ArticleThe European journal of neuroscience2013
Methamphetamine-induced neurotoxicity disrupts naturally occurring phasic dopamine signaling.
Article in The European journal of neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed.
- Altered striatal dopamine regulation in Adgrl3 knockout mice.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026Article
- Regional and sex differences in spontaneous striatal dopamine transmission.Journal of neurochemistry · 2022Article
- Effects of methamphetamine-induced neurotoxicity on striatal long-term potentiation.Psychopharmacology · 2022Article
- Optogenetic stimulation of striatal patches modifies habit formation and inhibits dopamine release.Scientific reports · 2021Article
- Distinct dose-dependent effects of methamphetamine on real-time dopamine transmission in the rat nucleus accumbens and behaviors.Journal of neurochemistry · 2021Article
- Accelerated development of cocaine-associated dopamine transients and cocaine use vulnerability following traumatic stress.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2020Article
- Mechanisms Regulating the Association of Protein Phosphatase 1 with Spinophilin and Neurabin.ACS chemical neuroscience · 2018Article
- Article
- Cross-talk between the epigenome and neural circuits in drug addiction.Progress in brain research · 2017Review
- Contrasting Regulation of Catecholamine Neurotransmission in the Behaving Brain: Pharmacological Insights from an Electrochemical Perspective.Pharmacological reviews · 2017Review
- Prior nicotine self-administration attenuates subsequent dopaminergic deficits of methamphetamine in rats: role of nicotinic acetylcholine receptors.Behavioural pharmacology · 2016Article
- Acute phenylalanine/tyrosine depletion of phasic dopamine in the rat brain.Psychopharmacology · 2016Article
- Article
- Three mechanisms by which striatal denervation causes breakdown of dopamine signaling.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- Methamphetamine-induced neurotoxicity disrupts pharmacologically evoked dopamine transients in the dorsomedial and dorsolateral striatum.Neurotoxicity research · 2014Article
- Illicit dopamine transients: reconciling actions of abused drugs.Trends in neurosciences · 2014Review
- Changes in neural circuitry regulating response-reversal learning and Arc-mediated consolidation of learning in rats with methamphetamine-induced partial monoamine loss.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2014Article
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5 authors.
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Abstract
Methamphetamine (METH) is a highly addictive drug that is also neurotoxic to central dopamine (DA) systems. Although striatal DA depletions induced by METH are associated with behavioral and cognitive impairments, the link between these phenomena remains poorly understood. Previous work in both METH-pretreated animals and the 6-hydroxydopamine model of Parkinson's disease suggests that a disruption of phasic DA signaling, which is important for learning and goal-directed behavior, may be such a link. However, previous studies used electrical stimulation to elicit phasic-like DA responses and were also performed under anesthesia, which alters DA neuron activity and presynaptic function. Here we investigated the consequences of METH-induced DA terminal loss on both electrically evoked phasic-like DA signals and so-called 'spontaneous' phasic DA transients measured by voltammetry in awake rats. Not ostensibly attributable to discrete stimuli, these subsecond DA changes may play a role in enhancing reward-cue associations. METH pretreatment reduced tissue DA content in the dorsomedial striatum and nucleus accumbens by ~55%. Analysis of phasic-like DA responses elicited by reinforcing stimulation revealed that METH pretreatment decreased their amplitude and underlying mechanisms for release and uptake to a similar degree as DA content in both striatal subregions. Most importantly, characteristics of DA transients were altered by METH-induced DA terminal loss, with amplitude and frequency decreased and duration increased. These results demonstrate for the first time that denervation of DA neurons alters naturally occurring DA transients and are consistent with diminished phasic DA signaling as a plausible mechanism linking METH-induced striatal DA depletions and cognitive deficits.
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