scholarly journals Calcium‐induced calcium release in proximity to hair cell BK channels revealed by PKA activation

2020 ◽  
Vol 8 (15) ◽  
Author(s):  
Jun‐ping Bai ◽  
Na Xue ◽  
Omolara Lawal ◽  
Anda Nyati ◽  
Joseph Santos‐Sacchi ◽  
...  
Keyword(s):  
Hair Cell ◽  
Calcium Release ◽  
Bk Channels ◽  
Calcium Induced Calcium Release

scholarly journals Pharmacology of Acetylcholine-Mediated Cell Signaling in the Lateral Line Organ Following Efferent Stimulation

2005 ◽  
Vol 93 (5) ◽  
pp. 2541-2551 ◽  
Author(s):  
Rosie Dawkins ◽  
Sarah L. Keller ◽  
William F. Sewell
Keyword(s):  
Hair Cell ◽  
Lateral Line ◽  
Nicotinic Receptor ◽  
Calcium Release ◽  
Afferent Fiber ◽  
Calcium Signal ◽  
Sk Channels ◽  
Lateral Line Organ ◽  
Calcium Induced Calcium Release ◽  
Line Organ

Cholinergic efferent fibers modify hair cell responses to mechanical stimulation. It is hypothesized that calcium entering the hair cell through a nicotinic receptor activates a small-conductance (SK), calcium-activated potassium channel to hyperpolarize the hair cell. The calcium signal may be amplified by calcium-induced calcium release from the synaptic cisternae. Pharmacological tests of these ideas in the intact cochlea have been technically difficult because of the complex and fragile structure of the mammalian inner ear. We turned to the Xenopus laevis lateral line organ, whose simplicity and accessibility make it a model for understanding hair cell organ function in a relatively intact system. Drugs were applied to the inner surface of the skin while monitoring the effects of efferent stimulation on afferent fiber discharge rate. Efferent effects were blocked by antagonists of SK channels including apamin (EC50 = 0.5 μM) and dequalinium (EC50 = 12 μM). The effect of apamin was not enhanced by co-administration of phenylmethylsulfonyl fluoride, a proteolysis inhibitor. Efferent effects were attenuated by ryanodine, an agent that can interfere with calcium-induced calcium release, although relatively high (mM) concentrations of ryanodine were required. Fluorescent cationic styryl dyes, 4-di-2-asp and fm 1–43, blocked efferent effects, although it was not possible to observe specific entry of the dye into the base of hair cells. These pharmacological findings in the Xenopus lateral line organ support the hypothesis that effects of efferent stimulation are mediated by calcium entry through the nicotinic receptor via activation of SK channels and suggest the generality of this mechanism in meditating cholinergic efferent effects.

scholarly journals Calcium induced calcium release in proximity to hair cell BK channels revealed by PKA activation

2019 ◽  
Author(s):  
Jun-ping Bai ◽  
Na Xue ◽  
Omolara Lawal ◽  
Anda Nyati ◽  
Joseph Santos-Sacchi ◽  
...  
Keyword(s):  
Calcium Release ◽  
Critical Role ◽  
Bk Channels ◽  
Ip3 Receptors ◽  
Spatial Spread ◽  
Synaptic Release ◽  
Close Proximity ◽  
Electrical Resonance ◽  
High Concentrations ◽  
Calcium Induced Calcium Release

AbstractLarge conductance calcium-activated potassium (BK) channels play a critical role in electrical resonance, a mechanism of frequency selectivity in chicken hair cells. We determine that BK currents are dependent on inward flow of Ca2+, and intracellular buffering of Ca2+. Entry of Ca2+ is further amplified locally by Ca2+ induced Ca2+ release (CICR) in close proximity to plasma membrane BK channels. Ca2+ imaging reveals peripheral clusters of high concentrations of Ca2+ that are suprathreshold to that needed to activate BK channels. PKA activation increases BK currents likely by recruiting more BK channels due to spatial spread of high Ca2+ concentrations in turn from increasing CICR. STORM imaging confirms the presence of nanodomains with ryanodine and IP3 receptors in close proximity to the Slo subunit of BK channels. Together, these data require a rethinking of how electrical resonance is brought about and suggest effects of CICR in synaptic release. Both genders were included in this study.

scholarly journals Calcium-induced calcium release supports recruitment of synaptic vesicles in auditory hair cells

