Ray A, Sen P, Alkondon M
Department of Pharmacology, University College of Medical Sciences, Delhi, India.
Pharmacol Biochem Behav. 1989 Apr;32(4):867-71. doi: 10.1016/0091-3057(89)90050-6.
Acetylcholinesterase (AChE) activity was estimated in brain and heart homogenates and plasma of 'aggressive' and 'nonaggressive' rats. Brain homogenates of 'nonaggressive' rats hydrolyzed significantly more substrate when compared to the 'aggressive' rats. Such differences were not seen in the heart homogenates or plasma of these two groups of rats. Acute DFP (0.1, 0.3 and 1.0 mg/kg) attenuated shock-induced aggression (SIA) 2 hr after treatment but facilitated SIA 24 hr and 48 hr after drug administration. Long-term DFP (0.3 mg/kg x 10 days), on the other hand, induced a significant enhancement in the SIA score, whereas atropine (1.0 and 5.0 mg/kg) produced a dose-related attenuation of the same. Pretreatment of rats with atropine (5 mg/kg) antagonized the long-term DFP-induced facilitation of SIA. These results are discussed in the light of an inhibitory central cholinergic mechanism in the regulation of SIA.
在“攻击性”和“非攻击性”大鼠的脑、心脏匀浆及血浆中对乙酰胆碱酯酶（AChE）活性进行了评估。与“攻击性”大鼠相比，“非攻击性”大鼠的脑匀浆水解的底物显著更多。在这两组大鼠的心脏匀浆或血浆中未观察到此类差异。急性给予二异丙基氟磷酸酯（DFP，0.1、0.3和1.0mg/kg）在给药后2小时减弱了休克诱导的攻击行为（SIA），但在给药后24小时和48小时促进了SIA。另一方面，长期给予DFP（0.3mg/kg×10天）导致SIA评分显著提高，而阿托品（1.0和5.0mg/kg）则产生了与剂量相关的SIA减弱作用。用阿托品（5mg/kg）预处理大鼠可拮抗长期DFP诱导的SIA促进作用。根据SIA调节中的抑制性中枢胆碱能机制对这些结果进行了讨论。
