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Sérotonine et capacité à différer une conduite un modèle psychobiologique

Published online by Cambridge University Press:  28 April 2020

Y. Lecrubier
Y. Lecrubier*
Affiliation:
Hôpital de La Salpêtrière, Unité Insertn 302, 47, bd de l’Hôpital, 75651 Paris Cedex 13, France
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Résumé

Des troubles du fonctionnement sérotoninergique ont été impliqués dans de nombreuses pathologies ou dysrégulations du système nerveux central: trouble dépressif, trouble anxieux, schizophrénie, psychopathie, agressivité, boulimie, éthylisme, etc.

Le rôle de cette amine dans l’inhibition de la survenue de certains comportements est décrit depuis longtemps. Chez l’animal, ce rôle semble organiser la capacité à différer une conduite et/ou à tolérer sans réponse comportementale une situation de contrainte. Chez l’homme, la sérotonine semble réguler une capacité à contrôler les réponses impulsives dans le cadre des troubles très différents tels que passage à l’acte suicidaire, conduite boulimique, compulsions itératives, conduite éthylique, etc. Les inhibiteurs du recaptage de la sérotonine semblent améliorer l’existence de ces troubles de façon transnosologique.

Nous faisons l’hypothèse que certains diagnostics pourraient être la conséquence d’un fonctionnement «limite» sur le plan biologique facilitant le passage à l’acte et des troubles de personnalité. Aucune des deux dimensions ne serait en soi pathologique. Le manque d’adaptabilité de certains fonctionnements mentaux (caractère, personnalité) ajoutée à un fonctionnement biologique «limite” (difficulté à différer sa réponse) seraient par leur coexistence responsables de la décompensation qui aboutit à ce qu’on appelle un diagnostic.

Summary

Summary

Serotoninergic function disorders have been implicated in numerous central nervous System pathologies or dysregulations: depressive or anxious disorders, schizophrenia, psychopathy, aggressivity, bulimia, alcoholisrn, etc.

The role of this amine in inhibiting the onset of certain behaviors was described long ago. In the animal, this rote seems to organize the capacity to delay a given conduct and/or tolerate a constraining condition without a behavioral response. In man, serotonin seems to regulate the capacity to control impulsive responses in the context of very different disorders sucli as passage to the suicidal act, bulimic conduct, iterative compulsions, alcoholisrn, etc. The inhibitors of serotonin reuptake seem to improve the existence of these disorders in a transnosological manner.

We propose that certain diagnoses may be the consequence of «limit» functioning at the biological level (facilitating passage to the act), in addition to personality disorders. While neither dimension seems to be intrinsically pathological, the decompensation resulting in what is called a diagnosis is apparently due to a coexisting lack of adaptability of certain mental functions (character, personality), added to «limit» biological functioning (difficulty to defer response).

Keywords

sérotoninepassage à l'actetrouble obsessionnel-compulsifboulimietransnosologieserotoninacting outobsessive-compulsive disorderbulimiatransnosology
Type
Research Article
Information
Psychiatry and Psychobiology , Volume 3 , Issue S1: Les Etats Dépressifs: vers une révision des concepts Paris, 20 Novembre 1987 , 1988 , pp. 95s - 100s
Copyright
Copyright © European Psychiatric Association 1998

