| Research Abstract |
Reduction of fertility or reproductive performance under malnutritional conditionsis is one of the major problems in animal production in the world as well as in Japan. Especially, the blockade of ovulation in milking cows with high milk yield or the delay of puberty in domestic animals of developing countries is considered to be caused by the malnutrition. Based on our previous results using fasted rat model, we have proposed that specific energy sensors and pathways in the brain mediate the malnutritional reduction of reproductive axis. We have also proposed that the brain glucose-sensing mechanism consists of ependymocytes and serotonergic neurons which have glucose transporter 2 and glucokinase, key proteins for the glucose-sensing unit in pancreatic B cells. In the present study, we tested if those cells can sense the glucose level using the intracellular calcium concentration as a parameter.
Ependymocytes and serotonergic neurons were isolated from the wall of the central canal and raphe obsculus, respectively. They were incubated in the medium containing either low or high level of glucose and intracellular calcium concentrations were measured using fura-2 and image analysis. Most of the glucokinase-immunoreactive ependymocytes and serotonergic neurons responded to either low or high level of glucose. The intracellular calcium concentration increased after increasing or decreasing the glucose level in the medium. Alloxan, a glucokinase inhibitor, blocked the increase in intracellular calcium concentrations in those cells, suggesting that the cells play a role in sensing the glucose level in the cerebrospinal fluid which may reflect the blood glucose level.
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