Cholinergic agonists increase intracellular calcium concentration in frog vestibular hair cells

Ohtani, Makiko; Devau, Gina; Lehouelleur, Jacques; Sans, Alain

doi:10.1016/0378-5955(94)90108-2

Cited by 10 publications

(8 citation statements)

References 37 publications

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“…We have previously reported that this phase is calcium-calmodulin dependent: removal of calcium from the extracellular medium significantly diminished the response to ionomycin; the calmodulin inhibitor, W-7 eliminated the iso-volumetric shortening . In the present report, we demonstrated that RAPHCs have a rather low resting [Ca 2+ ] i of 66 ± 19 nM, which is comparable with the level reported for frogs vestibular hair cells (Ohtani et al, 1994), but somewhat lower than that observed in mammalian outer hair cells (Ashmore and Ohmori, 1990;Frolenkov et al, 2003). Ionomycin-induced shape change in RAPHCs, however, required micromolar [Ca 2+ ] i (see Results), suggesting possible involvement of medium-affinity mediators in this response.…”

Section: Discussionsupporting

confidence: 90%

Slow motility in hair cells of the frog amphibian papilla: Myosin light chain-mediated shape change

Farahbakhsh

Narins

2008

Hearing Research

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Using video, fluorescence and confocal microscopy, quantitative analysis and modeling, we investigated intracellular processes mediating the calcium/calmodulin (Ca 2+ /CaM)-dependent slow motility in hair cells dissociated from the rostral region of amphibian papilla, one of the two auditory organs in frogs. The time course of shape changes in these hair cells during the period of pretreatment with several specific inhibitors, as well as their response to the calcium ionophore, ionomycin, were recorded and compared. These cells respond to ionomycin with a tri-phasic shape change: an initial phase of iso-volumetric length decrease; a period of concurrent shortening and swelling; and the final phase of increase in both length and volume. We found that both the myosin light chain kinase inhibitor, ML-7, and antagonists of the multifunctional Ca 2+ /CaM-dependent kinases, KN-62 and KN-93, inhibit the iso-volumetric shortening phase of the response to ionomycin. The type 1 protein phosphatase inhibitors, calyculin A and okadaic acid induce minor shortening on their own, but do not significantly alter the phase 1 response. However, they appear to counter effects of the inhibitors of Ca 2+ /CaM-dependent kinases. We hypothesize that an active actomyosin-based process mediates the iso-volumetric shortening in the frog rostral amphibian papillar hair cells.

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Section: Discussionsupporting

confidence: 90%

Slow motility in hair cells of the frog amphibian papilla: Myosin light chain-mediated shape change

Farahbakhsh

Narins

2008

Hearing Research

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“…Anatomical data indicate that EVS neurons receive significant input from the reticular formation, a major arousal system hub (Pfaff et al, 2005;Metts et al, 2006). Furthermore, several studies have implicated the EVS as a mechanism by which an enhancement of afferent sensitivity might be warranted during arousal state changes like sleep-to-awake transitions or postural threats (Horslen et al, 2014;Naranjo et al, 2015;Schwarz et al, 2015;Lim et al, 2016).…”

Section: Functional Considerationsmentioning

confidence: 99%

“…In fish and amphibians, efferent-mediated fast inhibition or excitation attenuates afferent responsiveness during self-generated movements (Boyle and Highstein, 1990;Chagnaud et al, 2015), but the evidence for similar attenuation in mammals has been less compelling Sadeghi et al, 2007b;Jamali et al, 2009). Recent studies in mice have indicated that the EVS modulates the amplitude of the vestibulo-ocular reflex (VOR) and vestibular stimulus-evoked potentials (Luebke et al, 2014;Hübner et al, 2015;Morley et al, 2016). While efferent-mediated fast inhibition or fast excitation may attenuate vestibular input (Boyle and Highstein, 1990;Chagnaud et al, 2015;Hübner et al, 2015), our data suggest that mAChRs and KCNQ closure could provide the EVS with a counter mechanism to enhance vestibular input.…”

Section: Functional Considerationsmentioning

confidence: 99%

“…The EVS may also alter afferent discharge regularity, action potential kinetics, and information transfer by modulating potassium channels and/or nAChRs in hair cells and afferents (Han et al, 2007;Pérez et al, 2009;Kalluri et al, 2010;Meredith and Rennie, 2015;Contini et al, 2016). This in turn may modify coding schemes to adjust how phasic and tonic pathways sense head movements and drive vestibular behaviors like the VOR (Sadeghi et al, 2007a;Hübner et al, 2015;Morley et al, 2016).…”

