Biomedical subjects
D Utzschneider
Publications and source records attributed to D Utzschneider.
Mutual excitation among dorsal root ganglion neurons in the rat.
Intracellular recordings were obtained from primary sensory neurons in excised dorsal root ganglia (DRGs). Most (90%) neurons sampled became depolarized during periods of repetitive stimulation of a branch of the dorsal root (DR) which contained only axons of neighboring neurons. DR stimulation also evoked a transient rise in extracellular K+ concentration ([K+]o), following similar kinetics. Thus, the mutual excitation among DRG neurons may be mediated by [K+]o. Activity-dependent cross-excitation in DRGs could contribute to neuropathic sensory abnormalities often triggered by nerve injury or disease.
Conduction properties of spinal cord axons in the myelin-deficient rat mutant.
Spinal cords of myelin-deficient and normal age-matched (control) rats were removed and their conduction and pharmacological properties studied in an in vitro brain slice chamber. The conduction velocity of the myelin-deficient dorsal column axons was reduced to about 25% of control axons; however, the amyelinated myelin-deficient axons displayed refractory periods and the ability to sustain high-frequency action potential discharge similar to that of dorsal column axons in control rats. Pharmacological results suggest that the myelin-deficient dorsal column axons qualitatively express a normal complement of ion channels and receptors. The demonstration of a normal representation of channels and receptors on these axons supports the proposal that the oligodendrocyte, and not the axon, is the site of the primary defect in the myelin-deficient rat mutant. It is concluded that, unlike acutely demyelinated axons which display marked frequency-dependent conduction block, amyelinated axons of the myelin-deficient rat spinal cord develop compensatory mechanisms to stabilize action potential conduction.