Dual regulation of heat-activated K+ channel in rat DRG neurons via α1 and β adrenergic receptors

Yamamoto, Satoshi; Kanno, Takeshi; Yamada, Kosaku; Yasuda, Yoh; Nishizaki, Tomoyuki

doi:10.1016/j.lfs.2009.05.009

Cited by 7 publications

(7 citation statements)

References 22 publications

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“…These channels may also be present in the plasma membrane of the cell bodies, where they are experimentally more accessible than in the much smaller terminals embedded in the peripheral tissues. Electrophysiological experiments on DRG or trigeminal neuron preparations using pharmacological agents of limited selectivity provided data in favor of (287), but also against (318,346), the contribution of TREK and TRAAK channels to the temperature-dependent K ϩ conductance changes. Recently, however, this apparent controversy was resolved by the application of gene knockout animals.…”

Section: Silencing Of Thermal and Mechanical Nociceptionmentioning

confidence: 99%

Molecular Background of Leak K⁺Currents: Two-Pore Domain Potassium Channels

Enyedi

Czirják

2010

Physiological Reviews

776

769

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Two-pore domain K+ (K2P) channels give rise to leak (also called background) K+ currents. The well-known role of background K+ currents is to stabilize the negative resting membrane potential and counterbalance depolarization. However, it has become apparent in the past decade (during the detailed examination of the cloned and corresponding native K2P channel types) that this primary hyperpolarizing action is not performed passively. The K2P channels are regulated by a wide variety of voltage-independent factors. Basic physicochemical parameters (e.g., pH, temperature, membrane stretch) and also several intracellular signaling pathways substantially and specifically modulate the different members of the six K2P channel subfamilies (TWIK, TREK, TASK, TALK, THIK, and TRESK). The deep implication in diverse physiological processes, the circumscribed expression pattern of the different channels, and the interesting pharmacological profile brought the K2P channel family into the spotlight. In this review, we focus on the physiological roles of K2P channels in the most extensively investigated cell types, with special emphasis on the molecular mechanisms of channel regulation.

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Section: Silencing Of Thermal and Mechanical Nociceptionmentioning

confidence: 99%

Molecular Background of Leak K⁺Currents: Two-Pore Domain Potassium Channels

Enyedi

Czirják

2010

Physiological Reviews

776

769

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“…From studies in a variety of systems we know that each of GPCRs affects a different complement of target ion channels. For example, NE binding to α-1 NE receptors (GqPCRs) suppress Cs + - sensitive K + channels in human osteoblast, Ba 2+ - and TEA-sensitive heat-activated K + channels in rat DRG neuron, and cardiac delayed rectifier K + currents (262, 583, 605). α-2 NE receptors (GiPCRs) modulate, for example, N-type voltage-gated Ca 2+ channels in cultured cerebellar neurons, delayed-rectifier K + current, and Na + current in rat sympathetic neurons (73, 292).…”

Section: G-protein Coupled Receptors and The Modulation Of Cellular Pmentioning

confidence: 99%

“…α-2 NE receptors (GiPCRs) modulate, for example, N-type voltage-gated Ca 2+ channels in cultured cerebellar neurons, delayed-rectifier K + current, and Na + current in rat sympathetic neurons (73, 292). β-NE receptors (GsPCRs) inhibit Ba 2+ - and TEA-sensitive heat-activated K + channels in rat DRG neurons (605). Within the respiratory network, we know that NE produces differential modulation on the two main types of respiratory pacemakers, resulting in an amplitude modulation of CS bursting pacemakers and frequency modulation for CI bursting pacemakers (578), but how exactly modulation of these bursting mechanisms is achieved remains unknown.…”

Section: G-protein Coupled Receptors and The Modulation Of Cellular Pmentioning

confidence: 99%

The Cellular Building Blocks of Breathing

Ramirez

Doi

Garcia

et al. 2012

Comprehensive Physiology

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Respiratory brainstem neurons fulfill critical roles in controlling breathing: they generate the activity patterns for breathing and contribute to various sensory responses including changes in O2 and CO2. These complex sensorimotor tasks depend on the dynamic interplay between numerous cellular building blocks that consist of voltage-, calcium-, and ATP-dependent ionic conductances, various ionotropic and metabotropic synaptic mechanisms, as well as neuromodulators acting on G-protein coupled receptors and second messenger systems. As described in this review, the sensorimotor responses of the respiratory network emerge through the state-dependent integration of all these building blocks. There is no known respiratory function that involves only a small number of intrinsic, synaptic, or modulatory properties. Because of the complex integration of numerous intrinsic, synaptic, and modulatory mechanisms, the respiratory network is capable of continuously adapting to changes in the external and internal environment, which makes breathing one of the most integrated behaviors. Not surprisingly, inspiration is critical not only in the control of ventilation, but also in the context of “inspiring behaviors” such as arousal of the mind and even creativity. Far-reaching implications apply also to the underlying network mechanisms, as lessons learned from the respiratory network apply to network functions in general.

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“…2 Briefly, nociception seems to involve protein kinase C 3 and Gq protein via α 1 adrenergic receptors and Gs protein and protein kinase A activation to β adrenoceptors. 4 Data obtained by our group demonstrated that the peripheral antinociceptive effect of the adrenoceptor agonist xylazine involves the activation of α 2C adrenoreceptor 5 thus inducing nitric oxide synthase to produce nitric oxide with a subsequent increase of cyclic guanosine monophosphate in peripheral nociceptors 6 and opening of adenosine triphosphate-sensitive K + channels. 7 Activation of the β adrenoceptor is responsible for analgesia in patients with rheumatoid arthritis 8 and in rats with adjuvant-induced arthritis.…”

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confidence: 96%