Ca(2+)‐induced Ca2+ release mediates Ca2+ transients evoked by single action potentials in rabbit vagal afferent neurones.

Cohen, Akiva S.; Moore, Kimberly A.; Bangalore, R.; Jafri, M. Saleet; Weinreich, Daniel; Kao, Joseph P. Y.

doi:10.1113/jphysiol.1997.sp021929

Cited by 47 publications

(34 citation statements)

References 41 publications

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“…In the presence of RY, DBHQ, and TG, the ⌬Ca t -AP relation exhibits slopes of 0.5, 1.1, and 0.8 nM per AP, respectively. When compared with the slope of 9.6 nM per AP in control neurons, Ca 2ϩ influx produced by a single nodose AP is amplified by 5-to 10-fold by CICR (16). Nodose neurons demonstrate a relatively low stimulus threshold for eliciting CICR.…”

Section: Resultsmentioning

confidence: 93%

Calcium regulation of a slow post-spike hyperpolarization in vagal afferent neurons

Cordoba-Rodriguez

Moore

Kao

et al. 1999

Proc. Natl. Acad. Sci. U.S.A.

109

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Activation of distinct classes of potassium channels can dramatically affect the frequency and the pattern of neuronal firing. In a subpopulation of vagal afferent neurons (nodose ganglion neurons), the pattern of impulse activity is effectively modulated by a Ca 2؉ -dependent K ؉ current. This current produces a post-spike hyperpolarization (AHP slow ) that plays a critical role in the regulation of membrane excitability and is responsible for spike-frequency accommodation in these neurons. Inhibition of the AHP slow by a number of endogenous autacoids (e.g., histamine, serotonin, prostanoids, and bradykinin) results in an increase in the firing frequency of vagal afferent neurons from <0.1 to >10 Hz. After a single action potential, the AHP slow in nodose neurons displays a slow rise time to peak (0.3-0.5 s) and a long duration (3-15 s Activation and sensitization of primary afferent nerve fibers during allergic inflammation are orchestrated by inflammatory mediators released from various cells, including tissue mast cells. Inf lammatory mediators provoke excitability changes in sensory nerves through diverse mechanisms, including (i) modification of the density and coupling efficacy of ligand-gated ionic channels; (ii) alteration in voltage-gated sodium, potassium, and calcium channels; and (iii) manipulation of cellular mechanisms that control spike-frequency adaptation.After immunologic activation of mast cells in airway in vivo or in sensory ganglia in vitro, a wide range of electrophysiological changes can be detected in peripheral sensory nerve terminals of the vagus (1) and in vagal primary afferent somata (located in the nodose and jugular ganglia) (2). These changes range from transient (minutes) membrane depolarizations that sometimes reach action potential (AP) threshold (3) to a sustained (days) unmasking of functional NK-2 tachykinin receptors (4, 5). One electrical membrane property that is particularly sensitive to inflammatory mediators is a slow post-spike afterhyperpolarization (AHP slow ; see Fig. 1 ) (3).This slow afterpotential influences neuronal excitability and determines the frequency and pattern of neuronal discharge. We have found that the amplitude and duration of the AHP slow are exquisitely sensitive to known inflammatory mediators such as prostanoids, amines, and kinins applied exogenously (Table 1) or released endogenously (i.e., after immunologic activation of mast cells) (3, 6). Inhibition of the AHP slow is accompanied by a loss of spike-frequency adaptation. Thus, modulation of the AHP slow amplitude and duration provides a mechanism for neuronal sensitization.We are interested in identifying the ionic channels and second-messenger transduction pathways that participate in the initiation and maintenance of the AHP slow in vagal primary afferent neurons. In this report, we describe the general properties of this slow afterpotential and our progress in its characterization. Our working hypothesis is that a close functional proximity between three separate channels [N t...

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Section: Resultsmentioning

confidence: 93%

Calcium regulation of a slow post-spike hyperpolarization in vagal afferent neurons

Cordoba-Rodriguez

Moore

Kao

et al. 1999

Proc. Natl. Acad. Sci. U.S.A.

109

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“…Importantly, cADPR/ryanodine-sensitive stores are also responsible for the Ca 2ϩ -induced Ca 2ϩ release triggered by action potentials (36, for review see ref 50). Hence, the elevations in [Ca 2ϩ ] i reported here may be expected to boost the action-potential evoked Ca 2ϩ transients and transmitter release, as found in the nodose ganglion cells (58) or neuroblastoma cell lines (59,60). Whether the NO-cGMP-cADPR-Ca 2ϩ pathway is sufficiently powerful to lead to action potential-independent GABA release is at present unclear, although some data suggest that this might be the case, at least in the hypothalamus (17).…”

Section: Ca 2؉ Release From Cadpr-ryanodine Sensitive Stores Is a Keymentioning

confidence: 87%

Mechanism of nitric oxide action on inhibitory GABAergic signaling within the nucleus tractus solitarii

Wang

Teschemacher²,

Paton³

et al. 2006

FASEB j.

