Neurons express extremely different sensitivity to ischemic insults. The neuronal vulnerability is region-specific and the striatum is among the most susceptible areas to ischemic damage. Projecting GABAergic medium-sized neurons are very sensitive to energy metabolism impairment, whereas interneurons are selectively spared. However, the reasons for this differential vulnerability are largely unknown. Calcium ions (Ca2+) are important intracellular messengers enabling several physiological processes. However, excessive Ca2+ influx from the extracellular space or release from internal stores can elevate Ca2+ to levels that exceed the capacity of single neurons to appropriately buffer such overload. This capacity also appears to be a peculiar feature of single neuronal subtypes. This review will provide a brief survey of the ionic basis underlying the differential responses to in vitro ischemia of distinct striatal neuronal subtypes, mainly focusing on the role of Ca2+. The potential relevance of these findings in the development of therapeutic strategies for acute stroke will be discussed.

Calcium signaling and neuronal vulnerability to ischemia in the striatum

PISANI, ANTONIO;
2004-01-01

Abstract

Neurons express extremely different sensitivity to ischemic insults. The neuronal vulnerability is region-specific and the striatum is among the most susceptible areas to ischemic damage. Projecting GABAergic medium-sized neurons are very sensitive to energy metabolism impairment, whereas interneurons are selectively spared. However, the reasons for this differential vulnerability are largely unknown. Calcium ions (Ca2+) are important intracellular messengers enabling several physiological processes. However, excessive Ca2+ influx from the extracellular space or release from internal stores can elevate Ca2+ to levels that exceed the capacity of single neurons to appropriately buffer such overload. This capacity also appears to be a peculiar feature of single neuronal subtypes. This review will provide a brief survey of the ionic basis underlying the differential responses to in vitro ischemia of distinct striatal neuronal subtypes, mainly focusing on the role of Ca2+. The potential relevance of these findings in the development of therapeutic strategies for acute stroke will be discussed.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11571/1356714
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