Noe Y
Department of Pedodontics, Hokkaido University, School of Dentistry, Sapporo.
Hokkaido Igaku Zasshi. 1988 Nov;63(6):897-912.
It is well established that plasma corticosterone levels in rats increase just prior to the meal (prefeeding peak), when animals are subjected to restricted feeding, in which daily food and water supply is restricted to a few hours at a fixed time of day. A self-sustained oscillatory mechanism is suggested underlying the prefeeding hormone peak, but its mechanism is different in origin from that involved in the light-entrainable circadian rhythm; the former dose not depend on the suprachiasmatic nucleus (SCN) but the latter dose. The purpose of the present study is to elucidate roles of the central noradrenergic system in the prefeeding corticosterone peak under restricted feeding. Male rats were bilaterally injected with 6-hydroxydopamine (6-OHDA) into the ventral noradrenergic ascending bundle (VNAB) and hypothalamic nuclei, the SCN, the paraventricular nucleus (PVN), the ventromedial hypothalamic nucleus, the lateral hypothalamic nucleus and the median eminence to examine effects of the catecholamine depletion on the circadian corticosterone rhythm under ad libitum feeding condition and the prefeeding corticosterone peak under restricted feeding. Blood samples were obtained from individual rats successively and plasma corticosterone was determined by competitive protein binding assay. Noradrenaline contents were measured in the individual hypothalamic nuclei by high performance liquid chromatograph to attest the effects of 6-OHDA injection. The prefeeding corticosterone peak was suppressed by 6-OHDA injected into the PVN and VNAB, but was not by 6-OHDA into the other brain regions. On the other hand, the circadian rhythm of plasma corticosterone was not affected by 6-OHDA injection into the PVN. These findings suggested that the noradrenergic projection to the PVN is responsible for the manifestation of the prefeeding corticosterone peak, but is not for the circadian rhythm of plasma corticosterone.
众所周知，当大鼠在定时限食（即每天的食物和水供应被限制在一天中的固定几个小时）条件下时，其血浆皮质酮水平会在进食前升高（进食前峰值）。有观点认为，进食前激素峰值背后存在一种自我维持的振荡机制，但其机制的起源与光可调节的昼夜节律不同；前者不依赖于视交叉上核（SCN），而后者依赖。本研究的目的是阐明在限食条件下，中枢去甲肾上腺素能系统在进食前皮质酮峰值中的作用。对雄性大鼠双侧腹侧去甲肾上腺素能上行束（VNAB）以及下丘脑核团（SCN、室旁核（PVN）、下丘脑腹内侧核、下丘脑外侧核和正中隆起）注射6-羟基多巴胺（6-OHDA），以研究儿茶酚胺耗竭对自由进食条件下昼夜皮质酮节律以及限食条件下进食前皮质酮峰值的影响。连续采集每只大鼠的血样，通过竞争性蛋白结合测定法测定血浆皮质酮水平。采用高效液相色谱法测定各个下丘脑核团中的去甲肾上腺素含量，以验证6-OHDA注射的效果。注射到PVN和VNAB的6-OHDA可抑制进食前皮质酮峰值，但注射到其他脑区的6-OHDA则无此作用。另一方面，注射到PVN的6-OHDA对血浆皮质酮的昼夜节律没有影响。这些结果表明，投射到PVN的去甲肾上腺素能神经通路负责进食前皮质酮峰值的表现，但不负责血浆皮质酮的昼夜节律。
