Serotonin 2A receptor clustering in peripheral lymphocytes is altered in major depression and may be a biomarker of therapeutic efficacy

Rivera-Baltanás, Tania; Olivares, J.M.; Martinez-Villamarin, Jose R.; Fenton, Erin Y.; Kalynchuk, Lisa E.; Caruncho, Héctor J.

doi:10.1016/j.jad.2014.03.011

Cited by 26 publications

(33 citation statements)

References 32 publications

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“…Preliminary evidence suggested that a trend of increased HTR2A mRNA levels in peripheral lymphocytes may be observed during the first 8 weeks of antidepressant treatment (Belzeaux et al 2010), suggesting that further studies should investigate this potential biomarker of antidepressant efficacy. Another preliminary study found that 5-HT2A receptor clustering in peripheral lymphocytes is altered in MDD and may be a bio-marker of therapeutic efficacy (Rivera-Baltanas et al 2014).…”

Section: Peripheral Biomarkersmentioning

confidence: 99%

Consensus paper of the WFSBP Task Force on Genetics: Genetics, epigenetics and gene expression markers of major depressive disorder and antidepressant response

Fabbri

Hosák

Mößner

et al. 2016

The World Journal of Biological Psychiatry

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Major depressive disorder (MDD) is a heritable disease with a heavy personal and socio-economic burden. Antidepressants of different classes are prescribed to treat MDD, but reliable and reproducible markers of efficacy are not available for clinical use. Further complicating treatment, the diagnosis of MDD is not guided by objective criteria, resulting in the risk of under-or overtreatment. A number of markers of MDD and antidepressant response have been investigated at the genetic, epigenetic, gene expression and protein levels. Polymorphisms in genes involved in anti-depressant metabolism (cytochrome P450 isoenzymes), antidepressant transport (ABCB1), glucocorticoid signalling (FKBP5) and serotonin neurotransmission (SLC6A4 and HTR2A) were among those included in the first pharmacogenetic assays that have been tested for clinical applicability. The results of these investigations were encouraging when examining patient-outcome improvement. Furthermore, a nine-serum biomarker panel (including BDNF, cortisol and soluble TNF-a receptor type II) showed good sensitivity and specificity in differentiating between MDD and healthy controls. These first diagnostic and response-predictive tests for MDD provided a source of optimism for future clinical applications. However, such findings should be considered very carefully because their benefit/cost ratio and clinical indications were not clearly demonstrated. Future tests may include combinations of different types of biomarkers and be specific for MDD subtypes or pathological dimensions.

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Section: Peripheral Biomarkersmentioning

confidence: 99%

Consensus paper of the WFSBP Task Force on Genetics: Genetics, epigenetics and gene expression markers of major depressive disorder and antidepressant response

Fabbri

Hosák

Mößner

et al. 2016

The World Journal of Biological Psychiatry

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“…5-HT receptors expressed in lymphocytes include 5HT1, 5HT1A, 5-HT1B, 5-HT2A, 5-HT3, 5-HT3A and 5-HT7. Activation of 5-HT2 receptors on T-cells by mast cell-derived 5-HT, results in delayed-type hypersensitivity (Mossner and Lesch, 1998;Rivera-Baltanas et al, 2014;Shajib and Khan, 2015). Similarly, platelet-secreted 5-HT initiates T cell-dependent contact sensitivity via immunoglobulin E (IgE) (Matsuda et al, 1997).…”

Section: Serotoninmentioning

confidence: 99%

“…Individuals with obsessive-compulsive disorder have reduced 5-HT transporter (5-HTT) levels and 5-HT2A with decreased binding capabilities (Hesse et al, 2005;Perani et al, 2008). 5-HT receptors are altered in patients with depression (Rivera-Baltanas et al, 2014). 5-HT2A is highly expressed in peripheral lymphocytes and the CNS (Inoue et al, 2011;Pandey et al, 1990).…”

