Rossi J, Zolovick A J, Davies R F, Panksepp J
Neurosci Biobehav Rev. 1982 Summer;6(2):195-204. doi: 10.1016/0149-7634(82)90055-0.
When dopamine-beta-hydroxylase is inhibited with FLA-63 (10 mg/kg) free feeding behavior is disrupted in satiated rats. While the average number of meals taken was not different from vehicle injected controls, meal size was decreased 58% in the first 9 hr after treatment with FLA-63. In starved animals, FLA-63, when given alone, produced little effect on feeding behavior, even though norepinephrine depletion was in excess of 40%. When given in combination with RO4-1284 (5 mg/kg), a vesicular reuptake inhibitor, feeding was reduced to 16% of control intake and norepinephrine was specifically depleted 99%. Feeding was reliably reinstated in animals which received FLA-63 plus RO4-1284 with either dl-threo-DOPs, a metabolic precursor to NE, or direct intrahypothalamic injections of NE. These findings suggest that the feeding inhibition observed after treatment with FLA-63 plus RO4-1284 is due to disruption of transmission in brain NE systems. A non-anorectic dosage of L110-140 (3.73 mg/kg), a specific FLA-63. Taken collectively, these findings suggest that the primary role of NE in feeding is maintenance of the consummatory response and that these effects are expressed in relation to activity in other neurochemical systems.
当用FLA - 63(10毫克/千克)抑制多巴胺-β-羟化酶时,饱足大鼠的自由进食行为会受到干扰。虽然进食餐数的平均值与注射赋形剂的对照组没有差异,但在用FLA - 63治疗后的最初9小时内,每餐食量减少了58%。在饥饿的动物中,单独给予FLA - 63对进食行为几乎没有影响,尽管去甲肾上腺素耗竭超过40%。当与囊泡再摄取抑制剂RO4 - 1284(5毫克/千克)联合使用时,进食量减少至对照摄入量的16%,去甲肾上腺素特异性耗竭99%。给接受FLA - 63加RO4 - 1284的动物注射NE的代谢前体dl-苏式-DOPs或直接下丘脑内注射NE后,进食行为可靠地恢复。这些发现表明,用FLA - 63加RO4 - 1284治疗后观察到的进食抑制是由于脑内去甲肾上腺素系统传递的破坏。一种非厌食剂量的L110 - 140(3.73毫克/千克),一种特异性的FLA - 63。总的来说,这些发现表明去甲肾上腺素在进食中的主要作用是维持进食反应,并且这些作用与其他神经化学系统的活性有关。