Raabe W, Gumnit R J
J Neurophysiol. 1975 Mar;38(2):347-55. doi: 10.1152/jn.1975.38.2.347.
The effect of intravenously administered ammonium salts on postsynaptic inhibition of pyramidal tract cells was investigated in cat motor cortex. Extracellular recordings revealed that pyramidally or thalamically mediated inhibition of antidromic action potentials is abolished by ammonia. Intracellular recordings demonstrated that hyperpolarizing IPSPs vanished and EPSPs appeared while the inhibitory stimuli still triggered a decrease of neuronal resistance and the resting membrane potential was unchanged. It is concluded that ammonia disinhibited action-potential generation and EPSPs by shifting E(IPSP) to the level of the resting membrane potential. With disinhibition and facilitation replacing inhibitation of action potentials, ammonia clearly disturbs those cortical functions involving postsynaptic inhibition.
在猫的运动皮层中,研究了静脉注射铵盐对锥体束细胞突触后抑制的影响。细胞外记录显示,氨可消除由锥体或丘脑介导的对逆向动作电位的抑制。细胞内记录表明,当抑制性刺激仍能引发神经元电阻降低且静息膜电位未改变时,超极化抑制性突触后电位消失,兴奋性突触后电位出现。得出的结论是,氨通过将抑制性突触后电位(E(IPSP))移至静息膜电位水平,解除了动作电位产生和兴奋性突触后电位的抑制。由于去抑制和易化取代了对动作电位的抑制,氨明显干扰了那些涉及突触后抑制的皮层功能。