This study examined the integrity of hypothalamic-pituitary-adrenal (HPA) axis in clomipramine model of depression. Male rat pups were treated twice daily from postnatal day 5 to 21 with clomipramine (15 mg/kg, s.c.). At three months of age, serum corticosterone level was estimated before and after dexamethasone (100 microg/kg, s.c.) administration and after subjected to REM sleep deprivation (RSD) for 4 days consecutively. Data indicated enhanced baseline corticosterone levels and nonsuppression to dexamethasone in clomipramine treated rats. The corticosterone levels however, reversed to the levels of control group in rats subjected to RSD. These findings thus indicated for the first time an HPA hyperactivity in rats treated with clomipramine during neonatal period and are in harmony with cholinergic hypersensitivity reported earlier in this model of depression.

Design: A total number of 100 subjects within 30 -70 years were considered for the study. 50 subjects with Stroke (both clinically as well as Computed tomographically proven cases) and 50 age and sex matched healthy individuals were taken for the study. Material and Methods: Total cholesterol, HDL cholesteroland Triglycerides are estimated by Enzymatic method using Semiautoanalyser. LDL cholesterol is estimated by Friedewald formula. Apo B and Apo A1 are estimated by Immunoturbidimetric method using Semiautoanalyser.Statistical Analysis: Student 't' test was used to compare the data between cases and controls. Diagnostic validity tests were conducted to assess the Diagnostic efficiency of Apo A1, Apo B and Apo B/Apo A1 ratio.Results: Total cholesterol, LDL cholesterol and Triglycerides are significantly increased in Cases compared to Controls. HDL -cholesterol is significantly decreased in Cases compared to Controls. Apo B and Apo B/Apo A1 ratio are significantly increased and Apo A1 is significantly decreased in Cases compared to Controls. Diagnostic validity tests showed that, Apo B , Apo A1 and Apo B /Apo A1 ratio have highest Sensitivity, Specificity and Diagnostic efficiency. Conclusion:Apo B , Apo A1 and Apo B / Apo A1 ratio can be used as predictors of stroke along with traditional lipid profile components.

This study examined whether corticotropin releasing factor (CRF), given prior to test, would produce an improved retrieval of aversive memory in the same way as pre-exposure to inescapable footshocks and the CRF antagonist, alpha-helical CRF 9-41 (a-h CRF), blocks this effect in rats. For this purpose animals conditioned in a T-maze with appetitive (10% sucrose) and aversive (2.0mA footshock) events were given intracerebroventricularly (i.c.v.) 20 min before testing, a single dose of 0.05, 0.1, 0.2 or 0.4 microgram/rat of CRF, or 5 micrograms/rat of a-h CRF, or both at 10 min interval. In the retention test conducted with the same training apparatus 72-hr after conditioning, CRF (0.05, 0.1 and 0.2 microgram) treated rats showed a dose-dependent increase in latencies to enter the previously shocked goalarm, with the absence of such a difference in responding to the nonshocked goalarm. The highest dose of CRF (0.4 microgram), however, increased the latencies to enter both the goalboxes. Alpha-helical CRF, administered 10 min before, antagonized the memory-enhancing effect of CRF. Further, CRF (0.1, 0.2 and 0.4 microgram) significantly decreased the total number of center entries in the open field, consistent with the view that i.c.v. administered CRF produces "anxiogenic-like" effect. Alpha-helical CRF reversed this effect. The effect of CRF on memory retrieval was similar to that seen following inescapable footshock in rats. The results thus suggest the possible involvement of central CRF mechanisms in the differential enhancement of memory of helplessness condition.

The effects of neonatal treatment with clomipramine on the sensitivity of cholinergic receptor and passive avoidance behavior were studied to examine the activity of the central cholinergic system. Rat pups were treated twice daily from postnatal day 5 to 21 with clomipramine (15 mg/kg, s.c.) and at 3 months of age the thermic responses to three different doses of oxotremorine were measured. One day following oxotremorine challenge study, the animals were subjected to passive avoidance training and retention was measured 24-hr later. Clomipramine treated animals showed an enhanced cholinomimetic-induced hypothermia and an increased latency in passive avoidance test. These findings may reflect an altered sensitivity of central cholinergic system in rats given clomipramine as neonates. The results were compared to other animal models of depression.

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The aim of the study was to examine whether ACTH and ACTH-fragment 4-10, given before the test would produce a selectively enhanced retrieval of aversive memories, in the same way as preexposure to inescapable footshocks, in rats. For this purpose animals conditioned in a T-maze with appetitive (10% sucrose) and aversive (2.0 mA footshock) events were administered (s.c.) a single dose of 10, 20 or 40 ug/rat of ACTH or 5, 10 or 20 ug/rat of ACTH-fragment 4-10, 20-min before testing. The retention test conducted in the same training apparatus 72-hrs after conditioning showed a dose-dependent increase in latencies to enter the previously shocked goalarm with the absence of such a difference in responding to the nonshocked goalarm, in ACTH and ACTH 4-10 treated groups. This differential response was not observed in saline treated rats. This effect of peptides on memory retrieval was similar to that seen following inescapable footshock in rats. The results suggest the possible involvement of ACTH in the differential enhancement of memory of helplessness condition.

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