Forebrain ischaemia/reperfusion injury (IRI) initiates cascade of events which eventually lead to cellular death. Dysregulation of calcium homeostasis is believed to be one of the causative phenomena linked with delayed neuronal death after IRI. Proper function of secretory pathways is important for neural cells. They secrete many neurotransmitters and secretory proteins necessary for growth and reorganization of neuronal circuits. A newly recognized calcium pump of Golgi apparatus, Ca²⁺ -ATPase (SPCA1) has important secretory function in rat forebrain. We investigated the presence and distribution of the SPCA1 pump protein in homogenates prepared from both the rat brain and the cell cultures of neurons and glial cells. Experiments show that SPCA1 pump protein in neural cells is localized to structures distinct from endoplasmic reticulum. In addition, mRNA expression pattern of SPCA1 gene was analyzed by RT-PCR after global forebrain IRI in rat. Forebrain ischaemia was initiated by four-vessel occlusion for 15min and reperfusion for 1h, 3h and 24h (IRI). RT-PCR analysis clearly detected expression of SPCA1 gene in injured area after IRI. In addition, mRNA expression pattern follows time dependent manner in reperfusion period. We observed, in reperfusion time, expression of SPCA1 gene follows a bell shaped pattern. In both areas of brain (cortex and hippocampus) the expression of SPCA1 was significantly increased with maximum at 3h after insult. Since the pump plays major role in the refilling of Ca²⁺ stores, we discuss here its possible contribution to altered intracellular Ca²⁺ signaling in neural cells in ischaemia/reperfusion event in context of involvement of secretory pathways in stress sensing and transduction of apoptotic signal. Supported by VEGA 3380/06, MVTS 39.