Cited by 29Treatment of Major DepressionNeurotransmitter Receptor Influence on BehaviorReceptor Mechanisms and Signaling

Heterotrimeric G Proteins: Insights into the Neurobiology of Mood Disorders

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Gonzalez-Maeso, Javier, Meana, J.·2006·Current Neuropharmacology

Abstract

Mood disorders such as major depression and bipolar disorder are common, severe, chronic and often life-threatening illnesses. Suicide is estimated to be the cause of death in up to approximately 10-15% of individuals with mood disorders. Alterations in the signal transduction through G protein-coupled receptor (GPCR) pathways have been reported in the etiopathology of mood disorders and the suicidal behavior. In this regard, the implication of certain GPCR subtypes such as alpha(2A)-adrenoceptor has been repeatedly described using different approaches. However, several discrepancies have been recently reported in density and functional status of the heterotrimeric G proteins both in major depression and bipolar disorder. A compilation of the most relevant research topics about the implication of heterotrimeric G proteins in the etiology of mood disorders (i.e., animal models of mood disorders, studies in peripheral tissue of depressive patients, and studies in postmortem human brain of suicide victims with mood disorders) will provide a broad perspective of this potential therapeutic target field. Proposed causes of the discrepancies reported at the level of G proteins in postmortem human brain of suicide victims will be discussed.

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  • The fighting reaction elicited in bulls in a corrida may temporarily antagonize the mechanisms implicated in low reactivity mental states, similar to those described in major depressive disorder.

    “The fighting reaction elicited in bulls in a corrida may temporarily antagonize the mechanisms implicated in low reactivity mental states, similar to those described in major depressive disorder [56].”
  • Heterotrimeric G-protein pathways are the main signaling pathways downstream of receptor activation and have been functionally associated with major depression and bipolar disorders.

    “These routes are the main signaling pathways downstream of receptor activation and have been functionally associated with major depression and bipolar disorders [56].”

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Research works printed but not linked: 3

  1. Callado, L. F., Meana, J. J., Grijalba, B., Pazos, A., Sastre, M., Garcia-Sevilla, J. A. (1998) Selective increase of alpha2A- Heterotrimeric G Proteins Current Neuropharmacology, 2006, Vol. 4, No. 2 135 adrenoceptor agonist binding sites in brains of depressed suicide victims. J. Neurochem., 70, 1114-1123.
  2. Gomperst, B. D. (2002) Signal Transduction. In: Gomperts, B. D., Kramer, I. M., Tatham, P. E. R. Eds, San Diego, Academic Press.
  3. Nemeroff, C. B. (2004) Mood Dissorders. In: Charney, D. S., Nestler, E. J. Eds, Neurobiology of Mental Illness. New York, Oxford.

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Authors
Gonzalez-Maeso, J., & Meana, J.
Affiliations
Mount Sinai Hospital (US)
Venue
Current Neuropharmacology
Published
2006-04-01
Volume
4
Issue
2
Pages
127-138
ISSN
1570-159X (ISSN-L)
OpenAlex
W2032985983
Cited by
29
References
125
Citations by year
2024: 1 · 2021: 8 · 2020: 3 · 2019: 2 · 2018: 2 · 2017: 1 · 2016: 2 · 2015: 1 · 2014: 2 · 2013: 1 · 2012: 1
FWCI
0.21
Type
journal article
Language
en
Open access
Locations
  • Current Neuropharmacology (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • Eusko Jaurlaritza
  • National Institutes of Health
  • National Institute on Drug Abuse (P01DA012923)
Topics
  • Health Sciences › Medicine › Pharmacology › Treatment of Major Depression
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Receptor Mechanisms and Signaling
Keywords
heterotrimeric G proteins, mood disorders, major depressive disorder, bipolar disorder, suicide, G protein-coupled receptors, alpha2A-adrenoceptor, signal transduction, postmortem brain, animal models of depression, therapeutic target

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