Obsessive-compulsive disorder and serotonin: Is there a connection?

Insel, Thomas R.; Mueller, Edward A.; Alterman, Ina; Linnoila, Markku; Murphy, Dennis L.

doi:10.1016/0006-3223(85)90176-3

Cited by 311 publications

(101 citation statements)

References 38 publications

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“…The main finding of our study is that CSF glutamate levels are significantly raised in OCD patients compared to normal controls, and that the difference is unrelated to age or gender of the subjects. To our knowledge, this is the first published report investigating CSF glutamate levels in OCD patients, although there have been previous studies investigating various biogenic amines in CSF in OCD patients (Thoren et al, 1980;Insel et al, 1985;Swedo et al, 1992;Leckman et al, 1995). The use of psychotropic drug-naïve patients in order to avoid the confounding effects of medications (Charney et al, 1981;Mellstrom et al, 1982;Garvey et al, 1984) and the use of a psychiatrically normal control sample constitute the other methodological advantages of our study.…”

Section: Discussionmentioning

confidence: 91%

Glutamatergic Dysfunction in OCD

Chakrabarty

Bhattacharyya

Christopher

et al. 2005

Neuropsychopharmacol

310

191

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The role of glutamatergic dysfunction in the pathophysiology of OCD has hardly been explored despite recent reports implicating glutamatergic dysfunction in OCD. We decided to investigate CSF glutamate levels in adult OCD probands compared to psychiatrically normal controls. In total, 21 consenting psychotropic drug-naïve adult OCD patients, diagnosed using SCID-IV-CV, and 18 consenting psychiatrically normal controls with age within 10 years of age of the patients, who did not have any history of head injury or neurological illness, were included into the study. Aseptically collected and stored CSF samples obtained from the patients and control subjects were used for glutamate estimation, which was carried out by a modification of the procedure described by Lund (1986). CSF glutamate (mmol/l) level was found to be significantly higher [F(1,31) ¼ 6.846, p ¼ 0.014] in OCD patients (47.1274.25) compared to control subjects (41.3673.63) on analysis of covariance. There was no effect of gender, age, duration of illness, Y-BOCS score, or CGI-S score on CSF glutamate levels. Our study provides preliminary evidence implicating glutamatergic excess in the pathophysiology of OCD, which needs to be further explored by studies from other centers involving larger sample sets from different age groups.

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Section: Discussionmentioning

confidence: 91%

Glutamatergic Dysfunction in OCD

Chakrabarty

Bhattacharyya

Christopher

et al. 2005

Neuropsychopharmacol

310

191

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“…Several studies suggest a genetic component in the etiology of OCD (3,4). In addition, the selective response of the illness to treatment with serotonin reuptake inhibiting agents has led to the hypothesis that OCD may be associated with dysregulation of serotonergic neurotransmission (5,6). Although serotonin reuptake inhibitors are clearly the first-line pharmacotherapy for OCD, complete relief of symptoms is rare during treatment with these medications, and 30-40% of patients remain clinically unchanged (7).…”

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confidence: 99%

Genotype determining low catechol-O-methyltransferase activity as a risk factor for obsessive-compulsive disorder

Karayiorgou

Altemus

Galke

et al. 1997

Proc. Natl. Acad. Sci. U.S.A.

Self Cite

288

182

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In the present study, we address the role of the gene for catechol-O-methyltransferase (COMT), a key modulator of dopaminergic and noradrenergic neurotransmission, in the genetic predisposition to obsessive-compulsive disorder (OCD). We show that a common functional allele of this gene, which results in a 3-to 4-fold reduction in enzyme activity, is significantly associated in a recessive manner with susceptibility to OCD, particularly in males. This association is further supported by psychiatric evaluation of patients who carry microdeletions encompassing the comt gene. The mechanism underlying this sex-selective association remains to be defined and may include a sexual dimorphism in COMT activity, although close linkage with a nearby disease susceptibility locus cannot be excluded at this point.

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“…Since the 1960s, serotonin has been repeatedly implicated in the pathophysiology of OCD (Insel et al 1985;Jenike et al 1990;Murphy and Pigott 1990;Zohar et al 1988;Barr et al 1992). This evidence was largely derived from the data about chronic administration of clomipramine and SSRIs, whose antiobsessive efficacy appears to be critically linked to the effects on the 5-HT system rather than other neurotransmitters (Pigott 1996).…”

Section: Discussionmentioning

confidence: 99%