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The cellular mechanisms mediating nitric oxide (NO) modulation of the inhibitory transmission in the nucleus tractus solitarii (NTS) remain unclear, even though this could be extremely important for various physiological and pathological processes. Specifically, in the NTS NO-evoked glutamate and gamma-aminobutyric acid (GABA) release might contribute to pathological hypertension. In cultured rat brainstem slices, NTS GABAergic neurons were targeted using an adenoviral vector to express enhanced green fluorescent protein and studied with a combination of patch clamp and confocal microscopy. Low nanomolar concentrations of NO increased intracellular Ca2+ concentration ([Ca2+]i) in somata, dendrites, and putative axons of GABAergic neurons, with axons being the most sensitive compartment. This effect was cGMP mediated and not related to depolarization or indirect presynaptic effects on glutamatergic transmission. Blockade of the cyclic adenosine diphosphate ribose (cADPR)/ryanodine-sensitive stores but not the inositol triphosphate-sensitive stores, inhibited NO effect. Since cADPR/ryanodine-sensitive stores are implicated in the Ca2+-induced Ca2+ release, NO can be expected to potentiate GABA release. In support of this notion, a cADPR antagonist abolished the NO-induced potentiation of GABAergic inhibitory postsynaptic potentials in the NTS. Thus, the NO-cGMP-cADPR-Ca2+ pathway, previously described in sea urchin eggs, also operates in mammalian GABAergic neurons. Potentiation of GABA release by NO may have implications for numerous brain functions.

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“…The large contribution of IK,Ca activated by superficial CICR to the negative feedback of membrane excitability andÏor the regulation of action potential shape is characteristic of smooth muscle cells (Imaizumi et al 1996a). Although the regulation of membrane excitability by CICR from SRÏER via activation of IK,Ca has been reported in some neurons (Kuba, 1994;Yoshizaki et al 1995;Cohen, Moore, Bangalore, Jafri, Weinreich & Kao, 1997), high time-resolution spatial analyses of Ca¥ release from the SRÏER have not yet been done.…”

Section: Discussionmentioning

confidence: 99%

Ca²⁺ images and K⁺ current during depolarization in smooth muscle cells of the guinea‐pig vas deferens and urinary bladder

Imaizumi

Torii

Ohi

et al. 1998

The Journal of Physiology

118

134

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Electrical events and intracellular calcium concentration ([Ca2+]) imaged using fluo‐3 and laser scanning confocal microscopy were simultaneously monitored in single smooth muscle cells freshly isolated from guinea‐pig vas deferens or urinary bladder. Images obtained every 8 ms, during stepping from ‐60 to 0 or +10 mV for 50 ms under voltage clamp, showed that a rise in [Ca2+] could be detected within 20 ms of depolarization in five to twenty small (< 2 μm diameter) ‘hot spots’, over 95 % of which were located within 1.5 μm of the cell membrane. Depolarization at 30 s intervals activated hot spots at the same places. Cd2+ or verapamil abolished both hot spots and Ca2+‐activated K+ current (IK,Ca). Caffeine almost abolished hot spots and markedly reduced IK,Ca. Cyclopiazonic acid, which raised basal global [Ca2+], decreased the rise in hot spot [Ca2+] and IK,Ca amplitude during depolarization. These results suggest that Ca2+ entry caused Ca2+‐induced Ca2+ release (CICR). Under voltage clamp, hot spot [Ca2+] closely paralleled the rise in IK,Ca and reached a peak within 20 ms of the start of depolarization, but the rise in global [Ca2+] over the whole cell area was much slower. Step depolarization to potentials positive to ‐20 mV caused hot spots to grow in size and coalesce, leading to a rise in global [Ca2+] and contraction. Ca2+ hot spots also occurred during the up‐stroke of an evoked action potential under current clamp. It is concluded that the entry of Ca2+ in the early stages of an action potential evokes CICR from discrete subplasmalemma Ca2+ storage sites and generates hot spots that spread to initiate a contraction. The activation of Ca2+‐dependent K+ channels in the plasmalemma over hot spots initiates IK,Ca and action potential repolarization.

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Ca(2+)‐induced Ca2+ release mediates Ca2+ transients evoked by single action potentials in rabbit vagal afferent neurones.

Cited by 47 publications

References 41 publications

Calcium regulation of a slow post-spike hyperpolarization in vagal afferent neurons

Calcium regulation of a slow post-spike hyperpolarization in vagal afferent neurons

Mechanism of nitric oxide action on inhibitory GABAergic signaling within the nucleus tractus solitarii

Ca²⁺ images and K⁺ current during depolarization in smooth muscle cells of the guinea‐pig vas deferens and urinary bladder

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Ca(2+)‐induced Ca2+ release mediates Ca2+ transients evoked by single action potentials in rabbit vagal afferent neurones.

Cited by 47 publications

References 41 publications

Calcium regulation of a slow post-spike hyperpolarization in vagal afferent neurons

Calcium regulation of a slow post-spike hyperpolarization in vagal afferent neurons

Mechanism of nitric oxide action on inhibitory GABAergic signaling within the nucleus tractus solitarii

Ca2+ images and K+ current during depolarization in smooth muscle cells of the guinea‐pig vas deferens and urinary bladder

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Ca²⁺ images and K⁺ current during depolarization in smooth muscle cells of the guinea‐pig vas deferens and urinary bladder