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The Potential Role of 5-HT1D Receptors in the Pathophysiology and Treatment of Obsessive-Compulsive Disorder

Published online by Cambridge University Press:  07 November 2014

Liat Stern ,
Joseph Zohar ,
Thalma Hendler ,
Iulian Ianco  and
Yehuda Sasson
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Extract

Obsessive-compulsive disorder (OCD) is a psychiatric disorder in which the patient suffers from recurrent intrusive ideas, impulses, thoughts (obsessions), and/or patterns of behavior (compulsions) that are ego-alien and produce anxiety if resisted. The ego-dystonic nature of OCD is one of the hallmarks of this disorder. OCD can be a disabling condition because the obsessions and compulsions are time-consuming and interfere with patients' everyday activities and their relationships with friends and family. In severe cases, OCD conflicts even with the simplest tasks of daily living.

Research interest in OCD has been growing steadily in the past decade. A search on MEDLINE reveals an over 300% increase in citations on OCD from 1986 to 1998. These range across the spectrum of research fields, from genetic studies, brain imaging, and neurobiological research examining the underlying pathogenesis of OCD to epidemiological studies evaluating the course of clinical symptoms, comorbidities, and outcomes. Each area represents an important piece in the complex jigsaw puzzle of OCD.

Type
Feature Article
Information
CNS Spectrums , Volume 3 , Issue 8: Serotonin Subsystems , September 1998 , pp. 46 - 49
Copyright
Copyright © Cambridge University Press 1998

