ArticleNeuroscience2016
Glycine blocks long-term potentiation of GABAergic synapses in the ventral tegmental area.
Article in Neuroscience, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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.
The trial behind it
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Who cites it
6 citing papers in PubMed, 11 citations in OpenAlex.
- Electroacupuncture Increases the Hippocampal Synaptic Transmission Efficiency and Long-Term Plasticity to Improve Vascular Cognitive Impairment.Mediators of inflammation · 2022Article
- Nitric Oxide Signaling Pathway in Ventral Tegmental Area is Involved in Regulation of 7,8-Dihydroxyflavone on Alcohol Consumption in Rats.Molecular neurobiology · 2022Article
- The Impact of Electronic Nicotine Delivery System (ENDS) Flavors on Nicotinic Acetylcholine Receptors and Nicotine Addiction-Related Behaviors.Molecules (Basel, Switzerland) · 2020Review
- Strength of resting state functional connectivity and local GABA concentrations predict oral reading of real and pseudo-words.Scientific reports · 2019Observational
- Could GABA, with a side of glycine, control glutamate receptors?The European journal of neuroscience · 2018Article
- Unravelling the Link Between Prenatal Stress, Dopamine and Substance Use Disorder.Neurotoxicity research · 2017Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 2 countries.
Funding
Abstract
The mesocorticolimbic dopamine system, originating in the ventral tegmental area (VTA) is normally constrained by GABA-mediated synaptic inhibition. Accumulating evidence indicates that long-term potentiation of GABAergic synapses (LTPGABA) in VTA dopamine neurons plays an important role in the actions of drugs of abuse, including ethanol. We previously showed that a single infusion of glycine into the VTA of rats strongly reduces ethanol intake for 24h. In the current study, we examined the effect of glycine on the electrophysiological activities of putative dopamine VTA neurons in midbrain slices from ethanol-naïve rats. We report here that a 15-min exposure to 10 μM glycine prevented trains of high-frequency stimulation (HFS) from producing LTPGABA, which was rescued by the glycine receptor (GlyR) antagonist strychnine. Glycine also concentration-dependently decreased the frequency of spontaneous excitatory postsynaptic currents (sEPSCs). By contrast, glycine pretreatment did not prevent potentiation of inhibitory postsynaptic currents (IPSCs) during a continuous exposure to the nitric oxide (NO) donor, SNAP (S-nitroso-N-acetylpenicillamine), or a brief exposure to 10 μM glycine and 10 μM NMDA (N-methyl-D-aspartate), an agonist of NMDA-type glutamate receptors. Thus, the blockade of LTPGABA by glycine is probably resulted from suppressing glutamate release by activating the GlyRs on the glutamatergic terminals. This effect of glycine may contribute to the reduction in ethanol intake induced by intra-VTA glycine observed in vivo.
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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.