2016 ◽  
Vol 115 (1) ◽  
pp. 226-239 ◽  
Author(s):  
Manuel Castellano-Muñoz ◽  
Michael E. Schnee ◽  
Anthony J. Ricci
Keyword(s):  
Hair Cell ◽  
Hair Cells ◽  
Synaptic Vesicles ◽  
Calcium Release ◽  
Resting Potential ◽  
Calcium Stores ◽  
Potential Contribution ◽  
Auditory Hair Cells ◽  
Ribbon Synapses ◽  
Calcium Induced Calcium Release

Hair cells from auditory and vestibular systems transmit continuous sound and balance information to the central nervous system through the release of synaptic vesicles at ribbon synapses. The high activity experienced by hair cells requires a unique mechanism to sustain recruitment and replenishment of synaptic vesicles for continuous release. Using pre- and postsynaptic electrophysiological recordings, we explored the potential contribution of calcium-induced calcium release (CICR) in modulating the recruitment of vesicles to auditory hair cell ribbon synapses. Pharmacological manipulation of CICR with agents targeting endoplasmic reticulum calcium stores reduced both spontaneous postsynaptic multiunit activity and the frequency of excitatory postsynaptic currents (EPSCs). Pharmacological treatments had no effect on hair cell resting potential or activation curves for calcium and potassium channels. However, these drugs exerted a reduction in vesicle release measured by dual-sine capacitance methods. In addition, calcium substitution by barium reduced release efficacy by delaying release onset and diminishing vesicle recruitment. Together these results demonstrate a role for calcium stores in hair cell ribbon synaptic transmission and suggest a novel contribution of CICR in hair cell vesicle recruitment. We hypothesize that calcium entry via calcium channels is tightly regulated to control timing of vesicle fusion at the synapse, whereas CICR is used to maintain a tonic calcium signal to modulate vesicle trafficking.

scholarly journals Postoperative malignant hyperthermia confirmed by calcium-induced calcium release rate after breast cancer surgery, in which prompt recognition and immediate dantrolene administration were life-saving: a case report

2021 ◽  
Vol 15 (1) ◽  
Author(s):  
Natsumi Miyazaki ◽  
Takayuki Kobayashi ◽  
Takako Komiya ◽  
Toshio Okada ◽  
Yusuke Ishida ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Body Temperature ◽  
Malignant Hyperthermia ◽  
Muscle Biopsy ◽  
Release Rate ◽  
Calcium Release ◽  
Cancer Surgery ◽  
Breast Cancer Surgery ◽  
Body Cooling ◽  
Calcium Induced Calcium Release

Abstract Background Malignant hyperthermia (MH) is a rare genetic disease characterized by the development of very serious symptoms, and hence prompt and appropriate treatment is required. However, postoperative MH is very rare, representing only 1.9% of cases as reported in the North American Malignant Hyperthermia Registry (NAMHR). We report a rare case of a patient who developed sudden postoperative hyperthermia after mastectomy, which was definitively diagnosed as MH by the calcium-induced calcium release rate (CICR) measurement test. Case presentation A 61-year-old Japanese woman with a history of stroke was hospitalized for breast cancer surgery. General anesthesia was introduced by propofol, remifentanil, and rocuronium. After intubation, anesthesia was maintained using propofol and remifentanil, and mastectomy and muscle flap reconstruction surgery was performed and completed without any major problems. After confirming her spontaneous breathing, sugammadex was administered and she was extubated. Thereafter, systemic shivering and masseter spasm appeared, and a rapid increase in body temperature (maximum: 38.9 °C) and end-tidal carbon dioxide (ETCO2) (maximum: 59 mmHg) was noted. We suspected MH and started cooling the body surface of the axilla, cervix, and body trunk, and administered chilled potassium-free fluid and dantrolene. After her body temperature dropped and her shivering improved, dantrolene administration was ended, and finally she was taken to the intensive care unit (ICU). Body cooling was continued within the target range of 36–37 °C in the ICU. No consciousness disorder, hypotension, increased serum potassium level, metabolic acidosis, or cola-colored urine was observed during her ICU stay. Subsequently, her general condition improved and she was discharged on day 12. Muscle biopsy after discharge was performed and provided a definitive diagnosis of MH. Conclusions The occurrence of MH can be life-threatening, but its frequency is very low, and genetic testing and muscle biopsy are required to confirm the diagnosis. On retrospective evaluation using the malignant hyperthermia scale, the present case was almost certainly that of a patient with MH. Prompt recognition and immediate treatment with dantrolene administration and body cooling effectively reversed a potentially fatal syndrome. This was hence a valuable case of a patient with postoperative MH that led to a confirmed diagnosis by CICR.

