OMIM Entry - * 182135 - 5-HYDROXYTRYPTAMINE RECEPTOR 2A; HTR2A

*182135

5-HYDROXYTRYPTAMINE RECEPTOR 2A; HTR2A

Alternative titles; symbols

SEROTONIN 5-HT-2A RECEPTOR
SEROTONIN 5-HT-2 RECEPTOR, FORMERLY; HTR2, FORMERLY

HGNC Approved Gene Symbol: HTR2A

Cytogenetic location: 13q14.2 Genomic coordinates (GRCh37): 13:47,405,676-47,471,210 (from NCBI)

Gene-Phenotype Relationships

Location	Phenotype	Phenotype MIM number	Phenotype mapping key
13q14.2	{Alcohol dependence, susceptibility to}	103780	3
{Anorexia nervosa, susceptibility to}	606788	3
{Major depressive disorder, response to citalopram therapy in}	608516	3
{Obsessive-compulsive disorder, susceptibility to}	164230	3
{Schizophrenia, susceptibility to}	181500	3
{Seasonal affective disorder, susceptibility to}	608516	3

TEXT

Description

Serotonin (5-hydroxytryptamine; 5-HT) is a neurotransmitter that occupies an important place in neurobiology because of its role in many physiologic processes such as sleep, appetite, thermoregulation, pain perception, hormone secretion, and sexual behavior. Abnormality of the serotonergic system has been implicated in a number of human diseases such as mental depression, migraine, epilepsy, obsessive-compulsive disorder, and affective disorder.. Like other neurotransmitters, 5-HT is released into the synaptic junction and exerts its effect on specific receptors on the postsynaptic membranes. Based on differential radioligand binding affinities, at least 6 types of 5-HT receptors have been identified: 5-HT-1A, -1B, -1C, -1D, -2, and -3 (summary by Sparkes et al., 1991; see reviews by Peroutka, 1988 and Paoletti et al., 1990).

Cloning and Expression

Using a restriction fragment of rat 5-HT2 receptor cDNA, Chen et al. (1992) identified 5-HT2 receptor clones from a human genomic library. The deduced amino acid sequences of the human, mouse, and rat 5-HT2 receptors are highly conserved; all 3 share 90% sequence identity (Chen et al., 1992).

Gene Structure

Chen et al. (1992) demonstrated that the HTR2 gene contains 3 exons and spans over 20 kb.

Mapping

Sparkes et al. (1991) used a rat cDNA clone for HTR2, which had been shown to cross-hybridize with human and mouse DNA, to map the gene in mouse and man by somatic cell hybrid and in situ hybridization studies. They concluded that the gene is located on chromosome 13q14-q21 in man and on chromosome 14 in the mouse. Hsieh et al. (1990) confirmed the assignment of the HTR2 locus to human chromosome 13 and mouse chromosome 14 by somatic cell hybrid analysis. Furthermore, linkage studies in CEPH families, using a PvuII RFLP detected with the HTR2 probe, showed tight linkage between HTR2 and the locus for esterase D (133280). They concluded that HTR2 is probably between ESD and RB1 (614041). Liu et al. (1991) demonstrated that mouse Htr2 gene is tightly linked to esterase-10 on mouse chromosome 14.

A mouse neurologic mutation, agitans (ag), maps to the region of chromosome 14 that, on the basis of syntenic homology, Hsieh et al. (1990) suggested may contain the Htr2 locus.

Gene Function

Kato et al. (1996) presented evidence for genomic imprinting of the HTR2 gene. They demonstrated that the HTR2 gene was expressed only from the maternal allele.

The human polyomavirus JCV causes the fatal demyelinating disease progressive multifocal leukoencephalopathy in immunocompromised patients. Elphick et al. (2004) found that the serotonergic receptor 5HT(2A)R could act as the cellular receptor for JCV on human glial cells. The 5HT(2A) receptor antagonists inhibited JCV infection, and monoclonal antibodies directed at 5HT(2A) receptors blocked infection of glial cells by JCV, but not by SV40. Transfection of 5HT(2A) receptor-negative HeLa cells with a 5HT(2A) receptor rescued virus infection, and this infection was blocked by antibody to the 5HT(2A) receptor. A tagged 5HT(2A) receptor colocalized with labeled JCV in an endosomal compartment following internalization. Thus, Elphick et al. (2004) suggested that serotonin receptor antagonists may be useful in the treatment of progressive multifocal leukoencephalopathy.

The liver can regenerate its volume after major tissue loss. Lesurtel et al. (2006) showed that in a mouse model of liver regeneration, thrombocytopenia resulted in the failure to initiate cellular proliferation in the liver. Platelets are major carriers of serotonin in the blood. In thrombocytopenic mice, a serotonin agonist reconstituted liver proliferation. The expression of 5-HT2A and 2B (601122) subtype serotonin receptors in the liver increased after hepatectomy. Antagonists of 5-HT2A and 2B receptors inhibited liver regeneration. Liver regeneration was also blunted in mice lacking tryptophan hydroxylase-1 (TPH1; 191060), which is the rate-limiting enzyme for the synthesis of peripheral serotonin. This failure of regeneration was rescued by reloading serotonin-free platelets with a serotonin precursor molecule. Lesurtel et al. (2006) concluded that platelet-derived serotonin is involved in the initiation of liver regeneration.