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References

Références

Asberg, M., Traskman, L. & Thoren, P. (1976) 5-HIAA in the cerebrospinal fluid: a biochemical suicide predictor? Arch. Gen. Psychiatry, 33, 1193–1197CrossRefGoogle ScholarPubMed
Banki, C.M. (1977) Correlation of anxiety and related symptoms with cerebrospinal fluid 5-HIAA in depressed women. J. Neurol. Transm. 41, 135–143CrossRefGoogle ScholarPubMed
Bioulac, B., Benezech, M., Renaud, B., Noel, B. & Roche, D. (1980) Serotonergic functions in 47.XYZ syndrome. Biol. Psychiatry 15, 917Google Scholar
Brodie, B.B. & Shore, P. (1957) A concept for a role of serotonin and norepinephrine as Chemical mediators in the brain. Ann. N.Y. Acad. Sci. 42, 66–631Google Scholar
Brown, G.L., Goodwin, F.K., Ballenger, J.C., Goyer, P.F. & Major, L.F. (1979) Aggression in humans correlates with cerebrospinal fluid amine metabolites. Psychiatry Res. 1, 131–139CrossRefGoogle ScholarPubMed
Foa, E.B., Steketee, G., Korak, M.J., Dugger, D. & Simpson, G.M. (1985) Effects of imipramine on depression and on obsessive-compulsive symptorns. Annual Meeting of the American College of Neuropsychopharmacology, p. 38(Abstr.)Google Scholar
Fontaine, R. & Chouinard, G. (1985) Antiobsessive effect of fluoxetine (letter). Am. J. Psychiatry 142, 989Google Scholar
Hudson, J.L. & Pope, H.G. (1987) Newer antidepressants in the treatment of Bulimia nervosa. Psychopharmacol. Bull. 23, 52–57Google ScholarPubMed
Insel, T.R., Mueller, E.A., Alterman, I., Linnoila, M. & Murphy, D.L. (1985) Obsessive-compulsive disorder and serotonin: is there a connection? Biol. Psychiatry 20, 1174–1188CrossRefGoogle ScholarPubMed
Kahn, R.S., Westcnberg, H.G.M. & Jolies, J. (1984) Zimelidine treatment of obsessive-compulsive disorder. Acta Psychiatr. Scand. 69, 259–261CrossRefGoogle ScholarPubMed
Kaye, W.H., Ebert, M.H., Gwirtman, H.E. & Weirs, S.R. (1984) Differences in brain serotoninergic metabolism between non-bulimic and bulimic patients with Anorexia nervosa. Am. J. Psychiatry 141, 1598–1601Google Scholar
Lidberg, C., Tuck, J.R., Asberg, M., Scalia, Tomba G.P. & Bertilsson, L. (1985) Homicide suicide and CSF 5-HIAA. Acta Psychiatr. Scand. 71, 230–236CrossRefGoogle ScholarPubMed
Linnoila, M., Virkhunem, M., Scheinin, M., Nuutila, A., Rimon, R. & Goodwin, F.K. (1983) Low cerebrospinal fluid 5-HIAA concentration differentiates impulsive front non-impulsive violent behavior. Life Sci. 33, 2609–2614CrossRefGoogle Scholar
Orland, L., Wiberg, A,Asberg, M., Traskman, L., Sjostrand, L., Thoren, P., Bertilsson, L. & Tybring, G. (1982) Platelet MAO activity and monoamine metabolites in cerebrospinal fluid in depressed and suicidai patients and in healthy Controls. Psychiatry Res. 4, 21–29CrossRefGoogle Scholar
Prasad, A. (1984a) A double-blind study of imipramine versus zimelidine in treatment of obsessive compulsive neurosis. Pharmacopsychiatry 17, 61–62CrossRefGoogle Scholar
Prasad, A. (1984b) Obsessive-compulsive disorder and trazodone (letter). Am. J. Psychiatry 141, 612–613Google Scholar
Price, L.H., Goodman, W.K., Charney, D.S., Rasmussen, S.A. & Heninger, G.R. (1987) Treatment of severe obsessive-compulsive disorder with fluvoxamine. Am. J. Psychiatry 144, 1059–1061Google ScholarPubMed
Sepinwall, J. & Cook, L. (1978) Behavioral pharmacology of anti-anxiety drugs. In: Handbook of Psychopharmacology (Iversen, L.L., Iversen, S.D. & Snyder, S.H., eds.), Plenum Press, vol. 13Google Scholar
Soubrié, P. (1986) Reconciling the role of central scrotonin neurons in human and animal behavior. Behav. Brain. Sci. 9, 319–364CrossRefGoogle Scholar
Thiébot, M.H., Le Bihan, C., Soubrié, P. & Simon, P. (1985) Benzodiazepines reduce the tolerance to reward delay in rats. Psychopharmacology 86, 147–152CrossRefGoogle ScholarPubMed
Thiébot, M.H. (1986) Are serotonergic neurons involved in the control of anxiety and in the anxiolytic activity of benzodiazepines? Pharmacol. Biochem. Behav. 24, 1471–1477CrossRefGoogle ScholarPubMed
Thoren, P., Asberg, M., Cronholm, B., Jornestedt, L. & Traskman, L. (1980) Clomipramine treatment of obsessive compulsive disorder: I. A controlled clinical trial. Arch. Gen. Psychiatry 37, 1281–1289CrossRefGoogle Scholar
Traskman, L., Asberg, M., Bertilsson, L. & Sjostrand, L. (1981) Monoamine metabolites in CSF and suicidai behavior. Arch. Gen. Psychiatry 38, 631–636CrossRefGoogle ScholarPubMed
Truffinet, P. & Lecrubier, Y. (1988) La sécrétion de cortisol chez le déprimé. Encephale XIV, 1—17Google Scholar
Turner, S.M., Jacob, R.G., Beidel, D.C. & Himmelhoch, J. (1985) Fluoxetine treatment of obsessive compulsive disorder. J. Clin. Psychopharmacol. 5, 207–212CrossRefGoogle ScholarPubMed
Van, Praag H.M. (1983a) CSF 5-HIAA and suicide in non-depressed schizophrenies. Lancet 977—978Google Scholar
Van, Praag H.M. (1983b) In search of the action mechanism of antidepressant 5-HTP tyrosine mixtures in depression. Neuroplwrmacology 22, 433–440Google Scholar
Van, Praag H.M. (1986) (Auto)aggression and CSF 5-HIAA in depression and schizophrenia. Psychopharmacol. Bull. 2, 669–673Google Scholar
Van, Praag H.M., Kahn, R.S., Asnis, G.M., Wetzler, S., Brown, S.L., Bleich, A. & Korn, M.L. (1987) Denosologization of biological psychiatry of the specificity of 5-HT disturbances in psychiatrie disorders. J. Affective Disord. 13, 1–8Google Scholar
Vindreau, C. & Ginestet, D. (1987) Boulimie sucrée, boulimie salée - Deux syndromes. Encephale XIII, 177-220Google Scholar
Wise, C.D., Berger, B.D. & Stein, L. (1973) Evidence of alpha-noradrenergic reward receptors and serotonergic punishment receptors in the rat brain. Biol. Psychiatry 6, 3–21Google Scholar
Wurtman, R.J. & Wurtman, J.J. (1986) Carbohydrate craving, obesity and brain serotonin. Appetite 7 (suppl.), 99–103CrossRefGoogle ScholarPubMed
Yagura-Tobias, J.A. & Bhagavan, H.N. (1977) L-Tryptophan in obsessive-compulsive disorders. Am. J. Psychiatry 234, 1298–1299Google Scholar
Zohar, J. & Insel, T.R. (1987) Obsessive-compulsive disorder: psychobiological approaches to diagnosis, treatment and pathophysiology. Biol. Psychiatry 10, 667–687Google Scholar
Zohar, J., Insel, T.R., Zohar-Katouch, R.C., Hill, J.L. & Murphy, D.L. (1988) Serotoninergic responsivity in obsessive compulsive disorder. Arch. Gen. Psychiatry 45, 88CrossRefGoogle Scholar
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