抄録
During food intake leptin released from the adipose tissues enters in the brain. The leptin concentration in the brain is 10−12 M. Leptin first reached to the hypothalamus and suppressed food intake and then to the hippocampus. We examined the effect of leptin on (1) behavioral performance in learning and memory tasks, (2) LTP at Schaffer collareral-CA1 synapses,(3) the intracellular Ca2+ concentration in hippocampal CA1 neurons, and (4) the activity of calmodulin kinase II (CaMKII)in the hippocampal CA1 tissue that exhibits LTP. Intravenous injections of leptin corresponding to 10−12 M, but not 10−10 M facilitated passive avoidance and Morris water-maze tasks. Bath application of 10−12 M leptin in slice experiments enhanced LTP in CA1 neurons, whereas 10−10 M suppressed it. The incease in the intracellular concentration of Ca2+ in CA 1 neurons induced by 10−10 M leptin was two times more greater than that induced by 10−12 M. This higher Ca2+ concentration suppressed the CAMK II activity. In addition, the facilitation and suppression of LTP by leptin was closely associated with an increse and decrease in activity of CAMK II. These results show that leptin not only affects hypothalamic functions, but also modulates higher nervous functions, such as the behavioral performance related to learning and memory and hippocampal synaptic plasticity. [J Physiol Sci. 2007;57 Suppl:S70]
