1. Changes in membrane and action potentials of cat spinal motoneurones during acute asphyxiation and re-oxygenation were recorded with an intracellular technique.2. The asphyxial potential of the grey matter, which develops in the first 2-2.5 min of asphyxiation, can be expected to interfere with the membrane potential record. After correcting for this effect a gradual depolarization of the soma at a rate of 3-4 mV/min was found, commencing within a fraction of a minute after the start of asphyxiation.3. The orthodromic responses of the motoneurones were the most vulnerable to O(2) lack. They failed earlier than the responses to antidromic and to direct excitation of the cell through the micro-electrode. After failure of the orthodromic spike an excitatory post-synaptic potential remained for a short time. Failure of antidromic excitation began by the dropping out of the some dendritic potential, followed by the arrest of the initial segment response.4. It was concluded that the early arrest of orthodromic excitation is caused by presynaptic failure.5. All changes in membrane and action potentials were completely reversible by re-oxygenation after periods of asphyxia lasting from 4 to 6 min. The orthodromic response recovered markedly slower than the antidromic and direct ones.

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PubMed1966

Asphyxial potentials of spinal grey matter, and of ventral and dorsal roots.

1. Asphyxial potentials of short latency (from a few to about 10 sec) were recorded with mono- and bipolar electrodes from the cat's spinal cord. Monopolarly, a zone of maximum negativity was found somewhat dorsal of the central canal in the dorsal horn. With bipolar leads potentials of opposite polarity were observed in the dorsal and ventral horns. In the dorsal horn the more ventral electrode tip became negative with respect to the more dorsal one, in the ventral horn the more ventral tip became more positive. In the centre of the cord where the monopolar potential showed a maximum the bipolar potentials were small in either direction, or reversed during asphyxiation.2. These observations can be explained by the development of two independent dipoles of opposite polarity, located in the dorsal and ventral horn respectively, oriented with their negative poles towards the centre of the cord.3. In the ventral as well as in the dorsal root a negativity of a proximal electrode with respect to a more distal one developed during asphyxiation after the same latency as the asphyxial cord potentials. The asphyxial root potentials continued to grow during periods of asphyxiation as long as 30 min, and recovered promptly upon re-oxygenation.4. Ventral and dorsal root potentials were abolished by asphyxiation of the cord for a period of 60 min, 2 weeks previously. This procedure destroys practically all the neurones, but not the dorsal root fibres. The dorsal root potential, but not the ventral one, was abolished by extradural sectioning of the roots, 2 weeks previously.5. The asphyxial ventral and dorsal root potentials were interpreted as the result of depolarization of the intraspinal part of the motoneurones and primary afferent endings respectively, conducted electrotonically along the roots. The short latency of these potentials suggests that an early depolarization of motoneurone, and of the primary afferent end knobs occurs. The latter, which may have some relation to presynaptic inhibition, explains the early failure of synaptic conduction during acute asphyxiation.

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