Evidence map›Paper›PMID 21906535›Full record

ReviewInternational review of neurobiology2011

Homeostatic control of neural activity: a Drosophila model for drug tolerance and dependence.

Alfredo Ghezzi, Nigel S Atkinson

Open access · greenAbstract readReview
In one paragraph

Review in International review of neurobiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.7field-weighted citation impact, top 11% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

22 citing papers in PubMed, 27 citations in OpenAlex.

  1. AlteredbioRxiv : the preprint server for biology · 2025
    Article
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  6. A Novel Peptide Restricts Ethanol Modulation of the BK Channel In Vitro and In Vivo.The Journal of pharmacology and experimental therapeutics · 2018
    Article
  7. Article
  8. Epigenetic Mechanisms of Alcohol Neuroadaptation: Insights fromJournal of experimental neuroscience · 2018
    Review
  9. Article
  10. Article
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  13. An alcohol-sensing site in the calcium- and voltage-gated, large conductance potassium (BK) channel.Proceedings of the National Academy of Sciences of the United States of America · 2014
    Article
  14. Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Alfredo GhezziWaggoner Center for Alcohol and Addiction Research, Section of Neurobiology, The University of Texas at Austin, 1 University Station C0920, Austin Texas 78712-0248, USA.
Nigel S Atkinson
The University of Texas at Austin · US

Funding

Epigenetic modification as a mechanism to produce functional toleranceR01AA018037 · NIAAA · UNIVERSITY OF TEXAS AT AUSTIN · PI ATKINSON, NIGEL S · 2008 to 2018
$3.3M
Chromatin Remodeling as a Mechanism to Produce Drug ToleranceR01DA022219 · NIDA · UNIVERSITY OF TEXAS AT AUSTIN · PI ATKINSON, NIGEL S · 2006 to 2009
$701k
NIAAA NIH HHS R01 AA018037NIDA NIH HHS R01 DA022219NIDA NIH HHS R01DA022219
6 · The paper itself

Abstract

Drug addiction is a complex condition of compulsive drug use that results in devastating physical and social consequences. Drosophila melanogaster has recently emerged as a valuable genetic model for investigating the mechanisms of addiction. Drug tolerance is a measurable endophenotype of addiction that can be easily generated and detected in animal models. The counteradaptive theory for drug dependence postulates that the homeostatic adaptations that produce drug tolerance become counteradaptive after drug clearance, resulting in symptoms of dependence. In flies, a single sedation with ethanol or with an organic solvent anesthetic (benzyl alcohol) induces functional tolerance, an adaptation of the nervous system that reduces the effect of these neural depressants. Here we review the role of the BK channel gene (slo) and genes that encode other synaptic proteins in the process of producing functional tolerance. These proteins are predicted to be part of an orchestrated response that involves specific interactions across a highly complex synaptic protein network. The response of the slo gene to drug exposure and the consequence of induced slo expression fit nicely the tenets of the counteradaptive theory for drug tolerance and dependence. Induction of slo expression represents an adaptive process that generates tolerance because it enhances neuronal excitability, which counters the sedative effects of the drugs. After drug clearance, however, the increase in slo expression leads to an allostatic withdrawal state that is characterized by an increase in the susceptibility for seizure. Together, these results demonstrate a common origin for development of drug tolerance and withdrawal hyperexcitability in Drosophila.

Indexed as

Disease Models, AnimalAnimalsDrosophilaDrug ToleranceHomeostasisHumansLarge-Conductance Calcium-Activated Potassium ChannelsModels, NeurologicalNeuronsSubstance-Related DisordersSubstance Withdrawal SyndromeSynaptic TransmissionLarge-Conductance Calcium-Activated Potassium Channels

Identifiers

PMID21906535
PMCPMC4862361
OpenAlexW1535640885

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.