Section: Serotoninmentioning

confidence: 99%

Interaction of neurotransmitters and neurochemicals with lymphocytes

Kerage

Sloan

Mattarollo

et al. 2019

Journal of Neuroimmunology

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Neurotransmitters and neurochemicals can act on lymphocytes by binding to receptors expressed by lymphocytes. This review describes lymphocyte expression of receptors for a selection of neurotransmitters and neurochemicals, the anatomical locations where lymphocytes can interact with neurotransmitters, and the effects of the neurotransmitters on lymphocyte function. Implications for health and disease are also discussed. As defined above, a neurotransmitter must be produced by neurons. Lymphocytes can be exposed to neurotransmitters in the blood or tissue. T-cells entering the central nervous system (CNS) encounter neurotransmitters at the site of release from neurons. Neurotransmitters are also found in blood. For example, acetylcholine can be detected in

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“…In fact, increases in EGR2 were observed only up to 5 h in rats (Nichols and Sanders-Bush, 2002; Gonzalez-Maeso et al, 2003; Nichols et al, 2003). Fourth, all changes in gene expression that are caused by LSD that have been reported to date have been observed animal brains, whereas our study focused solely on human blood cells as a peripheral biomarker of the central nervous system (Sullivan et al, 2006; Mohr and Liew, 2007; Desjardins et al, 2008; Belzeaux et al, 2010; Rollins et al, 2010; Rivera-Baltanas et al, 2014; Cattane et al, 2015). …”

Section: Limitationsmentioning

confidence: 99%

“…However, mRNA level changes in blood for candidate genes including EGR and HTR2A can cautiously be used as peripheral markers of transcription alterations in the CNS in response to interventions or to characterize patient groups (Sullivan et al, 2006; Mohr and Liew, 2007; Desjardins et al, 2008; Belzeaux et al, 2010; Rollins et al, 2010; Rivera-Baltanas et al, 2014; Cattane et al, 2015). The EGR and HTR2A genes are expressed in peripheral blood cells (Stefulj et al, 2000; Fukuda et al, 2006; Inoue et al, 2011; Cattane et al, 2015).…”

Section: Introductionmentioning

confidence: 99%

A Single Dose of LSD Does Not Alter Gene Expression of the Serotonin 2A Receptor Gene (HTR2A) or Early Growth Response Genes (EGR1-3) in Healthy Subjects

et al. 2017

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Rationale: Renewed interest has been seen in the use of lysergic acid diethylamide (LSD) in psychiatric research and practice. The repeated use of LSD leads to tolerance that is believed to result from serotonin (5-HT) 5-HT2A receptor downregulation. In rats, daily LSD administration for 4 days decreased frontal cortex 5-HT2A receptor binding. Additionally, a single dose of LSD acutely increased expression of the early growth response genes EGR1 and EGR2 in rat and mouse brains through 5-HT2A receptor stimulation. No human data on the effects of LSD on gene expression has been reported. Therefore, we investigated the effects of single-dose LSD administration on the expression of the 5-HT2A receptor gene (HTR2A) and EGR1-3 genes.Methods: mRNA expression levels were analyzed in whole blood as a peripheral biomarker in 15 healthy subjects before and 1.5 and 24 h after the administration of LSD (100 μg) and placebo in a randomized, double-blind, placebo-controlled, cross-over study.Results: LSD did not alter the expression of the HTR2A or EGR1-3 genes 1.5 and 24 h after administration compared with placebo.Conclusion: No changes were observed in the gene expression of LSD’s primary target receptor gene or genes that are implicated in its downstream effects. Remaining unclear is whether chronic LSD administration alters gene expression in humans.

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Serotonin 2A receptor clustering in peripheral lymphocytes is altered in major depression and may be a biomarker of therapeutic efficacy

Cited by 26 publications

References 32 publications

Consensus paper of the WFSBP Task Force on Genetics: Genetics, epigenetics and gene expression markers of major depressive disorder and antidepressant response

Consensus paper of the WFSBP Task Force on Genetics: Genetics, epigenetics and gene expression markers of major depressive disorder and antidepressant response

Interaction of neurotransmitters and neurochemicals with lymphocytes

A Single Dose of LSD Does Not Alter Gene Expression of the Serotonin 2A Receptor Gene (HTR2A) or Early Growth Response Genes (EGR1-3) in Healthy Subjects

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