Presynaptic BK type Ca2+-activated K+ channels are involved in prostanoid TP receptor-mediated inhibition of noradrenaline release from the rat gastric sympathetic nerves

Nakamura, Kumiko; Yokotani, Kunihiko

doi:10.1016/j.ejphar.2009.11.056

Cited by 3 publications

(1 citation statement)

References 55 publications

(24 reference statements)

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“…Group I mGluR activation can lead to the release of Ca 2+ from internal stores (Frenguelli et al, 1993; Kettunen et al, 2002; Larkum et al, 2003; Topolnik et al, 2009; Plotkin et al, 2013). Release from internal stores has been shown to activate Ca 2+ -dependent K + channels in many neurons and species (Kawai and Watanabe, 1989; Akita and Kuba, 2000; Yamada et al, 2004; Faber, 2010; Nakamura and Yokotani, 2010). It is unknown if such combinatory mechanisms are present in lamprey spinal neurons, but lamprey neurons do possess all the necessary components.…”

Section: Dendritic Ca2+ Signaling Is Dynamic and Determined By Cellulmentioning

confidence: 99%

A synaptic mechanism for network synchrony

Alford

Alpert

2014

Front. Cell. Neurosci.

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Within neural networks, synchronization of activity is dependent upon the synaptic connectivity of embedded microcircuits and the intrinsic membrane properties of their constituent neurons. Synaptic integration, dendritic Ca2+ signaling, and non-linear interactions are crucial cellular attributes that dictate single neuron computation, but their roles promoting synchrony and the generation of network oscillations are not well understood, especially within the context of a defined behavior. In this regard, the lamprey spinal central pattern generator (CPG) stands out as a well-characterized, conserved vertebrate model of a neural network (Smith et al., 2013a), which produces synchronized oscillations in which neural elements from the systems to cellular level that control rhythmic locomotion have been determined. We review the current evidence for the synaptic basis of oscillation generation with a particular emphasis on the linkage between synaptic communication and its cellular coupling to membrane processes that control oscillatory behavior of neurons within the locomotor network. We seek to relate dendritic function found in many vertebrate systems to the accessible lamprey central nervous system in which the relationship between neural network activity and behavior is well understood. This enables us to address how Ca2+ signaling in spinal neuron dendrites orchestrate oscillations that drive network behavior.

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Section: Dendritic Ca2+ Signaling Is Dynamic and Determined By Cellulmentioning

confidence: 99%

A synaptic mechanism for network synchrony

Alford

Alpert

2014

Front. Cell. Neurosci.

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Involvement of presynaptic voltage-dependent Kv3 channel in endothelin-1-induced inhibition of noradrenaline release from rat gastric sympathetic nerves

Nakamura

Shimizu

Tanaka

et al. 2012

European Journal of Pharmacology

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Interactions between thromboxane A2, thromboxane/prostaglandin (TP) receptors, and endothelium-derived hyperpolarization

Ellinsworth

Shukla

Fleming

et al. 2014

Cardiovascular Research

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Endothelium-dependent smooth muscle hyperpolarization (EDH) increasingly predominates over endothelium-derived nitric oxide (NO) as a participant in vasodilation as vessel size decreases. Its underlying nature is highly variable between vessel types, species, disease states, and exact experimental conditions, and is variably mediated by one or more transferable endothelium-derived hyperpolarizing factors and/or the electrotonic spread of endothelial hyperpolarization into the media via gap junctions. Although generally regarded (and studied) as a mechanism that is independent of NO and prostanoids, evidence has emerged that the endothelium-derived contracting factor and prostanoid thromboxane A2 can modulate several signalling components central to EDH, and therefore potentially curtail vasodilation through mechanisms that are distinct from those putatively involved in direct smooth muscle contraction. Notably, vascular production of thromboxane A2 is elevated in a number of cardiovascular disease states that promote endothelial dysfunction. This review will therefore discuss the mechanisms through which thromboxane A2 interacts with and modulates EDH, and will also consider the implications of such cross-talk in vasodilator control in health and disease.

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Presynaptic BK type Ca2+-activated K+ channels are involved in prostanoid TP receptor-mediated inhibition of noradrenaline release from the rat gastric sympathetic nerves

Cited by 3 publications

References 55 publications

A synaptic mechanism for network synchrony

A synaptic mechanism for network synchrony

Involvement of presynaptic voltage-dependent Kv3 channel in endothelin-1-induced inhibition of noradrenaline release from rat gastric sympathetic nerves

Interactions between thromboxane A2, thromboxane/prostaglandin (TP) receptors, and endothelium-derived hyperpolarization

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