Weisstaub et al. (2006) demonstrated that global disruption of Htr2a signaling in mice reduced inhibition in conflict anxiety paradigms without affecting fear-conditioned and depression-related behaviors. Selective restoration of Htr2a signaling in the cortex normalized conflict anxiety behaviors. Weisstaub et al. (2006) concluded that their findings indicate a specific role for cortical HTR2A function in the modulation of conflict anxiety, consistent with models of cortical, 'top-down' influences on risk assessment.

Bhattacharyya et al. (2006) found that dopamine acts as a partial agonist for rat Htr2a expressed in HEK293 cells. Dopamine also induced receptor internalization, although at significantly higher concentrations than serotonin. However, when the receptors were first sensitized by serotonin at a subthreshold concentration for internalization, then dopamine-induced internalization occurred at concentrations 10-fold lower than when dopamine was used alone. Dopamine-induced receptor internalization, unlike serotonin-induced internalization, did not depend on protein kinase C.

Gonzalez-Maeso et al. (2008) demonstrated that mGluR2 (604099) interacts through specific transmembrane helix domains with HTR2A, a member of an unrelated G protein-coupled receptor family, to form functional complexes in brain cortex. The serotonin HTR2A receptor-mGluR2 complex triggered unique cellular responses when targeted by hallucinogenic drugs, and activation of mGluR2 abolished hallucinogen-specific signaling and behavioral responses. In postmortem human brain from untreated schizophrenic subjects, HTR2A is upregulated and mGluR2 is downregulated, a pattern that could predispose to psychosis. Gonzalez-Maeso et al. (2008) concluded that the HTR2A-mGluR2 complex may be involved in the altered cortical processes of schizophrenia.

Molecular Genetics

Genomic imprinting describes a parent-of-origin-dependent epigenetic mechanism through which a subset of genes is expressed from only one allele. The allele-specific loss of expression can be polymorphic; that is, it can vary between individuals. Examples of genes that are polymorphically imprinted include the Wilms tumor-1 gene (WT1; 607102; Mitsuya et al., 1997) and the HTR2A gene (Bunzel et al., 1998).

Lohmueller et al. (2003) performed a metaanalysis of 301 published genetic association studies covering 25 different reported associations. For 8 of the associations, pooled analysis of follow-up studies yielded statistically significant replication of the first report, with modest estimated genetic effects. One of these associations was that of schizophrenia with the C allele of the 102T/C SNP in the HTR2A gene (182135.0001), as first reported by Inayama et al. (1996).

Harvey et al. (2003) investigated whether the agonist serotonin and antagonists loxapine and clozapine have an altered potency for 4 allelic variants (T25N, I197V, A447V, and H452Y) of the human 5HT2A receptor when compared with a wildtype allele. The studies were done by an in vitro functional assay system consisting of an insect cell line that was stably transformed with human wildtype and mutant alleles. This assay system measured release of calcium stores due to receptor activation by agonists and inhibition of this agonist stimulated response by antagonists. They found that the I197V allele required a 2-fold higher concentration of the atypical neuroleptic clozapine to inhibit serotonin stimulation compared to the wildtype receptor (P = 0.036). The I197V mutation did not affect the inhibition of serotonin stimulation by the typical neuroleptic loxapine nor did it alter the activation of the receptor by serotonin. The other 3 mutations did not significantly alter the response of the receptor to the agonist serotonin or to the antagonists loxapine and clozapine.

De Quervain et al. (2003) presented evidence that individuals with the H452Y polymorphism performed poorer on memory recall tests than individuals with a normal genotype, suggesting a role for the HTR2A receptor in memory functioning.

Enoch et al. (1998) and Walitza et al. (2002) found an association between the A allele of the -1438G-A promoter polymorphism (182135.0002) and obsessive-compulsive disorder (OCD; 164230).

Holmes et al. (1998) genotyped a total of 211 subjects from a population-based prospective study of psychopathology within late-onset Alzheimer disease (AD; 104300) for the 102T-C polymorphism and the cys23-to-ser polymorphism of the 5-HT-2C receptor gene (312861.0001). Associations were found between the presence of the 102C allele and the presence of both visual and auditory hallucinations. Among 96 AD patients, Assal et al. (2004) found that the 102T allele was associated with agitation/aggression and delusions, but not hallucinations.

