Kv7 Channels Can Function without Constitutive Calmodulin Tethering

9 p.

Water quality assessment and characterisation of chlorophyll-a variability related to river discharges, within the southeastern Bay of Biscay : evaluation and development of chlorophyll-a algorithms for MODIS and MERIS imagery

222 p. : il.

Role of G protein coupled inwardly rectifier K+ channels (GIRK) on the neurobiology depression

353 págs.

Controls on river terrace formation in New Zealand

[EUS] Artikulu honek, argitaratutako bibliografiaren bidez, Zeelanda Berriko ibai-terrazen garapenari eragiten dieten agente morfogenetikoak aztertzen ditu. Erreferentzia gisa Ipar Irlako 4 kasu eta Hego Irlako 3 kasu erabili dira. Oro har, ibai-terrazak sortzeko orduan, klima, sedimentuen erabilgarritasunan eta prezipitazioan duen eraginaren bitartez, eragile nagusiena da. Altxaketa tektonikoak forma hauen kontserbazioa eragiten du. Hainbat kasutan, gertaera asaldatzaileen ondorioz sortutako sedimentu kopuru handiek, fase morfogenetiko desberdinak eragin dituzte lokal/erregional mailan, nazional/kontinental mailan beharrean. Gertaera asaldatzaileen artean, besteak beste, ekarpen bolkaniko naturalak eta gizakiok bultzatutako lur erabilera aldaketen ondorioz sortutako sedimentu ekarpenak barneratzen dira.

Implementing Integrated Water Resources Management in the Ebro River Basin: From Theory to Facts

JA-925

CGP37157, an inhibitor of the mitochondrial Na+/Ca2+ exchanger, protects neurons from excitotoxicity by blocking voltage-gated Ca2+ channels

Inhibition of the mitochondrial Na+/Ca2+ exchanger (NCLX) by CGP37157 is protective in models of neuronal injury that involve disruption of intracellular Ca2+ homeostasis. However, the Ca2+ signaling pathways and stores underlying neuroprotection by that inhibitor are not well defined. In the present study, we analyzed how intracellular Ca2+ levels are modulated by CGP37157 (10 mu M) during NMDA insults in primary cultures of rat cortical neurons. We initially assessed the presence of NCLX in mitochondria of cultured neurons by immunolabeling, and subsequently, we analyzed the effects of CGP37157 on neuronal Ca2+ homeostasis using cameleon-based mitochondrial Ca2+ and cytosolic Ca2+ ([Ca2+](i)) live imaging. We observed that NCLX-driven mitochondrial Ca2+ exchange occurs in cortical neurons under basal conditions as CGP37157 induced a decrease in [Ca-2](i) concomitant with a Ca2+ accumulation inside the mitochondria. In turn, CGP37157 also inhibited mitochondrial Ca2+ efflux after the stimulation of acetylcholine receptors. In contrast, CGP37157 strongly prevented depolarization-induced [Ca2+](i) increase by blocking voltage-gated Ca2+ channels (VGCCs), whereas it did not induce depletion of ER Ca2+ stores. Moreover, mitochondrial Ca2+ overload was reduced as a consequence of diminished Ca2+ entry through VGCCs. The decrease in cytosolic and mitochondrial Ca2+ overload by CGP37157 resulted in a reduction of excitotoxic mitochondrial damage, characterized here by a reduction in mitochondrial membrane depolarization, oxidative stress and calpain activation. In summary, our results provide evidence that during excitotoxicity CGP37157 modulates cytosolic and mitochondrial Ca2+ dynamics that leads to attenuation of NMDA-induced mitochondrial dysfunction and neuronal cell death by blocking VGCCs.