Atypical Ca2+ currents in chromaffin cells from SHR and WKY rat strains result from the deficient expression of a splice variant of the α1D Ca2+ channel

Segura-Chama, Pedro; Rivera-Cerecedo, Claudia V.; González‐Ramírez, Ricardo; Felix, Ricardo; Hernández‐Guijo, Jesús M.; Hernández‐Cruz, Arturo

doi:10.1152/ajpheart.00849.2011

Cited by 8 publications

(2 citation statements)

References 42 publications

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“…In previous papers, we characterized the Ca 2+ ‐currents expressed in acute adrenal slices (Segura‐Chama et al . , ; Hernández et al . ), Now, we identify the Ca 2+ ‐channel subtypes that control the activation of Ca 2+ ‐activated K + ‐channels after Ca 2+ ‐influx.…”

Section: Discussionmentioning

confidence: 99%

Different contributions of calcium channel subtypes to electrical excitability of chromaffin cells in rat adrenal slices

Albiñana

Segura-Chama²,

Baraibar

et al. 2015

Journal of Neurochemistry

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We characterized the ionic currents underlying the cellular excitability and the Ca 2+ -channel subtypes involved in action potential (AP) firing of rat adrenal chromaffin cells (RCCs) preserved in their natural environment, the adrenal gland slices, through the perforated patch-clamp recording technique. RCCs prepared from adrenal slices exhibit a resting potential of À54 mV, firing spontaneous APs (2-3 spikes/s) generated by the opening of Na + and Ca 2+ -channels, and terminated by the activation of voltage and Ca-channels is involved in reaching threshold potential for AP firing, and is responsible for activation of BK-channels contributing to APrepolarization and afterhyperpolarization, whereas P/Q-type Ca 2+ -channels are involved only in the repolarization phase. BK-channels carry total outward current during AP-repolarization. Blockade of L-type Ca 2+ -channels reduces BK-current 60%, whereas blockade of N-or P/Q-type produces little effect. This study demonstrates that Ca 2+ influx through L-type Ca 2+ -channels plays a key role in modulating the threshold potential from RCCs in situ.

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Section: Discussionmentioning

confidence: 99%

Different contributions of calcium channel subtypes to electrical excitability of chromaffin cells in rat adrenal slices

Albiñana

Segura-Chama²,

Baraibar

et al. 2015

Journal of Neurochemistry

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“…Although T-type channel antagonist might have different specificity in turtle tissue, it should be noted, however, that NNC55-0396 may inhibit T-type channel activity in several biological preparations. Hence, the drug has been shown to block both recombinant Ca V 3 channels expressed in HEK-293 cells [23], [24], [29] as well as native T-type channels expressed in 3T3-L1 preadipocytes [30], as well as the Ca 2+ transients associated to T-type channel activity in human myometrium [31] and pregnant rat uterine smooth muscle [32]. NNC55-0396 also blocks T-type Ca 2+ channel-mediated rebound firing cerebellar neurons [33] and the T-type channel-mediated response to nerve stimulation in rat vas deferens [34].…”

Section: Discussionmentioning

confidence: 99%

Functional Expression of T-Type Ca2+ Channels in Spinal Motoneurons of the Adult Turtle

et al. 2014

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Voltage-gated Ca2+ (CaV) channels are transmembrane proteins comprising three subfamilies named CaV1, CaV2 and CaV3. The CaV3 channel subfamily groups the low-voltage activated Ca2+ channels (LVA or T-type) a significant role in regulating neuronal excitability. CaV3 channel activity may lead to the generation of complex patterns of action potential firing such as the postinhibitory rebound (PIR). In the adult spinal cord, these channels have been found in dorsal horn interneurons where they control physiological events near the resting potential and participate in determining excitability. In motoneurons, CaV3 channels have been found during development, but their functional expression has not yet been reported in adult animals. Here, we show evidence for the presence of CaV3 channel-mediated PIR in motoneurons of the adult turtle spinal cord. Our results indicate that Ni2+ and NNC55-0396, two antagonists of CaV3 channel activity, inhibited PIR in the adult turtle spinal cord. Molecular biology and biochemical assays revealed the expression of the CaV3.1 channel isotype and its localization in motoneurons. Together, these results provide evidence for the expression of CaV3.1 channels in the spinal cord of adult animals and show also that these channels may contribute to determine the excitability of motoneurons.

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Enhanced Ca2+-induced Ca2+ release from intracellular stores contributes to catecholamine hypersecretion in adrenal chromaffin cells from spontaneously hypertensive rats

Segura-Chama

López-Bistrain

Pérez-Armendáriz

et al. 2015

Pflugers Arch - Eur J Physiol

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Adrenal chromaffin cells (CCs) from spontaneously hypertensive rats (SHRs) secrete more catecholamine (CA) upon stimulation than CCs from normotensive Wistar Kyoto rats (WKY). Unitary CA exocytosis events, both spontaneous and stimulated, were amperometrically recorded from cultured WKY and SHR CCs. Both strains display spontaneous amperometric spikes but SHR CCs produce more spikes and of higher mean amplitude. After a brief stimulation with high K(+) or caffeine which produces voltage-gated Ca(2+) influx or intracellular Ca(2+) release, respectively, more spikes and of greater mean amplitude and unitary charge were recorded in SHR CCs. Consequently, peak cumulative charge was ~2-fold higher in SHR CCs. Ryanodine (10 μM), a specific blocker of the ryanodine receptors reduced depolarization-induced peak cumulative charge by ~10 % in WKY and ~77 % in SHR CCs, suggesting, a larger contribution of Ca(2+)-induced Ca(2+) release to CA exocytosis in SHR CCs. Accordingly, Ca(2+) imaging showed larger [Ca(2+)]i signals induced both by depolarization and caffeine in SHR CCs. Distribution amplitude histograms showed that small amperometric spikes (0-50 pA) are more frequent in WKY than in SHR CCs. Conversely, medium (50-190 pA) and large (190-290 pA) spikes are more numerous in SHR than in WKY CCs. This study reveals that the enhanced CA secretion in SHR CCs results from a combination of (1) larger depolarization-induced Ca(2+) transients, due to a greater Ca(2+)-induced intracellular Ca(2+) release, (2) more exocytosis events per time unit, and (3) a greater proportion of medium and large amperometric spikes probably due to a higher mean CA content per granule. Enhanced CA release by excessive amplification by Ca(2+) induced Ca(2+) release and larger granule catecholamine content contributes to the increased CA plasma levels and vasomotor tone in SHRs.

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Atypical Ca²⁺ currents in chromaffin cells from SHR and WKY rat strains result from the deficient expression of a splice variant of the α_1D Ca²⁺ channel

Cited by 8 publications

References 42 publications

Different contributions of calcium channel subtypes to electrical excitability of chromaffin cells in rat adrenal slices

Different contributions of calcium channel subtypes to electrical excitability of chromaffin cells in rat adrenal slices

Functional Expression of T-Type Ca2+ Channels in Spinal Motoneurons of the Adult Turtle

Enhanced Ca2+-induced Ca2+ release from intracellular stores contributes to catecholamine hypersecretion in adrenal chromaffin cells from spontaneously hypertensive rats

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