Bruno J P, Zigmond M J, Stricker E M
Behav Neurosci. 1986 Feb;100(1):125-8. doi: 10.1037//0735-7044.100.1.125.
Rats given near-total dopamine-depleting brain lesions as neonates exhibit none of the severe sensorimotor or ingestive dysfunctions that result when adult rats are given comparable lesions. These experiments showed that the apparent sparing of function is incomplete; when tested as adults, the brain-damaged animals did not eat in response to acute glucoprivation, nor did they drink water and saline in response to hypovolemia. Indeed, after receiving these homeostatic challenges, the animals became much less able to simply move about. In contrast to these marked effects, the dopamine-depleted rats ate normally after glucoprivation when they were handled hourly instead of being left alone. Similarly, administration of caffeine permitted them to drink while hypovolemic. These and other observations suggest that some central neurons other than those containing dopamine are responsible for maintaining behavioral activation in rats after neonatal destruction of dopaminergic fiber systems in the brain and that the homeostatic challenges compromise their function and thereby disrupt behavior.
新生大鼠若接受几乎能使多巴胺耗竭的脑部损伤，不会出现成年大鼠接受类似损伤时所产生的严重感觉运动或摄食功能障碍。这些实验表明，功能上明显的保留并不完全；当作为成年动物进行测试时，脑部受损的动物不会因急性糖剥夺而进食，也不会因血容量减少而饮水和摄入盐水。实际上，在受到这些内稳态挑战后，这些动物的活动能力大幅下降。与这些显著影响形成对比的是，多巴胺耗竭的大鼠若每小时接受一次处理而非任其独处，在糖剥夺后能正常进食。同样，给予咖啡因能使它们在血容量减少时饮水。这些以及其他观察结果表明，除含多巴胺的神经元外，一些中枢神经元负责在新生大鼠脑部多巴胺能纤维系统被破坏后维持其行为激活，并且内稳态挑战损害了这些神经元的功能，从而扰乱行为。
