Achapu M, Pompei P, Polidori C, de Caro G, Massi M
Instituto di Farmacologia, Facolta' di Farmacia, Universita' di Camerino, Italy.
Brain Res Bull. 1992 Feb;28(2):299-303. doi: 10.1016/0361-9230(92)90191-y.
The present study investigated the effect on water and food intake in the rat of the intracerebroventricular (ICV) injection of neuropeptide K (NPK), the N-terminally extended form of neurokinin A. NPK inhibited water deprivation-induced water intake even at 31.2 ng/rat. At higher doses, it inhibited also water intake induced by ICV angiotensin II or by subcutaneous hypertonic NaCl, and food-associated drinking, the threshold dose being 125 ng/rat. In response to 125 ng/rat, food intake following 16 h food deprivation was not reduced. NPK inhibited food intake only at 500 ng/rat, a dose that evoked excessive grooming in treated animals. Thus NPK is a potent inhibitor of water deprivation-induced drinking and at higher doses it exerts a general antidipsogenic effect towards several dipsogenic determinants, without affecting food intake. On the other hand, it inhibits food intake only at high doses, 500 ng/rat or more, but this inhibition might be just related to the intense grooming evoked. The effects of NPK on ingestive behavior are markedly different from those of neurokinin A, which selectively inhibits osmotic drinking and food-associated drinking. These differences suggest that NPK itself may exert its effects on the central nervous system, not necessarily through the conversion to neurokinin A.
本研究调查了脑室内（ICV）注射神经肽K（NPK，神经激肽A的N端延伸形式）对大鼠水和食物摄入的影响。即使剂量为31.2 ng/大鼠，NPK也能抑制缺水诱导的饮水。在更高剂量下，它还能抑制ICV注射血管紧张素II或皮下注射高渗氯化钠诱导的饮水以及与食物相关的饮水，阈值剂量为125 ng/大鼠。给予125 ng/大鼠时，16小时食物剥夺后的食物摄入量并未减少。NPK仅在500 ng/大鼠时抑制食物摄入，该剂量会使受试动物出现过度梳理行为。因此，NPK是缺水诱导饮水的有效抑制剂，在更高剂量时，它对几种致渴因素具有普遍的抗利尿作用，而不影响食物摄入。另一方面，它仅在高剂量（500 ng/大鼠或更高）时抑制食物摄入，但这种抑制可能仅与诱发的强烈梳理行为有关。NPK对摄食行为的影响与神经激肽A明显不同，神经激肽A选择性抑制渗透性饮水和与食物相关的饮水。这些差异表明，NPK本身可能对中枢神经系统发挥作用，不一定通过转化为神经激肽A来实现。
