Bromocriptine treatment of depressive disorders

Abstract

Fifteen depressed patients were treated with increasing doses of bromocriptine in an open study. Twelve were treated for 5 weeks (final dose 20-60 mg daily) and nine of these recovered almost completely. As expected from a dopamine agonist, bromocriptine decreased the level of homovanillic acid (HVA) in cerebrospinal fluid (CSF) by 15% (P less than 0.05) and 23% (P less than 0.01) after 2 and 5 weeks of treatment, respectively. After 2 but not after 5 weeks of treatment there was also a small but significant decrease (13%; P less than 0.001) of the noradrenaline metabolite HMPG in CSF. Although there was no mean effect on 5-HIAA in CSF, there was a significant relationship between the HVA and 5-HIAA levels (as % of pretreatment level) both after 2 and 5 weeks of treatment (r = 0.96 and r = 0.62, respectively). This may indicate that the drug has an effect on the serotonin system secondary to the dopamine receptor stimulation. The amelioration of depression was not related to HVA, but did correlate to HMPG in CSF (r = 0.65; P less than 0.05) both metabolites measured before treatment. These results indicate that bromocriptine may have antidepressant effects possibly mediated through the noradrenergic system rather than the dopaminergic system.

Effect of low-dose bromocriptine in treatment of psychosis: The dopamine autoreceptor-stimulation strategy

“…High-dose bromocriptine has been reported to have antidepressant effects in numerous studies (Agnoli et al 1977;Colonna et al 1979;Ose 1980;Nordin et al 1981 ;Waehrens and Gerlach 1981) as well as an antimanic effect in one study (Dorr and Sathananthan 1976), but not in another (Smith et al 1980), so it is possible that what we observed in our patient was only in antidepressant action. However, the impressive and rapid change in psychotic symptoms after bromocriptine on two occasions indicates that more than an antidepressant action was involved.…”

Blood serotonin and tryptophan in Tourette syndrome

“…Because of the response of the tics to haloperidol, a dopamine postsynaptic receptor antagonist, this has been interpreted as implicating predominantly a disturbance of dopamine, especially a hypersensitivity of postsynaptic dopamine receptors in TS. However, there is an intimate linkage between serotonin and dopamine metabolism [Comings, 1990;Faull et al, 1984;Hsiao et al, 1987;Jenner et al, 1983;Nordin et al, 1981;Samanin et al, 1978;Soubrie, 19861, and a primary defect in serotonin can lead to disinhibition dopamine neurons [Comings, 1990;Glowinski et al, 1984;Soubrie, 1986;Pycock et al, 19801. One of the major advantages of finding a biochemical abnormality in TS is the clues it may give toward identifying the basic genetic defect. The fact that the changes in tryptophan are even more impressive than the changes in serotonin places a genetic defect in tryptophan oxygenase (tryptophan pyrrolase, tryptophan 2,3, dioxygenase, indoleamine 2,3 dioxygenase) high on the list of candidate genes.…”

Tofisopam and midazolam: differences in clinical effects and in changes of CSF monoamine metabolites.

“…Nordin et al (1981) found a similar response following bromocriptine administration. Thus tofisopam appears to behave like a dopamine agonist in the central nervous system.…”