ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2000
Amphetamine blocks long-term synaptic depression in the ventral tegmental area.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
48 citing papers in PubMed, 151 citations in OpenAlex.
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- Spatio-temporal mechanisms of consolidation, recall and reconsolidation in reward-related memory trace.Molecular psychiatry · 2025Article
- Repeated chemogenetic activation of dopaminergic neurons induces reversible changes in baseline and amphetamine-induced behaviors.Psychopharmacology · 2023Article
- A Novel CaMKII Inhibitory Peptide Blocks Relapse to Morphine Seeking by Influencing Synaptic Plasticity in the Nucleus Accumbens Shell.Brain sciences · 2022Article
- Addiction-induced plasticity in underlying neural circuits.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2022Review
- Brain is modulated by neuronal plasticity during postnatal development.The journal of physiological sciences : JPS · 2021Review
- Methamphetamine pre-exposure induces steeper escalation of methamphetamine self-administration with consequent alterations in hippocampal glutamate AMPA receptor mRNAs.European journal of pharmacology · 2020Article
- Cocaine self-administration abolishes endocannabinoid-mediated long-term depression of glutamatergic synapses in the ventral tegmental area.The European journal of neuroscience · 2020Article
- On the Modulatory Roles of Neuregulins/ErbB Signaling on Synaptic Plasticity.International journal of molecular sciences · 2019Review
- mGluR1-Dependent Long Term Depression in Rodent Midbrain Dopamine Neurons Is Regulated by Neuregulin 1/ErbB Signaling.Frontiers in molecular neuroscience · 2018Article
- Opiates and Plasticity in the Ventral Tegmental Area.ACS chemical neuroscience · 2017Review
- Gene expression profiling of midbrain dopamine neurons upon gestational nicotine exposure.Medical & biological engineering & computing · 2017Article
- VTA dopamine neuron plasticity - the unusual suspects.The European journal of neuroscience · 2016Review
- Functional Relevance of Different Basal Ganglia Pathways Investigated in a Spiking Model with Reward Dependent Plasticity.Frontiers in neural circuits · 2016Article
- Article
- The role of D2-autoreceptors in regulating dopamine neuron activity and transmission.Neuroscience · 2014Review
- GABAA receptor drugs and neuronal plasticity in reward and aversion: focus on the ventral tegmental area.Frontiers in pharmacology · 2014Article
- A review of the abuse potential assessment of atomoxetine: a nonstimulant medication for attention-deficit/hyperactivity disorder.Psychopharmacology · 2013Review
- A-kinase anchoring protein-calcineurin signaling in long-term depression of GABAergic synapses.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- Monoamine oxidases in development.Cellular and molecular life sciences : CMLS · 2013Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The mesolimbic dopamine system is essential for reward-seeking behavior, and drugs of abuse are thought to usurp the normal functioning of this pathway. A growing body of evidence suggests that glutamatergic synapses on dopamine neurons in the ventral tegmental area (VTA) are modified during exposure to addictive drugs, producing sensitization, a progressive augmentation in the rewarding properties of psychostimulant drugs with repeated exposure. We have tested the hypothesis that psychostimulant exposure interferes with the synaptic plasticity of glutamatergic inputs to the VTA. We find that excitatory synapses onto VTA dopamine neurons exhibit long-term depression (LTD) in response to low-frequency stimulation and modest depolarization. LTD in the VTA is NMDA receptor-independent but is dependent on intracellular Ca(2+) and can be induced by driving Ca(2+) into the dopamine neuron. Brief exposure to amphetamine entirely blocks LTD at glutamatergic synapses in the VTA, by releasing endogenous dopamine that acts at D2 dopamine receptors. The block of LTD is selective, because amphetamine has no effect on hippocampal LTD. The LTD we have discovered in the VTA is likely to be an important component of excitatory control of the reward pathway; amphetamine will inhibit LTD, removing this normal brake on the glutamatergic drive to dopamine neurons. This effect of amphetamine represents an important mechanism by which normal function of the brain reward system may be impaired during substance abuse.
Indexed as
Identifiers
10908593PMC6772550W2155748117What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.