Elsevier

Brain Research

Volume 700, Issues 1–2, 27 November 1995, Pages 99-106
Brain Research

Effect of repeated methamphetamine administrations on dopamine and glutamate efflux in rat prefrontal cortex

https://doi.org/10.1016/0006-8993(95)00938-MGet rights and content

Abstract

Pretreatment with psychostimulants such as methamphetamine (METH) results in augmented mesostriatal dopamine transmission upon a challenge administration of the drug. This effect can be blocked by dopamine antagonists and excitatory amino acid antagonists. However, no direct comparisons have been made with respect to the effects of a low-dose pretreatment regimen of METH on impulse and transporter-mediated dopamine release or to what extent glutamate release is altered by a pretreatment regimen with METH. The purpose of this study was to examine dopamine and glutamate efflux in the prefrontal cortex and striatum in rats pretreated with METH following either high potassium (80 mM) infusion or after a systemic injection of a low dose of METH. Extracellular dopamine and glutamate concentrations in the prefrontal cortex and striatum were measured in vivo by microdialysis. Potassium infusion increased extracellular dopamine and glutamate concentrations to a greater extent in the prefrontal cortex than in the striatum of METH-pretreated rats compared to saline-pretreated controls. A low dose METH challenge significantly increased extracellular dopamine but not glutamate concentrations in both prefrontal cortex and striatum of all animals. Moreover, the acute METH-induced increase in cortical dopamine efflux was significantly greater in rats pretreated with METH. Overall, these data are the first evidence that repeated METH administrations can enhance cortical glutamate efflux and indicate that a low dose pretreatment regimen of METH enhances dopamine transmission in the prefrontal cortex through both transporter and depolarization-induced mechanisms.

Reference (57)

  • KazahayaY. et al.

    Subchronic methamphetamine treatment enhances methamphetamine- or cocaine-induced dopamine efflux in vivo

    Biol. Psychiatry

    (1989)
  • KoltaM.G. et al.

    Time course of the development of the enhanced behavioral and biochemical responses to amphetamine after pretreatment with amphetamine

    Neuropharmacology

    (1985)
  • KuczenskiR. et al.

    Chronic amphetamine: is dopamine a link in or a mediator of the development of tolerance and reverse tolerance?

    Pharmacol. Biochem. Behav.

    (1981)
  • LiangN.Y. et al.

    Comparison of the release of [3H]dopamine from isolated corpus striatum by amphetamine, fenfluramine and unlabelled dopamine

    Biochem. Pharmacol.

    (1982)
  • MullerP. et al.

    Presynaptic subsensitivity as a possible basis for sensitization by long-term dopamine mimetics

    Eur. J. Pharmacol.

    (1979)
  • MurakiA. et al.

    MK-801, a non-competitive antagonist of NMDA receptor, prevents methamphetamine-induced decrease of striatal dopamine uptake sites in the rat striatum

    Neurosci. Lett.

    (1992)
  • NakayamaM. et al.

    Long-lasting decrease in dopamine uptake sites following repeated administration of methamphetamine in the rat striatum

    Brain Res.

    (1993)
  • NashJ.F. et al.

    Methamphetamine neurotoxicity and striatal glutamate release: comparison to 3, 4-methylenedioxy-methamphetamine

    Brain Res.

    (1992)
  • NashJ.F. et al.

    Effect of d-amphetamine on the extracellular concentrations of glutamate and dopamine in iprindole-treated rats

    Brain Res.

    (1993)
  • NishikawaT. et al.

    Behavioral sensitization and relative hyperresponsiveness of striatal and limbic dopaminergic neurons after repeated methamphetamine treatment

    Eur. J. Pharmacol.

    (1983)
  • PatrickS.L. et al.

    Concomitant sensitization of amphetamine-induced behavioral stimulation and in vivo dopamine release from rat caudate nucleus

    Brain Res.

    (1991)
  • RobinsonT.E. et al.

    Behavioral sensitization is accompanied by an enhancement in amphetamine-stimulated dopamine release from striatal tissue in vitro

    Eur. J. Pharmacol.

    (1982)
  • RobinsonT.E. et al.

    Enduring enhancement in frontal cortex dopamine utilization in an animal model of amphetamine psychosis

    Brain Res.

    (1985)
  • RobinsonT.E. et al.

    The effects of footshock stress on regional brain dopamine metabolism and pituitary B-endorphin release in rats previously sensitized to amphetamine

    Neuropharmacology

    (1987)
  • RobinsonT.E. et al.

    Persistent sensitization of dopamine neurotransmission in ventral striatum (nucleus accumbens) produced by prior experience with (+)-amphetamine: a microdialysis study in freely moving rats

    Brain Res.

    (1988)
  • SeutinV. et al.

    Acute amphetamine-induced subsensitivity of A10 dopamine autoreceptors in vitro

    Brain Res.

    (1991)
  • StewartJ. et al.

    Microinjections of Sch-23390 into the ventral tegmental area and substantia nigra pars reticulata attenuate the development of sensitization to the locomotor activating effects of systemic amphetamine

    Brain Res.

    (1989)
  • SulzerD. et al.

    Amphetamine and other psychostimulants reduce pH gradients in midbrain dopaminergic neurons and chromaffin granules: A mechanism of action

    Neuron

    (1990)
  • Cited by (101)

    • The role of metabotropic glutamate receptors in neurobehavioral effects associated with methamphetamine use

      2023, International Review of Neurobiology
      Citation Excerpt :

      Alternatively, meth can directly affect presynaptic glutamate release (Andres et al., 2015; Shen et al., 2021), or neural activity of local glutamate neurons (Pu, Broening, & Vorhees, 1996; Stephans & Yamamoto, 1995). Though, it should be noted that both the mechanisms and magnitude of meth-induced glutamate levels likely depend both on the duration of meth exposure and the dose of meth used/administered (Earle & Davies, 1991; Jones et al., 2021; Pereira et al., 2012; Stephans & Yamamoto, 1995; Szumlinski et al., 2017). Preclinical research has also demonstrated that contingent and noncontingent delivery of meth over prolonged periods of time leads to a spectrum of glutamatergic aberrations.

    • Inhibitory regulation of the prefrontal cortex following behavioral sensitization to amphetamine and/or methamphetamine psychostimulants: A review of GABAergic mechanisms

      2019, Progress in Neuro-Psychopharmacology and Biological Psychiatry
      Citation Excerpt :

      For example, lidocaine-induced blockade of the mPFC blocks locomotor sensitization to AMPH (Degoulet et al., 2009) while sensitization to AMPH is associated with increased burst firing of neurons within the same region (Aguilar-Rivera et al. (2015). Furthermore, extracellular glutamate is increased in the mPFC following AMPH and METH exposure (Del Arco et al., 1998; Stephans and Yamamoto, 1995) suggesting that glutamatergic efferents of the PRL may be involved in the expression of sensitization. Therefore, the finding that GABAT was elevated in the PRL (Wearne et al., 2016b) provides molecular evidence that a hyperglutamatergic environment may be maintained by increased GABAergic metabolism.

    View all citing articles on Scopus
    View full text