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References

REFERENCES

1.American Psychiatric Association Diagnostic and Statistical Manual of Mental Disorders. 3rd ed rev. Washington, DC: American Psychiatric Association; 1987:245–247.Google Scholar
2.Zohar, J, Zohar-Kadouch, RC, Kindler, S. Current concepts in the pharmacological treatment of obsessive-compulsive disorder. Drugs. 1992;43:210–218.Google Scholar
3.Robins, LN, Helzer, JL, Weissman, MM, et al.Lifetime prevalence of specific psychiatric disorders in three sites. Arch Gen Psychiatry. 1984;41:949–958.Google Scholar
4.Weissman, MM, Bland, RC, Canino, GL. The cross national epidemiology of obsessive-compulsive disorder. J Clin Psychiatry. 1994;55:5–10.Google Scholar
5.Flament, MF, Withaker, A, Rapaport, JL, et al.Obsessive-compulsive disorder in adolescence: an epidemiological study. J Am Acad Child Adolesc Psychiatry. 1988;27:764–771.Google Scholar
6.Zohar, J, Insel, T. Obsessive-compulsive disorder psychobiological approaches to diagnosis, treatment and pathophysiology. Biol Psychiatry. 1987;22:667–687.Google Scholar
7.Zohar, J, Mueller, EA, Insel, TR. Serotonin responsivity in obsessive-compulsive disorder. Arch Gen Psychiatry. 1987;44:946–951.Google Scholar
8.Pigott, TA, L'Heureux, F, Bernstein, SE, Hill, JL, Murphy, DL. A controlled comparative therapeutic trial of clomipramine and m-chlorophenylpiperazine (mCPP) in patients with obsessive-compulsive disorder. NCDEU Annual Meeting. May 26–29, 1992; Orlando, FL.Google Scholar
9.Hollander, E, Fay, M, Cohen, B, Campeas, R, Gorman, JM, Leibovitz, MR. Serotonergic and adrenergic sensitivity in obsessive-compulsive disorder: behavioral findings. Am J Psychiatry. 1988;145:1015–1017.Google Scholar
10.Zohar, J, Insel, TR, Zohar-Kadouch, RC, Hill, JL, Murphy, DL. Serotonergic responsivity in obsessive-compulsive disorden effects of chronic clomipramine treatment. Arch Gen Psychiatry. 1998;45:167–172.Google Scholar
11.Marazziti, D, Hollander, E, Lensi, P, et al.Peripheral markers of serotonin and dopamine function in obsessive compulsive disorder. Psychiatry Res. 1992;42:41–51.Google Scholar
12.Flament, MF, Rapaport, JL, Murphy, DL, et al.Biochemical changes during clomipramine treatment of childhood obsessive-compulsive disorder. Arch Gen Psychiatry. 1987;44:219–225.Google Scholar
13.Thoren, P, Askeng, M, Bertlson, L, et al.Clomipramine treatment of obsessive-compulsive disorder. II. Biochemical aspects. Arch Gen Psychiatry. 1980;40:1085–1089.Google Scholar
14.Hollander, E, Decaria, CM, Nitescue, A, et al.Serotonergic function in obsessive-compulsive disorden behavioral and neuroendocrine to oral m-chlorophenylpiperazine and fenfluramine in patients and healthy volunteers. Arch Gen Psychiatry. 1992;49:21–28.Google Scholar
15.Pigott, TA, Zohar, J, Hill, JL, et al.Metergoline blocks behavioral and neuroendocrine effects of orally administrated in patients with obsessive-compulsive disorder. Biol Psychiatry. 1991;29:418–426.Google Scholar
16.Finberg, NA, Cowen, PJ, Kirk, JW, et al.Neuroendocrine response to intravenous L-tryptophan in obsessive-compulsive disorder. J Affective Disorder. 1994;32:97–104.Google Scholar
17.Lesch, KP, Hoh, A, Dissellcamp-Tietze, J, et al.5-Hydroxytryptamine 1A receptivity in obsessive-compulsive disorder: comparison of patients and controls. Arch Gen Psychiatry. 1991;48:540–547.Google Scholar
18.Jenike, M, Baer, L. Buspirone in OCD: an open trial. Am J Psychiatry. 1988;145:1285–1286.Google Scholar
19.Patto, UT, Pigott, TA, Hill, JL, et al.Controlled comparison of buspirone and clomipramine in obsessive-compulsive disorder. Am J Psychiatry. 1991;148:127–129.Google Scholar
20.McDougle, CJ, Goodman, WK, Leckman, JF, et al.Limited therapeutic effect of addition of buspirone in fluvoxamine-refractory obsessive-compulsive disorder. Am J Psychiatry. 1993;150:647–649.Google Scholar
21.Bastani, B, Nash, F, Meltzer, H. Prolactin and Cortisol response to MK-212, a serotonin agonist, in obsessive compulsive disorder. Arch Gen Psychiatry. 1990;47:946–951.Google Scholar
22.Ducharme, VG, Bouchard, C, Blier, P. Terminal 5-HT autore-ceptor desensitization in the orbitofrontal cortex is produced exclusively by drugs effective in obsessive-compulsive disorder (OCD). Society Neurosci. 1996;22:525–525.Google Scholar
23.Zohar, J, Kindler, S. Serotonergic probes in obsessive-compulsive disorder. Int Clin Psychopharmacol. 1992;7:39–40.Google Scholar
24.Starkey, SJ, Skingle, M. 5-HT1D as well as 5-HT1A autoreceptors modulate 5-HT release in guinea pig dorsal raphe nucleus. Neuropharmacohgy. 1994;33:393–402.Google Scholar
25.Pineyro, G, deMontigny, C, Blier, P. HT1D receptors regulate 5-HT release in the rat raphe nuclei. Neuropsychopharmacology. 1995;13:249–260.Google Scholar
26.Pineyro, G, deMontigny, C, Weiss, M, Blier, P. Autoregulatory properties of dorsal raphe 5-HT neurons: possible role of electronic coupling and 5-HT1D receptors in the rat brain. Synapse. 1996;22:54–62.Google Scholar
27.Benjamin, J, Greenberg, BD, Murphy, DL. Daily administration of m-chlorophenylpiperazine to health human volunteers rapidly attenuates many of its behavioral hormonal, cardiovascular and temperature effects. Psychopharmacobgy. 1996;127:140–149.Google Scholar
28.Peurotka, SJ, McCarthy, BG. Sumatriptan (GR43175) interacts selectively with 5-HT1B and 5-HT1D binding sites. Eur J Pharmacol. 1989;163:133–136.CrossRefGoogle Scholar
29.Peurotka, SJ. Drugs effective in the treatment of migraine. In: Hardman, JG, Limbrid, LE, Mollinof, PB, Ruddon, RW, Gilman, AG, eds. Goodman and Gilmans Pharmacological Basis of Therapeutics. 9th rev. ed New York, NY: McGraw-Hill; 1996;487–502.Google Scholar
30.Zohar, J. Is 5-HT1D involved in obsessive-compulsive disorder? Eur Neuropsychol. 1996;6:54–55.Google Scholar
31.Hendler, T, Goshen, E, Zwas, T, Lustig, M, Sasson, J, Zohar, J. Brain SPECT in obsessive-compulsive disorder during symptom provocation with sumatriptan. Eur J Neuropsychopharmacol. In press.Google Scholar
32.Stern, L, Zohar, J, Cohen, R, Sasson, Y. Treatment of severe, drag resistant obsessive compulsive disorder with the 5HT1D agonist sumatriptan. Eur Neuropsychopharmacol. In press.Google Scholar
33.Kaube, H, Hoskin, KL, Goadsby, PJ. Inhibition by sumatriptan of central trigeminal neurones only after blood-brain barrier disruption. Br J Pharmacol. 1993;109:788–792.Google Scholar
34.Rubin, RT, Villanueva-Meyer, J, Ananth, J, Traimar, PG, Mena, I. Regional 133Xe cerebral blood flow and cerebral 99mHMPAO uptake in unmedicated obsessive-compulsive disorder patients and matched normal control subject: determination by high resolution single photon emission computed tomography. Arch Gen Psychiatry. 1992;41:695–702.Google Scholar
35.Swedo, SE, Rappoport, JL, Cheslow, DL, et al.High prevalence of obsessive-compulsive symptoms in patients with Sydenham's chorea. Am J Psychiatry. 1989;146:246–249.Google Scholar