Evidence map›Paper›PMID 16049571›Full record

ArticleJournal of psychiatry & neuroscience : JPN2005

Evidence for the activity of lamotrigine at 5-HT(1A) receptors in the mouse forced swimming test.

Michel Bourin, Fabienne Masse, Martine Hascoët

Open access · greenAbstract read
In one paragraph

Article 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 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
5.7field-weighted citation impact, top 5% 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

15 citing papers in PubMed, 47 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Novel glutamatergic drugs for the treatment of mood disorders.Neuropsychiatric disease and treatment · 2013
    Article
  9. Case files of the University of California San Francisco Medical Toxicology Fellowship: lamotrigine toxicity.Journal of medical toxicology : official journal of the American College of Medical Toxicology · 2012
    Article
  10. Article
  11. Review
  12. The effectiveness of anticonvulsants in psychiatric disorders.Dialogues in clinical neuroscience · 2008
    Review
  13. The role of lamotrigine in the management of bipolar disorder.Neuropsychiatric disease and treatment · 2007
    Article
  14. Article
  15. 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

3 authors.

Michel BourinNeurobiologie de l'Anxiété et de la Dépression, Faculté de Médecine, Nantes, France. michel.bourin@univ-nantes.fr
Fabienne Masse
Martine Hascoët

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe antiepileptic drug lamotrigine is effective in the treatment of focal epilepsies. It is thought to act by inhibition of glutamate release through blockade of voltage-sensitive sodium channels and stabilization of the neuronal membrane. Lamotrigine is also effective in the treatment of mood disorders such as bipolar disorder. However, its exact mechanism of action in these conditions remains unclear. The aim of the present study was to evaluate the antidepressant-like effect of lamotrigine in a mouse model of depression, namely the forced swimming test (FST). Association studies using specific and nonspecific ligands acting on serotonin (5-hydroxytryptamine; 5-HT1) receptor subtypes were undertaken to evaluate the potential role of these receptors in the anti-immobility effect of lamotrigine.

methodsThe mouse FST was performed after single administration of lamotrigine. Subactive doses of lamotrigine were administered in association with subactive doses of the following 5-HT1 receptor agonists or antagonists: 8-hydroxy-2-(di-n-propilamino)-tetralin (8-OH-DPAT, a standard 5-HT(1A) receptor selective agonist), pindolol (a presynaptic and postsynaptic 5-HT(1A/1B) receptor antagonist), NAN-190 (a 5-HT(1A) receptor antagonist), RU 24969 (a 5-HT(1A/1B) receptor agonist) and anpirtoline (5-HT(1B) agonist).

resultsLamotrigine impaired spontaneous locomotor activity at doses of 4 mg/kg or greater, and activity decreased by more than 50% at the 16 mg/kg dose. When administered alone, lamotrigine (8 and 16 mg/kg) decreased immobility time in the FST. Only 8-OH-DPAT (1 mg/kg), pindolol (32 mg/kg) and RU 24969 (0.5 mg/kg) enhanced the antidepressant-like effect of lamotrigine in the FST.

conclusionsThese results suggest that postsynaptic 5-HT(1A) receptors might be involved in the activity of lamotrigine. Furthermore, they demonstrate that lamotrigine more closely resembles valproate and carbamazepine than lithium, with the advantage of an anti-immobility effect in the mouse FST when administered on its own.

Indexed as

CoercionSwimmingAnimalsAnticonvulsantsAntimanic AgentsLamotrigineMaleMiceReceptors, SerotoninTriazinesAnticonvulsantsAntimanic AgentsLamotrigineReceptors, SerotoninTriazines

Identifiers

PMID16049571
PMCPMC1160563
OpenAlexW1589481864

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.