Epileptic-like activity induces multiple forms of plasticity in hippocampal area CA1.
*Neuronal Plasticity; Animals; Calcium Channels; Electrophysiology; Epilepsy/chemically induced/*physiopathology; Hippocampus/*physiopathology; Ion Channels/physiology; L-Type/physiology; Long-Evans; Long-Term Potentiation/physiology; N-Methyl-D-Aspartate/metabolism; Potassium Chloride; Rats; Receptors; Synapses/physiology
Mesial temporal lobe epilepsy is a relatively common form of epilepsy that afflicts many thousands of people. It has been suggested that the development of primary and secondary foci may involve mechanisms similar to long-term potentiation (LTP). In vitro seizure models typically involve an increase in spontaneous asynchronous bursting activity (epileptiform activity) induced either by increasing excitation or decreasing inhibition. Previous experiments have indicated that these models often generate bursting activity that closely resembles epileptic activity. LTP is often observed following epileptiform activity. In area CA1 of the hippocampus two forms of LTP that are dependent on the activation of either the L-type voltage dependent calcium channel (vdccLTP) or the N-methyl-D-aspartate receptor/channel (nmdaLTP) have been described. It is unclear from previous experiments which type of LTP results from epileptiform activity. Recent evidence indicates that nmdaLTP is most likely a short-term type of plasticity while vdccLTP may be a long-lasting form of synaptic plasticity. Given the characteristics of vdccLTP it is a likely candidate mechanism to underlie the development and formation of secondary seizure foci. We have therefore tested the ability of epileptiform activity induced by elevated potassium chloride to induce multiple forms of LTP in area CA1 of the rat hippocampus. Elevation of extracellular potassium chloride resulted in spontaneous asynchronous bursting. The net result of the spontaneous asynchronous bursting was to induce a compoundLTP consisting of nmdaLTP and vdccLTP components.
Morgan S L; Teyler T J
Brain research
2001
2001-10
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
<a href="http://doi.org/10.1016/s0006-8993(01)02913-4" target="_blank" rel="noreferrer noopener">10.1016/s0006-8993(01)02913-4</a>
Calcium channel blocker toxicity.
Adult; Assisted Circulation; Calcium Channel Blockers/classification/pharmacokinetics/*poisoning; Calcium Channels; Calcium Chloride/therapeutic use; Cardiovascular Agents/therapeutic use; Cardiovascular Diseases/*chemically induced/drug therapy; Charcoal/therapeutic use; Child; Combined Modality Therapy; Drug Overdose/drug therapy/therapy; Enema; Extracorporeal Circulation; Fat Emulsions; Fluid Therapy; Glucagon/therapeutic use; Heart/drug effects; Humans; Hyperglycemia/*chemically induced/drug therapy; Infant; Intravenous/therapeutic use; L-Type/physiology; Muscle; Plasmapheresis; Poisoning/drug therapy/physiopathology/therapy; Practice Guidelines as Topic; Preschool; Smooth; Vascular/drug effects
Calcium channel blockers continue to be used for the management of a wide variety of adult and pediatric conditions including hypertension, angina pectoris, atrial arrhythmias, Raynaud phenomenon, and migraine headaches. With increased use comes increased potential for misuse and abuse. This article serves as a review of calcium channel blocker physiology with emphasis on presentation and management of the pediatric patient with calcium channel blocker toxicity.
Arroyo Anna Maria; Kao Louise W
Pediatric emergency care
2009
2009-08
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
<a href="http://doi.org/10.1097/PEC.0b013e3181b0a504" target="_blank" rel="noreferrer noopener">10.1097/PEC.0b013e3181b0a504</a>