A Cav3.2/Syntaxin-1A Signaling Complex Controls T-type Channel Activity and Low-threshold Exocytosis

Weiss, Norbert; Hameed, Shahid; Fernández-Fernández, José M.; Fablet, Katell; Karmažínová, Mária; Poillot, Cathy; Proft, Juliane; Chen, Lina; Bidaud, Isabelle; Monteil, Arnaud; Huc-Brandt, Sylvaine; Lacinová, Ľubica; Lory, Philippe; Zamponi, Gerald W.; Waard, Michel De

doi:10.1074/jbc.m111.290882

Cited by 116 publications

(78 citation statements)

References 51 publications

(43 reference statements)

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“…3Ab, 58 ) 57 and Cav3.1 channels are expressed at the terminals of inhibitory parvalbumin-positive interneuron in the CA1 hippocampal region. 66 In addition, Cav3.2 channels colocalize with proteins involved in synaptic release as syntaxin 1A in NRT neurons 67 while T-type channels are associated with syntaxin-1A and SNAP-25 in chromafin cells. 68 Functionally, Cav3.2 channels localized in layer III presynaptic-terminals of the entorhinal cortex were shown to contribute to the spontaneous release of glutamate (Fig.…”

Section: Subcellular Localization Of T-type Channels and Synaptic Plamentioning

confidence: 99%

T-type calcium channels in synaptic plasticity

Leresche

Lambert

2016

Channels

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The role of T-type calcium currents is rarely considered in the extensive literature covering the mechanisms of long-term synaptic plasticity. This situation reflects the lack of suitable T-type channel antagonists that till recently has hampered investigations of the functional roles of these channels. However, with the development of new pharmacological and genetic tools, a clear involvement of T-type channels in synaptic plasticity is starting to emerge. Here, we review a number of studies showing that T-type channels participate to numerous homo-and heterosynaptic plasticity mechanisms that involve different molecular partners and both pre-and postsynaptic modifications. The existence of T-channel dependent and independent plasticity at the same synapse strongly suggests a subcellular localization of these channels and their partners that allows specific interactions. Moreover, we illustrate the functional importance of T-channel dependent synaptic plasticity in neocortex and thalamus.

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Section: Subcellular Localization Of T-type Channels and Synaptic Plamentioning

confidence: 99%

T-type calcium channels in synaptic plasticity

Leresche

Lambert

2016

Channels

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“…It has been demonstrated that this co-localization is achieved using a specific interaction between HVA channels (Cav2.1 and Cav2.2) and SNARE proteins (syntaxin-1, SNAP-25 and synaptotagmin-1), through an interaction site called a synprint. It has recently been shown, that although T-type calcium channels lack this synprint interaction site, they closely associate with syntaxin-1A in central neurons [95]. This association between syntaxin-1A and Cav3.2 was also demonstrated in the same study to be essential for low-threshold exocytosis in chromaffin cells.…”

Section: Role Of T-type Calcium Channels In Secretionmentioning

confidence: 57%

Expression and Role of T-type Calcium Channels during Neuroendocrine Differentiation

Warnier¹,

Gackière²,

Roudbaraki³

et al. 2017

J Cell Signal

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Neuroendocrine cells release their secretion into the extracellular environment through calcium-dependent signalling pathways. These cells share common morphological and molecular features such as the expression of specific biomarkers, neurite outgrowth and dense core secretory granules. In order to elucidate the signalling pathways leading from undifferentiated to differentiated neuroendocrine cells, the role of voltage-dependent calcium channels, central actors in the excitation-secretion coupling, has been comprehensively investigated. T-type calcium channels appear to belong to the most important ion channel family involved in the neuroendocrine differentiation process. They could also participate in the development of neuroendocrine tumours.

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“…Hence, these T-type channels can be active in pinealocytes in their resting state, where they can contribute to changes in membrane potential and promote calcium flux. Work from our own laboratory has revealed that Cav3 calcium channels physically interact with syntaxin 1A, a key protein involved in vesicle release, and that this interaction supports low threshold exocytosis in chromaffin cells (Weiss et al 2012). We thus speculate that Cav3.1 channels may have a similar excretory function in the pineal gland, i.e.…”

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confidence: 70%