Diurnal and seasonal variation of cholecystokinin peptides in humans.

Cholecystokinin (CCK) was determined in plasma obtained from 10 female (aged 23.4+/-SD 2.3 years) and nine male (aged 22.0+/-SD 1.4 years) healthy volunteers. Blood samples were drawn three times (8.00a.m., 12 noon and 8.00a.m.) on each of two sessions, one in the winter (November-December) and one in the summer (April-July). The participants had fasted (and were nicotine-free) since midnight preceding the sampling. A standardized breakfast was served after the first sampling. CCK was determined by radioimmunoassay. The area under the curve 0-24h (AUC)(CCK Winter) was lower than AUC(CCK Summer) (F(1:17)=4.73; P=0.0440) in the whole group of volunteers. On comparing the CCK concentrations within each session, there was an overall difference in winter (F(2:36)=14.81; P<0.0001) as well in summer (F(2:36)=18.39; P<0.0001). Post hoc comparisons yielded a difference between the 8.00a.m. and 12 noon concentrations on the first day in winter (t=-3.96; P=0.0009) as well as in summer (t=-4.64; P=0.0002). The difference between the summer and winter AUCs(CCK) correlated with the difference between AUCs for temperatures in summer and winter (r=0.58; P=0.0089). The correlation was accounted for by the females (r=0.73; P=0.0171). The results are in accord with a diurnal and a seasonal variation of CCK in human plasma.

CSF monoamine patterns in pathological gamblers and healthy controls.

Previous reports on compounds in the cerebrospinal fluid (CSF) of pathological gamblers have focused on disturbed NA, DA and 5-HT function in the central nervous system. We have analysed precursors, transmitters and transmitter metabolites in 3 x 6 ml of CSF obtained from one female and 11 male pathological gamblers and 11 healthy male controls lumbar punctured at the L4-5 level after 8 h of fasting without preceding strict bedrest. Pathological gamblers displayed lower CSF levels of tryptophan and 5-HT while the opposite was the case for 5-HIAA, tyrosine, DA, HVA, DOPAC and HMPG. In contrast to previous studies, the NA level did not differ between pathological gamblers and healthy controls. A disrupted CSF gradient was noted for tryptophan, 5-HT, DA, HVA, DOPAC, NA and HMPG, but only in pathological gamblers. A disrupted gradient was found for 5-HIAA in both pathological gamblers and healthy controls. The results are in line with the presence of altered indoleamine and catecholamine function in pathological gamblers as well as an altered CSF transport from the brain to the lumbar compartment in such gamblers.