Capacitative calcium entry (CCE) is a signifi cant component of calcium homeostasis in non-excitable cells. In neurons, an increasing number of evidence points to CCE as an important event in neuronal physiology and pathology. STIM1 is an endoplasmic reticulum (ER) residing protein, where it serves as a calcium sensor. Low level of calcium in ER drives STIM1 oligomerize and interact with plasma membrane protein Orai1, hence leading to calcium entry. Previously, we showed STIM1 expression in neurons, where it exhibits the same mode of action as described for non-excitable cells. Here we present description of STIM1 distribution in the mouse brain. The highest STIM1 immunoreactivity was observed in Purkinje neurons and their dendrites. Very high immunoreactivity was found in the basal ganglia. High immunoreactivity was present in the hippocampal formation, in the piriform cortex, also in infragranular layers and layer V pyramidal neurons in the neocortex. In amygdala most nuclei showed strong immunoreactivity, only the basolateral complex was weakly stained. The thalamus was very weakly stained, and the hypothalamus showed immunoreactivity of both cells and neuropil. Observed differences in STIM1 distribution in the brain indicates that various brain structures depends on CCE to different extend. Prominent dissimilarity of STIM1 immunoreactivity between amygdaloid nuclei is, in our opinion, the most interesting in light of anatomical and functional organization of the amygdala.
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