Ca2+ homeostasis, Ca2+ signalling and somatodendritic vasopressin release in adult rat supraoptic nucleus neurones

Komori, Yoko; Tanaka, Megumi; Kuba, Motoko; Ito, Masahiro; Abe, Maiko; Naoki, Katsuhiko; Verkhratsky, Alexei; Shibuya, Izumi; Dayanithi, Govindan

doi:10.1016/j.ceca.2010.10.002

Cited by 29 publications

(28 citation statements)

References 49 publications

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“…Our results showing that TG prolonged the NMDA-⌬Ca 2ϩ signal both in sham and HF rats, indicate that the ER indeed acts as an important intracellular Ca 2ϩ buffering mechanism shaping the NMDA-⌬Ca 2ϩ waveform. This is in agreement with previous studies showing that blockade of the ER-SERCa prolonged the decay of a K ϩ -induced increase in Ca 2ϩ in MNCs (30). However, the fact that TG prolonged the NMDA-⌬Ca 2ϩ waveform in both experimental groups to a similar extent would argue against a blunted ER-SERCa function during HF.…”

Section: Discussionsupporting

confidence: 81%

“…MNCs possess numerous Ca 2ϩ buffering/clearance mechanisms, including plasmalemmal (PMCa) and endoplasmic reticulum (ER-SERCa) Ca 2ϩ transport ATPases, and the mitochondrial Ca 2ϩ selective uniporter (10), all of which have been shown to efficiently shape somatic Ca 2ϩ transients in these neurons (28,30). These Ca 2ϩ buffering mechanisms slowly decrease the levels of cytosolic free Ca 2ϩ , resulting in a slow decaying Ca 2ϩ time course following the initial transient rise.…”

Section: Discussionmentioning

confidence: 99%

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Enhanced NMDA receptor-mediated intracellular calcium signaling in magnocellular neurosecretory neurons in heart failure rats

Stern

Potapenko

2013

American Journal of Physiology-Regulatory, Integrative and Comp

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Stern JE, Potapenko ES. Enhanced NMDA receptor-mediated intracellular calcium signaling in magnocellular neurosecretory neurons in heart failure rats. Am J Physiol Regul Integr Comp Physiol 305: R414 -R422, 2013. First published June 19, 2013 doi:10.1152/ajpregu.00160.2013.-An enhanced glutamate excitatory function within the hypothalamic supraoptic and paraventricluar nuclei is known to contribute to increased neurosecretory and presympathetic neuronal activity, and hence, neurohumoral activation, during heart failure (HF). Still, the precise mechanisms underlying enhanced glutamate-driven neuronal activity in HF remain to be elucidated. Here, we performed simultaneous electrophysiology and fast confocal Ca 2ϩ imaging to determine whether altered N-methyl-D-aspartate (NMDA) receptor-mediated changes in intracellular Ca 2ϩ levels (NMDA-⌬Ca 2ϩ ) occurred in hypothalamic magnocellular neurosecretory cells (MNCs) in HF rats. We found that activation of NMDA receptors resulted in a larger ⌬Ca 2ϩ in MNCs from HF when compared with sham rats. The enhanced NMDA-⌬Ca 2ϩ was neither dependent on the magnitude of the NMDA-mediated current (voltage clamp) nor on the degree of membrane depolarization or firing activity evoked by NMDA (current clamp). Differently from NMDA receptor activation, firing activity evoked by direct membrane depolarization resulted in similar changes in intracellular Ca 2ϩ in sham and HF rats. Taken together, our results support a relatively selective alteration of intracellular Ca 2ϩ homeostasis and signaling following activation of NMDA receptors in MNCs during HF. The downstream functional consequences of such altered ⌬Ca 2ϩ signaling during HF are discussed.NMDA; vasopressin; supraoptic; glutamate; Ca 2ϩ SYMPATHOHUMORAL ACTIVATION involving augmented sympathetic tone and elevated hormonal plasma levels, including vasopressin (VP) and angiotensin II, among others (37,43,73), is a key central nervous system pathophysiological process in congestive heart failure (HF). Chronically elevated plasma VP levels have been reported both in animal models and human patients with HF (15, 19, 52, 62) being an important factor contributing to altered fluid/electrolyte balance, as well as detrimental myocardial effects (17,18,40,44,53). The importance of VP in HF is also underscored by several clinical trials demonstrating that VP receptor antagonism efficiently improves water balance and hemodynamic parameters in HF patients (2, 9, 41). Thus the VP system is currently emerging as a novel therapeutic target for the treatment of HF (14). Despite its major impact on morbidity and mortality in HF patients (7), the precise mechanisms contributing to neurohumoral activation, including elevated VP release in HF, remain incompletely understood.The hypothalamic supraoptic (SON) and paraventricular (PVN) nuclei are crucial centers involved in autonomic and neuroendocrine regulation of the circulation (23, 60). Within these nuclei, magnocellular neurosecretory cells (MNCs) directly control VP (and oxytocin) release into...

