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Involvement of glycine and GABA_A receptors in the pathogenesis of spinal myoclonus

In vitro studies in the isolated neonatal rodent spinal cord

From the Laboratory of Neural Control and Medical Neurology Branch, NINDS, National Institutes of Health, Bethesda, MD.
Received December 20, 1994. Accepted in final form February 20, 1995.
Address correspondence and reprint requests to Dr. Ely S. Simon, Laboratory of Neural Control, NIH, Building 49, Room 3A50, 9000 Rockville Pike, Bethesda, MD 20892.

Studies of pathogenetic mechanisms of myoclonus and spinal spasticity have established a strong association between deficient inhibitory glycinergic transmission and pathologic rigidity and tremor.Consistent with known cases in the clinical literature, electrophysiologic data from animal models of myoclonus implicate dysfunction of segmental spinal cord circuitry. The present study sought to further explore pathogenetic mechanisms at the circuit level. In vitro preparations of isolated spinal cord from neonatal rodents allowed for stable recordings of individual cells as well as populations of motoneurons. Blockade of glycine receptors enhanced 5- to 15-Hz sinusoidal oscillations that were synchronous in entire populations of motoneurons as well as along multiple segments of the spinal cord. Oscillations at motoneurons were mediated largely by non-NMDA excitatory synaptic inputs. Blockade of GABA_A receptors, and not GABA (_B) receptors, abolished sinusoidal oscillations, suggesting a critical role for GABA_A receptors in the premotoneuronal circuitry responsible for generation or transmission of the sinusoidal oscillations. These data offer new insights into possible pathogenetic mechanisms of spinal myoclonus and may help guide future research leading to specific therapies for hyperkinetic movement disorders of spinal origin.

NEUROLOGY 1995;45: 1883-1892

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