Immunological and Functional Identification of Intracellular Ca²⁺ Store from Gerbil Forebrain

Abstract

An increasing body of evidence has been presented to prove that endoplasmic reticulum plays an important role as rapidly exchanging intracellular Ca²⁺-store in the neural cells during normal and pathological conditions (1). This organelle appears to include an intracellular Ca²⁺-store able: i) to sequester Ca²⁺ via Ca²⁺ pumping activity (sarco/end-oplasmic reticulum Ca²⁺-ATPase — SERCA), ii) to respond to InsP₃-mediated agonists (metabotropic signals) and/or to Ca²⁺ (ionotropic signals), iii) to buffer Ca²⁺ via Ca²⁺-bind-ing proteins (2,3). From the functional point of view, the Ca²⁺-store not only initiates the Ca²⁺-signal releasing Ca²⁺ in the deeper cell structures in response to plasmalemnal receptor stimulation (acting as a source) but acts also as a buffering system or regulating barrier (sink) to protect the cell from Ca²⁺ overload (4).