Willis G L, Smith G C
Appetite. 1984 Sep;5(3):239-67, 277-9. doi: 10.1016/s0195-6663(84)80019-7.
Lesions of the lateral hypothalamus produce ascending catecholamine neuron degeneration which results in terminal depletion and proximal accumulation above the lesions. The occurrence of deficits in ingestive behaviour has been attributed traditionally to the loss of functional dopamine neurotransmitter in the terminal fields. However, release of functional amines may occur in the lateral hypothalamus at areas of accumulation, to produce at least some of the behavioural symptoms characterizing the lateral hypothalamic syndrome. Recovery from behavioural deficits as a result of various pharmacological treatments, after dopamine-depleting lesions, may be mediated by changes in amine release or modified sensitivity of receptors affected by released amines. We conclude that amine accumulation should be considered when interpreting experiments implicating central catecholamine systems in the control of consumatory behaviour and the regulation of body weight.
下丘脑外侧的损伤会导致去甲肾上腺素能神经元上行性变性，从而造成损伤上方的终末耗竭和近端蓄积。传统上，摄食行为缺陷的出现被归因于终末区域功能性多巴胺神经递质的丧失。然而，在蓄积区域的下丘脑外侧可能会释放功能性胺类，从而产生至少部分表征下丘脑外侧综合征的行为症状。多巴胺耗竭性损伤后，各种药物治疗导致行为缺陷的恢复，可能是由胺类释放的变化或受释放胺类影响的受体敏感性改变介导的。我们得出结论，在解释涉及中枢去甲肾上腺素系统对摄食行为控制和体重调节的实验时，应考虑胺类的蓄积。
