Strejcková A, Jakoubek B, Kraus M, Mares P
Physiol Bohemoslov. 1985;34(6):567-73.
The effect of microiontophoretically administered beta-endorphin on the activity of 62 cortical and hippocampal neurones was studied in acute experiments on 14 rats. The effectiveness of beta-endorphin was first of all verified in the isolated guinea pig ileum, the mouse was deferens and in a study if its analgetic and catatonic effect in rats. Beta-endorphin only mildly depressed the spontaneous activity of cortical neurones, but markedly inhibited the activity stimulated by the microiontophoretic administration of glutamate. In the hippocampus, beta-endorphin stimulated the activity of all the studied neurones when only low ejection currents were used and activation persisted for 1-4 min after terminating administration. With higher ejection currents, the discharge frequency rose enormously and not even GABA blocked this effect. The excitatory effect of beta-endorphin on the hippocampal neurones may possibly be the basis of the epileptogenic action of this substance.
在对14只大鼠进行的急性实验中,研究了微量离子导入法给予β-内啡肽对62个皮质和海马神经元活动的影响。首先在离体豚鼠回肠、小鼠输精管中验证了β-内啡肽的有效性,并研究了其对大鼠的镇痛和木僵作用。β-内啡肽仅轻微抑制皮质神经元的自发活动,但显著抑制微量离子导入谷氨酸所刺激的活动。在海马体中,当仅使用低喷射电流时,β-内啡肽刺激所有研究神经元的活动,给药终止后激活持续1-4分钟。当喷射电流较高时,放电频率大幅上升,甚至γ-氨基丁酸也无法阻断这种效应。β-内啡肽对海马神经元的兴奋作用可能是该物质致癫痫作用的基础。