Section: Functional Considerationsmentioning

confidence: 99%

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Muscarinic Acetylcholine Receptors and M-Currents Underlie Efferent-Mediated Slow Excitation in Calyx-Bearing Vestibular Afferents

Holt

Jordan²,

Lysakowski

et al. 2017

J. Neurosci.

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Stimulation of vestibular efferent neurons excites calyx and dimorphic (CD) afferents. This excitation consists of fast and slow components that differ Ͼ100-fold in activation kinetics and response duration. In the turtle, efferent-mediated fast excitation arises in CD afferents when the predominant efferent neurotransmitter acetylcholine (ACh) activates calyceal nicotinic ACh receptors (nAChRs); however, it is unclear whether the accompanying efferent-mediated slow excitation is also attributed to cholinergic mechanisms. To identify synaptic processes underlying efferent-mediated slow excitation, we recorded from CD afferents innervating the turtle posterior crista during electrical stimulation of efferent neurons,incombinationwithpharmacologicalprobesandmechanicalstimulation.Efferent-mediatedslowexcitationwasunaffectedbynAChR compounds that block efferent-mediated fast excitation, but were mimicked by muscarine and antagonized by atropine, indicating that it requires ACh and muscarinic ACh receptor (mAChR) activation. Efferent-mediated slow excitation or muscarine application enhanced the sensitivity of CD afferents to mechanical stimulation, suggesting that mAChR activation increases afferent input impedance by closing calyceal potassium channels. These observations were consistent with suppression of a muscarinic-sensitive K ϩ -current, or M-current. Immunohistochemistry for putative M-current candidates suggested that turtle CD afferents express KCNQ3, KCNQ4, and ERG1-3 potassium channel subunits. KCNQ channels were favored as application of the selective antagonist XE991 mimicked and occluded efferent-mediated slow excitation in CD afferents. These data highlight an efferent-mediated mechanism for enhancing afferent sensitivity. They further suggest that the clinical effectiveness of mAChR antagonists in treating balance disorders may also target synaptic mechanisms in the vestibular periphery, and that KCNQ channel modulators might offer similar therapeutic value.

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“…The intracellular calcium concentration ([Ca 2+ ] i ) is elevated by the following: (1) entry of Ca 2+ via the MET channel; (2) entry of Ca 2+ via the voltage-dependent Ca channel after depolarization of the membrane potential, and (3) mediation through an efferent nerve transmitted by ATP [7], acetylcholine [8,9], and other substances. To study the effect of intracellular Ca 2+ on the MET channel, we altered [Ca 2+ ] i directly in the same cell by applying two methods: (1) flash-induced photolysis of a caged calcium compound, Nitr-5 [10], and (2) perfusion of the interior solution of a patch electrode by the application of negative pressure [11].…”

Section: Introductionmentioning

confidence: 99%

Intracellular Calcium Suppresses Mechano-Electrical Transduction Current in Chick CochlearHair Cells

Kimitsuki

Taira²,

Komune³

et al. 1998

ORL

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Intracellular calcium concentration ([Ca²⁺]_i) was elevated by photolysis of the caged calcium compound, Nitr-5, and by use of the intrapipette perfusion technique in hair cells dissociated from the chick cochlea. An increase in [Ca²⁺]_i induced an outward-going current at a membrane potential of –40 mV, as recorded with an intracellular medium of 160 mM KCl. This current was carried by the Ca²⁺-activated K⁺ current. In contrast, an increase of [Ca²⁺]_i induced an inward-going current at –50 mV with a 160 mM CsCl-based intracellular medium. This inward-going current was carried by the Ca²⁺-activated non-selective cation current. The amplitude of the mechano-electrical transduction current was suppressed by the increase of [Ca²⁺]_i, achieved both by photolysis and by use of the intrapipette perfusion method.

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Cholinergic agonists increase intracellular calcium concentration in frog vestibular hair cells

Cited by 10 publications

References 37 publications

Slow motility in hair cells of the frog amphibian papilla: Myosin light chain-mediated shape change

Slow motility in hair cells of the frog amphibian papilla: Myosin light chain-mediated shape change

Muscarinic Acetylcholine Receptors and M-Currents Underlie Efferent-Mediated Slow Excitation in Calyx-Bearing Vestibular Afferents

Intracellular Calcium Suppresses Mechano-Electrical Transduction Current in Chick CochlearHair Cells

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