Effects of hypoxia on the monosynaptic reflex pathway in the cat spinal cord.

Publisher Website
Google Scholar
Abstract
Cat spinal monosynaptic reflexes were studied during hypoxia induced by ventilation with 0-5% oxygen in nitrogen. Increase followed by decrease and disappearance of reflexes. Changes in excitability of presynaptic elements and in ortho-dromic motor nuclei focal potentials interpreted as due to progressive depolarization and conduction block in afferent nerve terminals. A small and gradual depolarization of motoneurones (less than 2 mV/min.). Small reductions in maximum rate of rise and fall, in overshoot, and in after-hyperpolarization of motoneurone action potentials. No significant changes in excitability and resistance of motoneurone membranes. Increase followed by decrease and disappearance of monosynaptic excitatory postsynaptic potentials (EPSPs). Hypoxia probably acts by depressing active ion fluxes. Motoneurones are less sensitive to hypoxia than are presynaptic nerve terminals in which depolarization cause conduction block and therby decrease in EPSPs and number of cells firing which then explain the decrease and block of monosynaptic reflexes. Initial increase in monosynaptic reflexes may be due to increased release of transmitter substance causing increase in EPSPs and number of cells firing.