[The biological basis of suicidal behavior: neuroendocrine and psychophysiological approach to the role of catecholamines].
The current main neurochemical theories of the biological correlates of suicidal behavior principally involve the serotonergic system. Few data are available about the possible role of the catecholaminergic (noradrenergic and dopaminergic) function. In the present study, in a first part, we assessed the growth hormone (GH) response to clonidine, a selective alpha 2-adrenergic agonist, and to apomorphine, a dopaminergic agonist, in 22 DSM-III-R major depressive male inpatients with a history of suicide attempts compared to 22 age-matched major depressive inpatients without history of suicidal behavior. Hormonal responses to clonidine and apomorphine were also compared with 4.00 PM postdexamethasone cortisol levels. The two groups differed significantly in the GH peak response after apomorphine: 6.27 +/- 3.18 ng/ml in suicide attempters vs 17.40 +/- 14.87 ng/ml in nonattempters (F = 11.78, p = 0.001). There was no statistically significant difference between the two groups for GH peak responses after clonidine. Moreover, mean postdexamethasone cortisol levels did not exhibit any significant difference between suicide attempters and nonattempters. Violent and nonviolent attempters did not differ on any of the biological measures. In a second part, P300 and contingent negative variation (CNV) were recorded in 20 depressive inpatients subgrouped into suicide attempters (n = 10) and nonattempters (n = 10). The results showed a significant reduction of both P300 and CNV amplitudes in patients who attempted suicide compared to patients without history of suicide attempts. Moreover, a significant correlation was found between the Suicidal Risk scale and CNV amplitude. In conclusion, these results suggest that a dopaminergic hypoactivity as assessed by a blunted GH response to apomorphine and by a reduction of both P300 and CNV amplitudes, could be considered as a biological correlate of suicidal behavior. In contrast, noradrenergic disturbances, particularly at the level of alpha 2-adrenergic receptors, seem to play a more minor role. Moreover, DST nonsuppression cannot be considered as a biological marker of suicidal behavior.
Unité de Psychiatrie, C.H.U. du Sart Tilman, Liége, Belgique.
W
W
Pitchot
M
M
Hansenne
A
A
Gonzalez Moreno
J
J
Wauthy
M
M
Ansseau
D000293:Adolescent; D000316:Adrenergic alpha-Agonists / Q000494:pharmacology; D000328:Adult; D001058:Apomorphine / Q000494:pharmacology; D003000:Clonidine / Q000494:pharmacology; D003265:Contingent Negative Variation; D003866:Depressive Disorder / Q000097:blood* / Q000523:psychology; D003907:Dexamethasone; D018491:Dopamine Agonists / Q000494:pharmacology; D018913:Event-Related Potentials, P300; D013006:Growth Hormone / Q000097:blood*; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D008297:Male; D013406:Suicide, Attempted / Q000523:psychology
D000316:Adrenergic alpha-Agonists; D018491:Dopamine Agonists; D003907:Dexamethasone; D013006:Growth Hormone; D003000:Clonidine; D001058:Apomorphine; D006854:Hydrocortisone
Bases biologiques du comportement suicidaire: approche neuroendocrinienne et psychophysiologique du rôle des catécholamines.