Role of RyRs and IP3 Receptors after Traumatic Injury to Spinal Cord White Matter
| Autor: | L. G. Leibrock, Sandeep K. Agrawal, W. E. Thorell |
|---|---|
| Rok vydání: | 2002 |
| Předmět: |
Boron Compounds
Male medicine.medical_specialty Central nervous system Neural Conduction Action Potentials Receptors Cytoplasmic and Nuclear chemistry.chemical_element In Vitro Techniques Calcium Biology Dantrolene Caffeine Internal medicine medicine Animals Inositol 1 4 5-Trisphosphate Receptors Rats Wistar Receptor Egtazic Acid Spinal cord injury Spinal Cord Injuries Chelating Agents Voltage-dependent calcium channel Muscle Relaxants Central Ryanodine Ryanodine receptor Calcium-Binding Proteins Ryanodine Receptor Calcium Release Channel Anatomy medicine.disease Spinal cord Rats Electrophysiology Endocrinology medicine.anatomical_structure chemistry Models Animal Central Nervous System Stimulants Calcium Channels Neurology (clinical) medicine.drug |
| Zdroj: | Journal of Neurotrauma. 19:335-342 |
| ISSN: | 1557-9042 0897-7151 |
| DOI: | 10.1089/089771502753594909 |
| Popis: | Calcium influx and elevation of intracellular free calcium (Ca2+i), with subsequent activation of degenerative enzymes is hypothesized to cause cell injury and death after trauma. We examined the effects of traumatic compressive injury on (Ca2+)i dynamics in spinal cord white matter. We conducted electrophysiological studies with ryanodine and inositol (1,4,5)-triphosphate (IP3) receptor agonists and antagonists in an in vitro model of spinal cord injury (SCI). A 25-30-mm length of dorsal column was isolated from the spinal cord of adult rats, pinned in an in vitro recording chamber (37 degrees C) and injured with a modified clip (2-g closing force) for 15 sec. The functional integrity of the dorsal column was monitored electrophysiologically by quantitatively measuring the compound action potential (CAP) with glass microelectrodes. The CAP decreased to 55.2+/-6.8% of control (p < 0.05) after spinal cord injury (SCI). Chelation of Ca2+i with BAPTA-AM (a high-affinity calcium chelator) promoted significantly greater recovery of CAP amplitude (83.2+/-4.2% of control; p < 0.05) after injury. Infusion of caffeine (1 and 10 mM) exacerbated CAP amplitude decline (45.1+/-5.9% of control; p < 0.05; 44.6+/-3.1% of control; p < 0.05) postinjury. Blockade of Ca2+i release through ryanodine-sensitive receptors (RyRs) with dantrolene (10 microM) and ryanodine (50 microM), conferred significant (p < 0.05) improvement in CAP amplitude after injury. On the other hand, blockade of Ca2+i with inositol (1,4,5)-triphosphate receptor (IP3Rs) blocker 2APB (10 microM) also conferred significant improvement in CAP amplitude after injury (82.9+/-7.9%; p < 0.05). In conclusion, the injurious effects of Ca2+i in traumatic central nervous system (CNS) white matter injury appear to be mediated both by RyRs and through IP3Rs calcium-induced calcium release receptors (CICRs). |
| Databáze: | OpenAIRE |
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