Calmyrin 2 (CaMy2, Cib2) represents a novel calmyrin subfamily of Ca2+ binding proteins that coordinate Ca2+ in the EF-hand motives. CaMy2 mRNA was recently detected in brain, but nothing is known about CaMy2 protein localization and properties in the brain. We have cloned CaMy2 from rat brain, demonstrated CaMy2 Ca2+- sensor properties and determined its neuronal pattern of rat brain expression. CaMy2 protein is expressed mainly in hippocampal neurons and localizes together with Golgi apparatus and dendrite markers. Our studies in primary cultures of hippocampal neurons demonstrate that expression of CaMy2 protein is induced upon neuronal activation with pharmacological agents that stimulate Ca2+ infl ux through such types of Ca2+ channels as glutamate excitatory receptors and voltage-operated Ca2+ channels. In addition, increase in CaMy2 protein level was induced by soluble amyloid β and BDNF. However, most prominent increase in CaMy2 protein (7-fold), and mRNA (2-fold) occurs upon stimulation of NMDA receptor (NMDAR). The induction is blocked by translation inhibitors, specifi c antagonists of NMDAR, the Ca2+-chelator BAPTA, and inhibitors of ERK1/2 and PKC, kinases transmitting NMDAR-linked Ca2+ signal. Our results show that CaMy2 level is controlled by NMDAR and Ca2+ and suggest CaMy2 role in Ca2+ signaling underlying NMDAR activation. This work was supported by the Polish Ministerial Research grant N301 109 32/3854.
JavaScript jest wyłączony w Twojej przeglądarce internetowej. Włącz go, a następnie odśwież stronę, aby móc w pełni z niej korzystać.