Abstract: Repeated administration of high doses of methamphetamine (MAP) to rats can induce long-lasting neurotoxicity

Cited by 24 publications

References 27 publications

Neuronal dysfunction of a long projecting multisynaptic pathway in response to methamphetamine using manganese-enhanced MRI

Neuronal dysfunction of a long projecting multisynaptic pathway in response to methamphetamine using manganese-enhanced MRI

Cortical ionotropic glutamate receptor antagonism protects against methamphetamine-induced striatal neurotoxicity

Neurotoxicity of methamphetamine and 3,4-methylenedioxymethamphetamine

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