Ramos J M, Castillo M E, Puerto A
Laboratorio de Psicobiología, Area de Psicobiología, Universidad de Granada, Spain.
Behav Neural Biol. 1989 Nov;52(3):422-9. doi: 10.1016/s0163-1047(89)90562-1.
The neuropharmacological mechanisms involved in the prandial drinking pattern seen in rats with superior salivatory nucleus lesions + parotidectomy were investigated with behavioral methods. Results showed that the administration of low doses (0.1 mg/kg body wt) of atropine in lesioned rats potentiated previously established prandial drinking. Higher doses of atropine (1.0 mg/kg), however, were required to induce a similar degree of prandiality in control rats (parotidectomy alone). These findings suggest that the salivatory nucleus lesions affected a cholinergic brainstem-salivary gland system involved in the neural control of food-associated drinking.
采用行为学方法,对患有上唾液核损伤+腮腺切除的大鼠出现的餐时饮水模式所涉及的神经药理学机制进行了研究。结果显示,给损伤大鼠注射低剂量(0.1毫克/千克体重)的阿托品可增强先前已确立的餐时饮水行为。然而,对照组大鼠(仅行腮腺切除术)则需要更高剂量的阿托品(1.0毫克/千克)才能诱导出相似程度的餐时饮水行为。这些发现表明,唾液核损伤影响了一个参与食物相关饮水神经控制的胆碱能脑干-唾液腺系统。