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Section: Discussionsupporting

confidence: 81%

Section: Discussionmentioning

confidence: 99%

Enhanced NMDA receptor-mediated intracellular calcium signaling in magnocellular neurosecretory neurons in heart failure rats

Stern

Potapenko

2013

American Journal of Physiology-Regulatory, Integrative and Comp

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“…Importantly, NCX plays a role in the regulation of somatodendritic Ca 2ϩ and AVP release (Komori et al 2010). Along the same line of thinking, the ability of NCX to regulate somatic, and likely also dendritic, Ca 2ϩ in the SCN neurons also suggests a possible involvement in the release of neuropeptides such as AVP, VIP, and GRP.…”

Section: Ncx1 Is the Major Ncx Isoform Involved In Regulating Somaticmentioning

confidence: 93%

Role of Na⁺/Ca²⁺exchanger in Ca²⁺homeostasis in rat suprachiasmatic nucleus neurons

Wang

Chen

Cheng

et al. 2015

Journal of Neurophysiology

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Wang YC, Chen YS, Cheng RC, Huang RC. Role of Na ϩ /Ca 2ϩ exchanger in Ca 2ϩ homeostasis in rat suprachiasmatic nucleus neurons. J Neurophysiol 113: 2114 -2126, 2015. First published January 7, 2015 doi:10.1152/jn.00404.2014 is critical to the central clock of the suprachiasmatic nucleus (SCN). However, the role of Na ϩ /Ca 2ϩ exchanger (NCX) in intracellular Ca 2ϩ concentration ([Ca 2ϩ ] i ) homeostasis in the SCN is unknown. Here we show that NCX is an important mechanism for somatic Ca 2ϩ clearance in SCN neurons. In control conditions Na ϩ -free solution lowered [Ca 2ϩ ] i by inhibiting TTX-sensitive as well as nimodipine-sensitive Ca 2ϩ influx. With use of the Na ϩ ionophore monensin to raise intracellular Na ϩ concentration ([Na ϩ ] i ), Na ϩ -free solution provoked rapid Ca 2ϩ uptake via reverse NCX. The peak amplitude of 0 Na ϩ -induced [Ca 2ϩ ] i increase was larger during the day than at night, with no difference between dorsal and ventral SCN neurons. Ca 2ϩ extrusion via forward NCX was studied by determining the effect of Na ϩ removal on Ca 2ϩ clearance after high-K ϩ -induced Ca 2ϩ loads. The clearance of Ca 2ϩ proceeded with two exponential decay phases, with the fast decay having total signal amplitude of ϳ85% and a time constant of ϳ7 s. Na ϩ -free solution slowed the fast decay rate threefold, whereas mitochondrial protonophore prolonged mostly the slow decay. In contrast, blockade of plasmalemmal and sarco(endo)plasmic reticulum Ca 2ϩ pumps had little effect on the kinetics of Ca 2ϩ clearance. RT-PCR indicated the expression of NCX1 and NCX2 mRNAs. Immunohistochemical staining showed the presence of NCX1 immunoreactivity in the whole SCN but restricted distribution of NCX2 immunoreactivity in the ventrolateral SCN. Together our results demonstrate an important role of NCX, most likely NCX1, as well as mitochondrial Ca 2ϩ uptake in clearing somatic Ca 2ϩ after depolarization-induced Ca 2ϩ influx in SCN neurons. Ca 2ϩ homeostasis; Ca 2ϩ imaging; circadian rhythm; Na ϩ /Ca 2ϩ exchanger; suprachiasmatic nucleus

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“…Data acquisition was performed using a procedure reported previously (7,10). Data were obtained at a sampling frequency of 0.2 Hz using Aqua Cosmos Software (Hamamatsu Photonics).…”

Section: Effects Of Gymnopilin On Cultured Dorsal Root Ganglion Cellsmentioning

confidence: 99%

Gymnopilin-a substance produced by the hallucinogenic mushroom, Gymnopilus junonius-mobilizes intracellular Ca2+ in dorsal root ganglion cells

et al. 2012

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Gymnopilus junonius is a widely spread mushroom in Japan and well known as a hallucinogenic mushroom. Gymnopilin was purified from the fruiting body of G. junonius and was reported to act on the spinal cord and depolarize motoneurons. This is the only evidence that gymnopilin has a biological effect on animals and no mechanism of the action has been determined at all. In this study, we examined effects of gymnopilin on intracellular Ca . These results indicate that gymnopilin activated phospholipase C and mobilize Ca 2+ from the intracellular Ca 2+ store in non-neuronal cells from the DRG. This is the first report to show that gymnopilin directly acts on cells isolated from the mammalian nervous system.

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Ca2+ homeostasis, Ca2+ signalling and somatodendritic vasopressin release in adult rat supraoptic nucleus neurones

Cited by 29 publications

References 49 publications

Enhanced NMDA receptor-mediated intracellular calcium signaling in magnocellular neurosecretory neurons in heart failure rats

Enhanced NMDA receptor-mediated intracellular calcium signaling in magnocellular neurosecretory neurons in heart failure rats

Role of Na⁺/Ca²⁺exchanger in Ca²⁺homeostasis in rat suprachiasmatic nucleus neurons

Gymnopilin-a substance produced by the hallucinogenic mushroom, Gymnopilus junonius-mobilizes intracellular Ca2+ in dorsal root ganglion cells

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Ca2+ homeostasis, Ca2+ signalling and somatodendritic vasopressin release in adult rat supraoptic nucleus neurones

Cited by 29 publications

References 49 publications

Enhanced NMDA receptor-mediated intracellular calcium signaling in magnocellular neurosecretory neurons in heart failure rats

Enhanced NMDA receptor-mediated intracellular calcium signaling in magnocellular neurosecretory neurons in heart failure rats

Role of Na+/Ca2+exchanger in Ca2+homeostasis in rat suprachiasmatic nucleus neurons

Gymnopilin-a substance produced by the hallucinogenic mushroom, Gymnopilus junonius-mobilizes intracellular Ca2+ in dorsal root ganglion cells

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Role of Na⁺/Ca²⁺exchanger in Ca²⁺homeostasis in rat suprachiasmatic nucleus neurons