Enhancement of whole cell calcium currents following transient MCAO

Cerebral infarctions have been shown to cause widespread changes of neurona l excitability in non-infarcted tissue. Calcium currents are major determin ants of neuronal behavior, and pathological modulation of Ca2+-channels is known to lead to altered excitability states in a variety of paradigms. In the present study we addressed the question to what extent whole cell calci um currents are altered after middle cerebral artery occlusion (MCAO) in bo th the ipsi- and contralateral sensory cortex. Transient middle cerebral ar tery occlusion was induced for 1 h in rats using the intraluminal thread mo del. After 7 or 28 days survival, whole cell patch clamp studies were carri ed out on freshly isolated neurons of the ipsi- and contralateral sensory c ortex, and high voltage activated (HVA) calcium currents were examined. In lesioned animals, we found a significant increase of calcium current amplit ude and maximal conductance in the sensory cortex contralateral to the infa rcts. This was paralleled by a prominent positive shift of the potential of half-maximal activation (V-h,V-a) in these cells. Changes were long-lastin g and at least stable for the following 28 days. These alterations were pre sent in animals with lesions of moderate size, but not in those with massiv e infarction, and only in the cortex contralateral to the lesion. Following cortical infarctions, changes of calcium current properties are selectivel y observed in neurons contralateral to the lesion. At the behavioral level, compensatory mechanisms involving the unaffected hemisphere may induce thi s alteration of calcium current properties. (C) 2000 Elsevier Science BN. A ll rights reserved.