The -1438G-A polymorphism has been implicated in other neuropsychiatric disorders such as schizophrenia (181500) (Arranz et al., 1998), seasonal affective disorder (see 608516) (Enoch et al., 1999), alcohol dependence (103780) (Nakamura et al., 1999), and anorexia nervosa (606788) (Collier et al., 1997).

Hinney et al. (1997) and Campbell et al. (1998) found no association of the A allele of the -1438G-A polymorphism with anorexia nervosa.

Nakamura et al. (1999) suggested that the A allele of the -1438G-A polymorphism could be associated with restrictive behavior while the G allele could be associated with food and alcohol addiction. Aubert et al. (2000) reported that the -1438G-A polymorphism influences food and alcohol intake in obese (601665) French subjects.

Patients with major depressive disorder (608516) whose treatment is unsuccessful with one medication often have a response when treated with an antidepressant of a different chemical class. McMahon et al. (2006) searched for genetic predictors of treatment outcome in 1,953 patients with major depressive disorder who were treated with the antidepressant citalopram and were prospectively assessed. They detected significant and reproducible association between treatment outcome and a marker in intron 2 of HTR2A, rs7997012. Other markers in HTR2A also showed evidence of association with treatment outcome in the total sample. The serotonin-2A receptor, which is encoded by the HTR2A gene, is downregulated by citalopram. Participants who were homozygous for the A allele had an 18% reduction in absolute risk of having no response to treatment compared with those homozygous for the other allele. The A allele was over 6 times more frequent in white than in black participants, and treatment was less effective among black participants. The A allele may contribute to racial differences in outcomes of antidepressant treatment. Taken together with previous neurobiologic findings, these new genetic data made a compelling case for a key role of HTR2A in the mechanism of antidepressant action.

Nomenclature

HTR2 became HTR2A with description of HTR2B (601122) and HTR2C (312861).

ALLELIC VARIANTS (3 Selected Examples):

Table View

.0001 SCHIZOPHRENIA, SUSCEPTIBILITY TO

HTR2A, 102T-C - [ClinVar]

Williams et al. (1996) looked for an association between schizophrenia (181500) and the 102T-C polymorphism of the HTR2A gene in a large multicenter study. Seven countries recruited 1,210 participants: 571 white schizophrenic patients and 639 ethnically matched controls. All patients had a diagnosis of schizophrenia or schizoaffective disorder. Williams et al. (1996) found a significant overall association between schizophrenia and the C allele with an odds ratio of 1.3 (95% CI 1.1-1.53); a highly significant excess of the TC/CC genotypes in schizophrenia (p = 0.008) with a relative risk of 1.7 and an attributable fraction of 0.35.

Williams et al. (1997) reported a metaanalysis of the association between the 102T-C polymorphism of the HDR2A gene and schizophrenia.

.0002 OBSESSIVE-COMPULSIVE DISORDER, SUSCEPTIBILITY TO

HTR2A, -1438G-A - [ClinVar]

Enoch et al. (1998) demonstrated an association between the A allele of an A-to-G polymorphism at position -1438 in the HTR2A promoter and obsessive-compulsive disorder (OCD; 164230). Walitza et al. (2002) confirmed this finding in an association analysis of the -1438G-A promoter polymorphism in 55 children and adolescents with OCD and in 223 controls consisting of unrelated students. Statistically significant differences in genotype (p less than 0.05) and allele frequencies (p less than 0.05) were observed that suggested an association of the -1438A allele with OCD.

The -1438G-A SNP lies upstream of 2 alternative promoters for the HTR2A gene. To investigate possible functional effects of this polymorphism on either promoter, Parsons et al. (2004) used 2 different reporter gene assays in 3 cell lines. In the presence of the SV40 enhancer, promoter activity was significantly greater with the A allele relative to the G allele, but only in cell lines expressing endogenous HTR2A, suggesting that transcriptional factors and the presence of both promoters might be necessary to elicit this effect.

.0003 MAJOR DEPRESSIVE DISORDER, RESPONSE TO CITALOPRAM THERAPY IN

HTR2A, IVS2, A-G [dbSNP:rs7997012] [ClinVar]

In 1,953 patients with major depressive disorder (608516) who were treated with the antidepressant citalopram and were prospectively assessed, McMahon et al. (2006) found an association between the HTR2A intron 2 rs7997012 and treatment outcome. The allele frequency of the A allele of this SNP was 0.42 in white participants and 0.06 in black participants. Participants who were homozygous for the A allele had an 18% reduction in absolute risk of having no response to treatment compared with those homozygous for the other allele. The serotonin-2A receptor, which is encoded by the HTR2A gene, is downregulated by citalopram. McMahon et al. (2006) concluded that the A allele of the rs7997012 may contribute to racial differences in outcomes of antidepressant treatment.

See Also:

Murray and Lopez (1996)

REFERENCES

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▸ Contributors:

Ada Hamosh - updated : 5/9/2008

Creation Date:

Victor A. McKusick : 1/14/1991

▸ Edit History:

carol : 10/01/2014

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