Carregal E J
J Neurobiol. 1975 Jan;6(1):103-13. doi: 10.1002/neu.480060113.
Asphyxiation of the spinal cord for periods of 2-4 min leads to block of the monosynaptic pathway. At about the same time this blockage takes place, the afferent action potentials fail to invade the presynaptic terminals. Asphyxiation also interferes with the antidromic invasion of motoneurons, and the failure of the antidromic action potentials to invade the motoneuron dendrites coincides with the time of the disappearance of the orthodromic monosynaptic responses. During reoxygenation, both the presynaptic terminals and the dendrites recover their function, or rather their polarization, in a few seconds and yet synaptic transmission reappears only after several minutes. It is postulated that failure of synaptic transmission during asphyxia is due to depolarization of both the presynaptic terminals and the dendrites of the postsynaptic elements. However, repolarization of these elements during reoxygenation, is not sufficient to reestablish synaptic transmission, but recovery of some unidentified biochemical process is apparently necessary.
脊髓窒息2 - 4分钟会导致单突触通路阻断。大约在发生这种阻断的同时,传入动作电位无法侵入突触前终末。窒息还会干扰运动神经元的逆向传入,而逆向动作电位无法侵入运动神经元树突的时间与顺向单突触反应消失的时间一致。在复氧过程中,突触前终末和树突在几秒钟内恢复其功能,或者更确切地说是恢复其极化状态,但突触传递仅在几分钟后才重新出现。据推测,窒息期间突触传递失败是由于突触前终末和突触后元件树突的去极化。然而,复氧过程中这些元件的复极化不足以重新建立突触传递,显然还需要一些未明确的生化过程恢复。