Evidence map›Paper›PMID 15944741›Full record

ReviewJournal of psychiatry & neuroscience : JPN2005

Selective GABAergic treatment for panic? Investigations in experimental panic induction and panic disorder.

Peter Zwanzger, Rainer Rupprecht

Open access · greenAbstract readReview
In one paragraph

Review in Journal of psychiatry & neuroscience : JPN, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
8.7field-weighted citation impact, top 2% 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

27 citing papers in PubMed, 86 citations in OpenAlex.

  1. Acute shift in glutamate concentrations following experimentally induced panic with cholecystokinin tetrapeptide--a 3T-MRS study in healthy subjects.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2013
    Trial
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Pediatric Migraine and Academics.Current pain and headache reports · 2020
    Review
  9. Article
  10. Article
  11. Biological markers for anxiety disorders, OCD and PTSD: A consensus statement. Part II: Neurochemistry, neurophysiology and neurocognition.The world journal of biological psychiatry : the official journal of the World Federation of Societies of Biological Psychiatry · 2017
    Review
  12. Pseudopheochromocytoma induced by anxiolytic withdrawal.European journal of medical research · 2014
    Article
  13. Hippocampal hyperexcitability underlies enhanced fear memories in TgNTRK3, a panic disorder mouse model.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013
    Article
  14. Article
  15. Review
  16. Biomarkers in development of psychotropic drugs.Dialogues in clinical neuroscience · 2011
    Review
  17. The GABA transporter 1 (SLC6A1): a novel candidate gene for anxiety disorders.Journal of neural transmission (Vienna, Austria : 1996) · 2009
    Article
  18. Article
  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

2 authors at 1 institution in 1 country.

Peter ZwanzgerAnxiety Research Unit and Anxiety Outpatient Clinic, Department of Psychiatry, Ludwig-Maximilians-Universität, Munich, Germany. zwanzger@med.uni-muenchen.de
Rainer Rupprecht
Ludwig-Maximilians-Universität München · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

gamma-Aminobutyric acid (GABA) is the most important inhibitory neurotransmitter in the central nervous system (CNS). It exerts its rapid inhibitory action mostly through GABA(A) receptors, which are targets for benzodiazepines, barbiturates, neuroactive steroids and distinct anticonvulsive agents. There is considerable evidence that dysfunction of GABA(A) receptors or dysregulation of GABA concentrations in the CNS (or both) plays an important role in the pathophysiology of panic disorder. Currently, benzodiazepines are the only drugs directly targeting the GABA(A) receptors that are approved for the treatment of anxiety disorders. Because of their well-known anxiolytic effects, they are widely used in this setting, but side effects limit their use in long-term treatment. The question of whether drugs that selectively increase GABA concentrations in the CNS could improve symptoms of anxiety has been discussed. Recent investigations by our group have demonstrated that enhancement of endogenous GABA (through blockade of GABA transaminase by vigabatrin or through inhibition of GABA transporters by tiagabine) exerts anxiolytic effects on experimentally induced panic. Our studies in healthy volunteers have shown that both compounds lead to a significant reduction in panic symptoms elicited by cholecystokinin-tetrapeptide. Moreover, benzodiazepine-like effects on the activity of the hypothalamic-pituitary-adrenal axis have been observed in association with vigabatrin treatment. Small open studies in patients with panic disorder also showed an improvement in panic and anxiety with both compounds. This review summarizes our recent research on the effects of selective GABAergic treatment in experimentally induced panic and outlines the possible role of compounds targeting the GABA binding site of the GABA(A)-benzodiazepine receptor for the treatment of panic and anxiety.

Indexed as

AnimalsAnti-Anxiety AgentsGABA AgentsGABA AgonistsHumansPanicPanic DisorderReceptors, GABA-AAnti-Anxiety AgentsGABA AgentsGABA AgonistsReceptors, GABA-A

Identifiers

PMID15944741
PMCPMC1089777
OpenAlexW2139938825

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.