ArticleBehavioural brain research2011
Substantia nigra pars reticulata is crucially involved in barbiturate and ethanol withdrawal in mice.
Article in Behavioural brain research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
8 citing papers in PubMed, 9 citations in OpenAlex.
- A Circuit-Based Information Approach to Substance Abuse Research.Trends in neurosciences · 2021Review
- Progress in opioid reward research: From a canonical two-neuron hypothesis to two neural circuits.Pharmacology, biochemistry, and behavior · 2021Review
- The kappa opioid receptor modulates GABA neuron excitability and synaptic transmission in midbrainprojections from the insular cortex.Neuropharmacology · 2020Article
- Acute ethanol withdrawal impairs contextual learning and enhances cued learning.Alcoholism, clinical and experimental research · 2015Article
- Mpdz expression in the caudolateral substantia nigra pars reticulata is crucially involved in alcohol withdrawal.Genes, brain, and behavior · 2014Article
- Genetics and genomics of alcohol sensitivity.Molecular genetics and genomics : MGG · 2014Review
- Striatal involvement in human alcoholism and alcohol consumption, and withdrawal in animal models.Alcoholism, clinical and experimental research · 2011Review
- Rostroventral caudate putamen involvement in ethanol withdrawal is influenced by a chromosome 4 locus.Genes, brain, and behavior · 2010Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Sedative-hypnotic CNS depressant drugs are widely prescribed to treat a variety of disorders, and are abused for their sedative and euphoric effects. Physiological dependence and associated withdrawal episodes are thought to constitute a motivational force that sustains their use/abuse and may contribute to relapse in dependent individuals. Although no animal model duplicates depressant dependence, models for specific factors, like withdrawal, are useful for identifying potential neural determinants of liability in humans. Recent analyses implicate the caudolateral substantia nigra pars reticulata (clSNr) in withdrawal following acute and repeated ethanol exposures in mice, but did not assess its impact on withdrawal from other sedative-hypnotics or whether intrinsic neurons or fibers of passage are involved. Here, we demonstrate that bilateral chemical (ibotenic acid) lesions of the clSNr attenuate barbiturate (pentobarbital) and ethanol withdrawal. Chemical lesions did not affect convulsions in response to pentylenetetrazole, which blocks GABA(A) receptor-mediated transmission. Our results demonstrate that the clSNr nucleus itself rather than fibers of passage is crucial to its effects on barbiturate and ethanol withdrawal. These findings support suggest that clSNr could be one of the shared neural substrates mediating withdrawal from sedative-hypnotic drugs.
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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.