Intracerebroventricular administration of adiponectin attenuates streptozotocin-induced memory impairment in rats.

Alzheimer's disease (AD) has been reported to be linked with diabetes mellitus and insulin resistance. Adiponectin (ADN), an adipocytokine secreted from adipose tissue, is involved in the regulation of insulin sensitivity, energy homeostasis, and mitochondrial dysfunction. In this study, we examined the effect of ADN on passive avoidance memory in animal model of sporadic AD (sAD). On days 1 and 3 after cannulation, rats received intracerebroventricular (icv) injection of streptozotocin (STZ) (3 mg/kg). Thirty minutes before the learning process, animals received saline or ADN in different doses (6, 60, and 600 µg). The step-through latency (STL) and total time spent in the dark compartment (TDC) were recorded and analyzed. In STZ-treated rats, STL was significantly decreased, whereas TDC showed a dramatic increase. In ADN-treated rats, STL was significantly increased (P < 0.01) in all treatment doses. The number of entries was decreased in all applied doses; however, TDC was reduced only by the application of 6 ng of ADN (P < 0.05). It can be concluded that ADN is useful to improve the STZ-induced memory impairment. This study showed, for the first time, that icv administration of ADN could improve the memory acquisition in animal model of sAD.

Examining the effect of the CaMKII inhibitor administration in the locus coeruleus on the naloxone-precipitated morphine withdrawal signs in rats.

Drug addiction is an occurrence with physiological, psychological, and social outcomes. Repeated drug exposure causes neuronal adaptations and dependency. It has been shown that CaMKIIα enzyme contributes to morphine dependency. The locus coeruleus nucleus has been implied in the morphine withdrawal syndrome. This research focuses on the behavioral and molecular adaptations that occur in the locus coeruleus neurons in response to the chronic morphine exposure. Adult male Wistar rats were injected by morphine sulfate (10 mg/kg/s.c.) at an interval of 12 h for a period of nine subsequent days. On the tenth day, naloxone (1 mg/kg/i.p.) was injected 2 h after the morphine administration. Somatic withdrawal signs were investigated for 30 min. We concluded that the inhibition of CaMKIIα by administration of KN-93, the specific inhibitor of this enzyme, significantly attenuated some of the withdrawal signs. In molecular method, the expression of CaMKIIα protein has been enhanced in locus coeruleus of the morphine dependent rats. These findings indicate that CaMKIIα may be involved in the modulation of the naloxone-induced withdrawal syndrome, and treatment with KN-93 may have some effects on this system.

Effects of Nepeta menthoides aqueous extract on retention and retrieval of memory in mice.

There are several evidences that plants and vegetables with antioxidant activity can reduce oxidative damages in brain and improve cognitive functions. The aim of this study was evaluation of Nepeta menthoides aqueous extract on memory retention and retrieval of mice by using passive avoidance apparatus. For this purpose, mice were classified, coded, weighted and grouped (n = 8) as follow as: control group (Only electric shock), blank group (electric shock plus normal saline) and test groups (electric shock plus Nepeta menthoides extract by doses: 100, 200, 400 and 800 mg kg(-1), i.p.). Delay time of leaving the platform was measured for retention and retrieval test of memory in all mentioned groups. In retention test, plant extract was administered immediately after receiving electric shock while it was administered 24 h after receiving electric shock in retrieval. The results revealed that Nepeta menthoides aqueous extract significantly (p<0.05) increased memory retention and retrieval. The best response for memory retention and retrieval was achieved with 800 mg kg(-1) of Nepeta extract. In conclusion, enhancement of memory retention and retrieval by Nepeta menthoides could be cause of antioxidant activity of its components such as rosmarinic acid, caffeic acid and phenolic acids.