HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text (PDF) Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Collewijn, H. Articles by Van Harreveld, A. Search for Related Content PubMed PubMed Citation Articles by Collewijn, H. Articles by Van Harreveld, A.

1. Intracellular recordings were obtained from lumbar spinal motoneurones in cats with post-asphyxial rigidity of the hind limbs.

2. Membrane potentials, latencies and (or) appearance of excitatory post-synaptic potentials, initial segment responses and soma-dendritic spikes were not materially different from those observed in cells of normal cords.

3. Dorsal root stimulation activated all the motoneurones examined through monosynaptic pathways in contrast to cells in normal cords in which such a stimulus sometimes elicits only a post-synaptic potential. In a number of cells subsequent polysynaptic activation caused a spike about 10 msec after the monosynaptic response, notwithstanding the serious interneuronal destruction which characterized these preparations.

4. In a few preparations the effects of acute asphyxiation could be examined. The soma depolarized at a rate of 3-4 mV/min. Synaptic activation was more resistant to O₂ lack than antidromic and direct excitation, in contrast to the experience with normal cells. Survival times of 8·5, 11 and 16 min were found. At certain levels of depolarization `spontaneous' spikes were observed, which, since they were preceded by post-synaptic potentials, could be considered as the result of synaptic activation.

5. To account for the enhanced reflex activity of rigid preparations, it was postulated that the substantial loss of interneurones in the cord had caused denervation supersensitivity of the motoneurones to the transmitter compound without materially changing their electrical excitability.

6. It was postulated that the early presynaptic failure during asphyxiation in normal preparations was dependent on a mechanism resembling presynaptic inhibition. The prolonged asphyxial survival of reflex activity in rigid preparations may be due to the destruction of interneurones involved in this form of inhibition.