The effects of phosphatidylserine (BC-PS) on cognitive, affective and behavioural symptoms were studied in a group of 10 elderly women with depressive disorders. Patients were treated with placebo for 15 days, followed by BC-PS (300 mg/day) for 30 days. The Hamilton Rating Scale for Depression, Gottfries-Bråne-Steen Rating Scale, Nurse's Observation Scale for Inpatient Evaluation and Buschke Selective Reminding Test were administered before and after placebo and after BC-PS therapy, to monitor changes in depression, memory and general behaviour. At the same time, basal plasma levels of noradrenaline, MHPG, DOPAC, HVA and 5-HIAA, and GH/beta-endorphin/beta-lipotropin responses to clonidine stimulation were measured. BC-PS induced consistent improvement of depressive symptoms, memory and behaviour. No changes in amine metabolite levels or in hormonal responses to alpha 2-adrenoceptor stimulation were observed.

Ten chronic undifferentiated schizophrenics, 6 men and 4 women, aged 28–63, with 6- to 31-year histories of the disease were given DDAVP to observe the effects of this neuropeptide on the prevalent negative symptoms of their illness. Patients were maintained on neuroleptic therapy and first given a 20-day course of placebo followed by 20 days of DDAVP i.m., 4 µg. Andreasen Scale for assessment of negative symptoms, the Brief Psychiatric Rating Scale, the NOSIE Rating Scale and the Luria-Nebraska Rating Scale were administered to monitor negative symptomatology, behavior and memory before the study began, after placebo and after DDAVP administration. Patients were also given a growth hormone-clonidine test and in addition plasma basal concentrations of 3-methoxy-4-hydroxyphenylglycol (MHPG), homovanillic acid, 3,4-dihydroxyphenylacetic acid (DOPAC) and 5-hydroxyindoleacetic acid (5-HIAA) were measured at the same intervals. DDAVP therapy induced a significant improvement of negative symptomatology and a trend toward improvement of short- to medium-term memory. No changes in homovanillic acid, MHPG, 5-HIAA and DOPAC, nor of growth hormone response to clonidine stimulation were observed.

Plasma and ventricular cerebro-spinal fluid (CSF) Beta-endorphin concentrations were evaluated after chromatographic separation in patients carrying a ventricular shunt before and after the administration of diclofenac or placebo. In the same subjects the ventricular CSF concentrations of the serotonin and the catecholamine metabolites 5-hydroxyindole-acetic acid (5-HIAA), homovanillic acid (HVA) and MOPEG were also evaluated. Plasma, but not ventricular, Beta-endorphin concentrations increased significantly after diclofenac, while placebo was ineffective. No significant changes in ventricular 5-HIAA, HVA or MOPEG levels were observed. These data suggest a role for Beta-endorphin in the analgesic effect of diclofenac.

Mounting behavior of rats induced by several drugs, such as e.g. p-CPA, 5,7-dihydroxytryptamine, L-DOPA or lisuride, appears to result from a combined decrease of 5-hydroxytryptamine (5-HT) and increase of dopamine (DA) neurotransmission. In this paper, lisuride-induced mounting is proposed as a behavioral model for detecting pharmacologically active drugs that interact with monoaminergic mechanisms, e.g. 5-HT reuptake blockers and type A monoamine oxidase inhibitors. With regard to sleep, 5-HT appears to sustain a relevant part in controlling the sleep-wakefulness cycle. However, other transmitters or neuromodulators (catecholamines, oligopeptides etc.) may also be involved in sleep mechanisms.

In 11 preoperative women, plasma adrenaline (A) concentrations were lower after oral administration of an antianxiety dose (19.25 micrograms/kg) of chlordemethyldiazepam (Cl-DMDZ) than the predrug values, or those in 12 patients given placebo. No significant differences in supine plasma noradrenaline (NA), blood pressure (BP) and heart rate values were observed. Digital plethysmography showed finger vasoconstriction after placebo and vasodilatation after Cl-DMDZ. A mental arithmetic test caused equivalent rises in plasma A in both groups. Standing caused plasma NA to rise to similar levels in both groups of patients, but the BP decrease was less and there was a markedly lower incidence of orthostatic hypotension in the Cl-DMDZ treated group. It is concluded that the effect of Cl-DMDZ on the release of catecholamines from the peripheral sympathetic system consists essentially of decreasing basal adrenomedullary activity. CL-DMDZ appears to prevent the orthostatic hypotension which occurs when neurosympathetic reflex activation is normal.