It is known that noradrenergic projections from brainstem has a stimulatory effect on oxytocin secretion, and intravenous administration of cholecystokinin (CCK) causes an increase of noradrenaline (NA) contcentration in supraoptic and paraventricular nucleus (PVN), and plasma oxytocin levels. It is suggested that melatonin inhibits basal and induced oxytocin secretion but the precise mechanism of this effect is yet to be discovered. The aim of this study was to investigate the effect of melatonin on the CCK-induced NA release in PVN. Virgin female rats (250-300 g) were anaesthetized with choral hydrate (400mg/kg) and placed on a stereotaxic frame. A microdialysis probe was set into PVN with the guaidance of the rat stereotaxic atlas, and artificial cerebrospinal fluide was run through a micropump throughout the experimental period. One hour later, microdialysis samples were collected with 20 minutes intervals for 80 min. After collection of the first sample (control), 50μg/kg CCK was intravenously administered to the CCK group (n=8). In addition to CCK, 1μg melatonin was intracerebroventricularly infused to the melatonin group (MLT, n=8). The control (n=10) and CCK groups were received intracerebroventricularly vehicle infusion. NA content of samples were analysed by a high performance liquid chromatography-electrochemical detector system. Data were evaluated and expressed as percentages of the baseline levels. NA levels were normalized by nominating the control level as 100%, and its levels in 20-mins samples were expressed as percentage of these values. Data were statistically analysed by One-way Analysis of Variance (ANOVA) followed by a pairwise comparison between control and each CCK and MLT groups using a Tukey’s t-test for multiple comparisons. P<0.05 was considered statistically significant. In the second interval (20-40 min), NA content of PVN was significantly elevated in the CCK group (p<0.001) compared to control values. But melatonin did not alter this CCK-induced rise in NA content compared to CCK administered group for this interval. Melatonin group also had significantly higher NA levels than both the control group (p<0.005) and its initial control values (p0.05). The results of the present study indicate that CCK has stimulatory effect on NA content in PVN which is not subject to modulation by melatonin. Our results does not rule out the possibility that, the reported inhibitory effect of melatonin on oxytocin secretion may involve mechansim(s) other than NA mediation.