scholarly journals LIM Domain Only 4 (LMO4) Regulates Calcium-Induced Calcium Release and Synaptic Plasticity in the Hippocampus

2012 ◽  
Vol 32 (12) ◽  
pp. 4271-4283 ◽  
Author(s):  
Z. Qin ◽  
X. Zhou ◽  
M. Gomez-Smith ◽  
N. R. Pandey ◽  
K. F. H. Lee ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Calcium Release ◽  
Lim Domain ◽  
Calcium Induced Calcium Release

Teaching calcium-induced calcium release in cardiomyocytes using a classic paper by Fabiato

2008 ◽  
Vol 32 (1) ◽  
pp. 1-10 ◽  
Author(s):  
Willmann Liang
Keyword(s):  
Teaching And Learning ◽  
Calcium Release ◽  
Cell Model ◽  
Learning Experience ◽  
Review Article ◽  
Supporting Evidence ◽  
Cardiac Sarcoplasmic Reticulum ◽  
Technical Issues ◽  
Calcium Induced Calcium Release ◽  
Physiology Students

This teaching paper utilizes the materials presented by Dr. Fabiato in his review article entitled “Calcium-induced release of calcium from the cardiac sarcoplasmic reticulum.” In the review, supporting evidence of calcium-induced calcium release (CICR) is presented. Data concerning potential objections to the CICR theory are discussed as well. In closing, technical issues associated with the skinned cell model are mentioned. Based on this review article, teaching and learning points are put forth in this article to highlight two concepts: 1) the regulatory mechanisms of CICR in cardiomyocytes and 2) the recognition of contradicting hypotheses and limitations in experimental design. The first concept is certainly an important one for physiology students. The second concept is universally applicable to researchers in all fields of science. It is thus the aim of this article to cultivate a rewarding teaching and learning experience for both instructors and students.

Angiotensin II Ca2+ signaling in rat afferent arterioles: stimulation of cyclic ADP ribose and IP3 pathways

2005 ◽  
Vol 288 (4) ◽  
pp. F785-F791 ◽  
Author(s):  
Susan K. Fellner ◽  
William J. Arendshorst
Keyword(s):  
Calcium Release ◽  
Rat Kidney ◽  
Ang Ii ◽  
High Concentration ◽  
Inositol Trisphosphate Receptor ◽  
Cyclic Adp Ribose ◽  
Specific Antagonist ◽  
Afferent Arterioles ◽  
Trisphosphate Receptor ◽  
Calcium Induced Calcium Release

ANG II induces a rise in cytosolic Ca2+ ([Ca2+]i) in vascular smooth muscle (VSM) cells via inositol trisphosphate receptor (IP3R) activation and release of Ca2+ from the sarcoplasmic reticulum (SR). The Ca2+ signal is augmented by calcium-induced calcium release (CICR) and by cyclic adeninediphosphate ribose (cADPR), which sensitizes the ryanodine-sensitive receptor (RyR) to Ca2+ to further amplify CICR. cADPR is synthesized from β-nicotinamide adenine dinucleotide (NAD+) by a membrane-bound bifunctional enzyme, ADPR cyclase. To investigate the possibility that ANG II activates the ADPR cyclase of afferent arterioles, we used inhibitors of the IP3R, RyR, and ADPR cyclase. Afferent arterioles were isolated from rat kidney with the magnetized microsphere and sieving technique and loaded with fura-2 to measure [Ca2+]i. In Ca2+-containing buffer, ANG II increased [Ca2+]i by 125 ± 10 nM. In the presence of the IP3R antagonists TMB-8 and 2-APB, the peak responses to ANG II were reduced by 74 and 81%, respectively. The specific antagonist of cADPR 8-Br ADPR and a high concentration of ryanodine (100 μM) inhibited the ANG II-induced increases in [Ca2+]i by 75 and 69%, respectively. Nicotinamide and Zn2+ are known inhibitors of the VSM ADPR cyclase. Nicotinamide diminished the [Ca2+]i response to ANG II by 66%. In calcium-free buffer, Zn2+ reduced the ANG II response by 68%. Simultaneous blockade of the IP3 and cADPR pathways diminished the [Ca2+]i response to ANG II by 83%. We conclude that ANG II initiates Ca2+ mobilization from the SR in afferent arterioles via the classic IP3R pathway and that ANG II may lead to activation of the ADPR cyclase to form cADPR, which, via its action on the RyR, substantially augments the Ca2+ response.

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