Baklavadzhian O G, Darbinian A G, Hecht K, Poppaĭ M, Taturian I Kh
Zh Vyssh Nerv Deiat Im I P Pavlova. 1980 Nov-Dec;30(6):1187-95.
The part of noradrenergic mechanisms in self-stimulation (SS) operant behaviour was studied in rats. In all experiments systolic blood pressure (BP) in the tail artery was measured by means of photocells. It was found, that small doses of noradrenaline facilitate the SS, while high doses depress or stop it. The depressive effect is accompanied by a marked increase of BP. Effective blockade of beta-adrenoceptive structures by inderal suppresses SS, and the inhibitory effect is accompanied by a small decrease of BP. Suppressing effect of alpha-adrenoblocking agent, phentolamine, is even more pronounced, but is accompanied by a marked decrease of BP. Beta-agonist isadrin causes a marked facilitation of SS without changes of BP. It is suggested that positive reward in the lateral hypothalamus is due to a direct stimulation of beta-adrenoceptive noradrenergic neuronal elements. Chronic neurogenic hypertension is developed by an overloading of the higher nervous activity. In chronic hypertensive rats there is a pronounced suppression of SS. A transient fail of BP caused by injection of catapresan (hemiton) results in a temporary recovery of normal SS behaviour. It may be concluded that reduction of lever-pressing rate during acute and chronic neurogenic hypertensions is related to baroreceptor mechanisms. The role of the autonomic nervous system in SS behaviour is discussed.
研究了去甲肾上腺素能机制在大鼠自我刺激(SS)操作性行为中的作用。在所有实验中,通过光电管测量尾动脉的收缩压(BP)。研究发现,小剂量去甲肾上腺素促进自我刺激,而大剂量则抑制或终止自我刺激。抑制作用伴随着血压显著升高。心得安对β-肾上腺素能结构的有效阻断抑制了自我刺激,且抑制作用伴随着血压小幅下降。α-肾上腺素能阻断剂酚妥拉明的抑制作用更为明显,但伴随着血压显著下降。β-激动剂异丙肾上腺素显著促进自我刺激,而血压无变化。提示下丘脑外侧的正性奖赏是由于直接刺激了β-肾上腺素能去甲肾上腺素能神经元成分。慢性神经源性高血压是由高级神经活动过度负荷引起的。在慢性高血压大鼠中,自我刺激受到明显抑制。注射可乐定(海米托)引起的血压短暂下降导致正常自我刺激行为暂时恢复。可以得出结论,急性和慢性神经源性高血压期间按压杠杆速率的降低与压力感受器机制有关。讨论了自主神经系统在自我刺激行为中的作用。