Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0040822 (tremor)
 18,428 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. This study was undertaken to examine changes of excitatory drive to the triceps surae alpha-motoneuron pool during fatiguing submaximal isometric contractions in man. Eight healthy subjects maintained isometric plantar flexions at 30 percent of maximum voluntary contraction (MVC) until the limit of endurance (range, 6-9 min). 2. Excitability of the alpha-motoneuron pool to Ia afferent stimulation (H reflex), electromyograms (EMG) and maximum compound motor unit action potentials (Mmax) from the lateral (LG) and medial heads (MG) of the gastrocnemius as well as from the soleus muscle (Sol) were recorded throughout the contraction. Superimposed maximum twitch torques (twitch occlusion) and isometric torque fluctuations (tremor) were also recorded as indirect measures of excitatory drive. 3. H reflexes were studied at different levels of underlying voluntary contraction to assess the relationship between H reflex amplitude and excitatory drive. With increasing levels of underlying contraction up to MVC, superimposed H reflex amplitude increased for LG in six subjects, for MG in all eight and for Sol in five. In the remaining cases, H reflex amplitude first increased and then plateaued between 30-50% of MVC. 4. H/Mmax ratios increased during fatigue in those muscles that showed an H reflex amplitude increase with high levels of underlying contraction. In these cases, LG and MG H/Mmax increased significantly after about 50 and 20% of endurance time onward, respectively, whereas Sol H/Mmax demonstrated a significant increase up to 40% of endurance time. 5. EMG root mean square (r.m.s.) increased linearly throughout the contraction for all three muscles, while tremor r.m.s. increased in a non-linear way, with a steeper increase from 60% of endurance time onward. Superimposed twitch amplitude decreased significantly from 25% of endurance time onward. 6. It is concluded that during fatiguing isometric contractions at 30% of MVC, the excitatory drive to the triceps surae alpha-motoneuron pool increases. This is thought to be a compensatory mechanism to facilitate recruitment of new, unfatigued motor units (MUs), and/or to increase MU firing rates. The facts that the twitch is not abolished at endurance limit and that the EMG does not attain its unfatigued MVC level are strong indications that central fatigue occurred during the sustained submaximal contraction.
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PMID:Excitatory drive to the alpha-motoneuron pool during a fatiguing submaximal contraction in man. 901 19

The pathogenesis of neuropathic pain is incompletely understood and treatments are often inadequate. Cytoplasmic Ca(2+) regulates numerous cellular processes in neurons. This review therefore examines the pathogenic contribution of altered inward Ca(2+) flux (I(Ca)) through voltage-gated Ca(2+) channels in sensory neurons after peripheral nerve injury. We reviewed studies that recorded membrane currents through intracellular and patch-clamp techniques, as well as intracellular Ca(2+) levels using fluorimetric indicators, and performed behavioral analysis of rodent nerve injury models. Following nerve injury by partial ligation, a response characterized by sustained lifting, shaking, and licking of the paw after sharp mechanical stimulation is a reliable indicator or neuropathic pain. Primary sensory neurons isolated from animals with this behavior show a decrease in high-voltage activated I(Ca) by approximately one third. Low voltage-activated I(Ca) is nearly eliminated by peripheral nerve injury. Loss of I(Ca) leads to decreased activation of Ca(2+)-activated K(+) currents, which are also directly reduced in traumatized neurons. As a result of these changes in membrane currents, membrane voltage recordings show increased action potential duration and diminished afterhyperpolarization. Excitability is elevated, as indicated by resting membrane potential depolarization and a decreased current threshold for action potential initiation. Traumatized nociceptive neurons develop increased repetitive firing during sustained depolarization after axotomy. Concurrently, cytoplasmic Ca(2+) transients are diminished. In conclusions, axotomized neurons, especially pain-conducting ones, develop instability and elevated excitability after peripheral injury. Treatment of neuronal I(Ca) loss at the level of injury of the dorsal root ganglion may provide a novel therapeutic pathway.
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PMID:Role of decreased sensory neuron membrane calcium currents in the genesis of neuropathic pain. 1730 35