Evidence map›Paper›PMID 17519508›Full record

ReviewMolecular neurobiology2007

Cocaine withdrawal and neuro-adaptations in ion channel function.

Xiu-Ti Hu

Abstract readReview
PubMed Publisher
In one paragraph

Review in Molecular neurobiology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
0.9field-weighted citation impact, top 32% 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

25 citing papers in PubMed, 39 citations in OpenAlex.

  1. Article
  2. Review
  3. Cocaine induces paradigm-specific changes to the transcriptome within the ventral tegmental area.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2021
    Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. The serotonin 5-HTJournal of psychopharmacology (Oxford, England) · 2017
    Review
  9. Article
  10. Article
  11. Article
  12. Repeated cocaine treatment enhances HIV-1 Tat-induced cortical excitability via over-activation of L-type calcium channels.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2014
    Article
  13. Article
  14. Article
  15. Article
  16. Role of nucleus accumbens glutamatergic plasticity in drug addiction.Neuropsychiatric disease and treatment · 2013
    Review
  17. Article
  18. Novel therapeutic strategies for alcohol and drug addiction: focus on GABA, ion channels and transcranial magnetic stimulation.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2012
    Review
  19. Article
  20. Article
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

1 author at 1 institution in 1 country.

Xiu-Ti HuDepartment of Cellular and Molecular Pharmacology, Rosalind Franklin University of Medicine and Science, The Chicago Medical School, North Chicago, IL, USA. xiu-ti.hu@rosalind-franklin.edu
Rosalind Franklin University of Medicine and Science · US

Funding

NIDA NIH HHS DA-00456NIDA NIH HHS DA-04093
6 · The paper itself

Abstract

Chronic exposure to psychostimulants induces neuro-adaptations in ion channel function of dopamine (DA)-innervated cells localized within the medial prefrontal cortex (mPFC) and nucleus accumbens (NAc). Although neuroplasticity in ion channel function is initially found in drug-sensitized animals, it has recently been believed to underlie the withdrawal effects of cocaine, including craving that leads to relapse in human addicts. Recent studies have also revealed remarkable differences in altered ion channel activities between mPFC pyramidal neurons and medium spiny NAc neurons in cocaine-withdrawn animals. In response to psychostimulant or certain "excitatory" stimuli, increased intrinsic excitability is found in mPFC pyramidal neurons, whereas decreased excitability is observed in medium spiny NAc cells in drug-withdrawn animals compared to drug-free control animals. These changes in ion channel function are modulated by interrupted DA/Ca2+ signaling with decreased DA D2 receptor function but increased D1 receptor signaling. More importantly, they are correlated to behavioral changes in cocaine-withdrawn human addicts and sensitized animals. Based on growing evidence, researchers have proposed that cocaine-induced neuro-adaptations in ion channel activity and DA/Ca2+ signaling in mPFC pyramidal neurons and medium spiny NAc cells may be the fundamental cellular mechanism underlying the cocaine withdrawal effects observed in human addicts.

Indexed as

Adaptation, PhysiologicalAnimalsCalciumCocaineDopamineHumansIon ChannelsNeuronsPrefrontal CortexReceptors, DopamineRewardSignal TransductionSubstance Withdrawal SyndromeCalciumCocaineDopamineIon ChannelsReceptors, Dopamine

Identifiers

PMID17519508
OpenAlexW1979912812

What OpenQuestion holds

Textmetadata
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.