Transcriptional Regulation of T-type Calcium Channel CaV3.2

Loo, Karen M.J. van; Schaub, Christina; Pernhorst, Katharina; Yaari, Yoel; Beck, Hanno; Schoch, Susanne; Becker, Albert

doi:10.1074/jbc.m111.310763

Cited by 66 publications

(32 citation statements)

References 53 publications

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“…A consistent finding in our experiments was the suppression of frequency bands adjacent to the theta peak. Notably, slow oscillations between 1 and 3 Hz were suppressed, similar to results obtained in visual cortex during stimulation of basal forebrain cholinergic neurons (Pinto et al, 2013).…”

Section: Discussionsupporting

confidence: 66%

“…Nevertheless, a more precise timing of CA3 neuron firing might promote plasticity in either the autoassociative CA3 network or in CA3-CA1 projections (Pavlides et al, 1988;Hölscher et al, 1997;Orr et al, 2001;Hyman et al, 2003). Such an effect has been observed in the human medial temporal lobe and is predictive of subsequent memory performance (Rutishauser et al, 2010). In monkeys, phase locking of single unit activity was observed in the cortex during working memory tasks and this is likewise predictive of memory performance (Liebe et al, 2012).…”

Section: Discussionmentioning

confidence: 90%

“…When more extensive lesions of either the MSDB or the fimbriafornix pathway were performed in urethane-anesthetized animals (Andersen et al, 1979) or awake animals (Green and Arduini, 1954;Donovick, 1968;Rawlins et al, 1979), hippocampal theta rhythms were completely abolished. Likewise, global inhibition of MSDB activity in freely moving animals eliminates theta oscillations (Chrobak et al, 1989;Lawson and Bland, 1993;Givens and Olton, 1994).…”

Section: Introductionmentioning

confidence: 99%

“…The presence of rhythmically bursting cells in the MSDB, initially discovered in rabbits (Petsche et al, 1962;Stumpf et al, 1962), gave rise to the hypothesis that the MSDB serves as a "pacemaker" for the hippocampal theta rhythm. Indeed, lowerfrequency theta oscillations (3-6 Hz) during alert immobility and under urethane anesthesia are fully abolished by muscarinic blocker injection into the MSDB (Kramis et al, 1975).…”

Section: Introductionmentioning

confidence: 99%

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Synergy of Direct and Indirect Cholinergic Septo-Hippocampal Pathways Coordinates Firing in Hippocampal Networks

Dannenberg¹,

Pabst²,

Braganza³

et al. 2015

J. Neurosci.

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131

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The medial septum/diagonal band of Broca complex (MSDB) is a key structure that modulates hippocampal rhythmogenesis. Cholinergic neurons of the MSDB play a central role in generating and pacing theta-band oscillations in the hippocampal formation during exploration, novelty detection, and memory encoding. How precisely cholinergic neurons affect hippocampal network dynamics in vivo, however, has remained elusive. In this study, we show that stimulation of cholinergic MSDB neurons in urethane-anesthetized mice acts on hippocampal networks via two distinct pathways. A direct septo-hippocampal cholinergic projection causes increased firing of hippocampal inhibitory interneurons with concomitantly decreased firing of principal cells. In addition, cholinergic neurons recruit noncholinergic neurons within the MSDB. This indirect pathway is required for hippocampal theta synchronization. Activation of both pathways causes a reduction in pyramidal neuron firing and a more precise coupling to the theta oscillatory phase. These two anatomically and functionally distinct pathways are likely relevant for cholinergic control of encoding versus retrieval modes in the hippocampus.

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Section: Discussionsupporting

confidence: 66%

Section: Discussionmentioning

confidence: 90%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Synergy of Direct and Indirect Cholinergic Septo-Hippocampal Pathways Coordinates Firing in Hippocampal Networks

Dannenberg¹,

Pabst²,

Braganza³

et al. 2015

J. Neurosci.

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131

155

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“…7,8 Over the last few years, various pathways and mechanisms underlying the modulation of T-type channels have been identified. [9][10][11] Besides numerous small molecules that acutely modulate channel activity, 12 T-type channels are subject to regulation at the levels of transcription, [13][14][15] alternative splicing, [16][17][18][19] protein interaction, [20][21] and post-translational modification including ubiquitination 22 and phosphorylation. 23 In addition, asparagine (N)-linked glycosylation has emerged as an essential level of control of T-type channel expression.…”

Section: Introductionmentioning

confidence: 99%

Modulation of Ca_v3.2 T-type calcium channel permeability by asparagine-linked glycosylation

et al. 2016

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Low-voltage-gated T-type calcium channels are expressed throughout the nervous system where they play an essential role in shaping neuronal excitability. Defects in T-type channel expression have been linked to various neuronal disorders including neuropathic pain and epilepsy. Currently, little is known about the cellular mechanisms controlling the expression and function of T-type channels. Asparagine-linked glycosylation has recently emerged as an essential signaling pathway by which the cellular environment can control expression of T-type channels. However, the role of N-glycans in the conducting function of T-type channels remains elusive. In the present study, we used human Ca v 3.2 glycosylation-deficient channels to assess the role of N-glycosylation on the gating of the channel. Patch-clamp recordings of gating currents revealed that N-glycans attached to hCa v 3.2 channels have a minimal effect on the functioning of the channel voltage-sensor. In contrast, N-glycosylation on specific asparagine residues may have an essential role in the conducting function of the channel by enhancing the channel permeability and / or the pore opening of the channel. Our data suggest that modulation of N-linked glycosylation of hCa v 3.2 channels may play an important physiological role, and could also support the alteration of T-type currents observed in disease states.

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Roles of Ca_v3.2 and TRPA1 channels targeted by hydrogen sulfide in pancreatic nociceptive processing in mice with or without acute pancreatitis

Terada

Fujimura

Nishimura

et al. 2014

J of Neuroscience Research

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Hydrogen sulfide (H(2)S), formed by multiple enzymes, including cystathionine-γ-lyase (CSE), targets Ca(v)3.2 T-type Ca(2+) channels (T channels) and transient receptor potential ankyrin-1 (TRPA1), facilitating somatic pain. Pancreatitis-related pain also appears to involve activation of T channels by H(2)S formed by the upregulated CSE. Therefore, this study investigates the roles of the Ca(v)3.2 isoform and/or TRPA1 in pancreatic nociception in the absence and presence of pancreatitis. In anesthetized mice, AP18, a TRPA1 inhibitor, abolished the Fos expression in the spinal dorsal horn caused by injection of a TRPA1 agonist into the pancreatic duct. As did mibefradil, a T-channel inhibitor, in our previous report, AP18 prevented the Fos expression following ductal NaHS, an H(2)S donor. In the mice with cerulein-induced acute pancreatitis, the referred hyperalgesia was suppressed by NNC 55-0396 (NNC), a selective T-channel inhibitor; zinc chloride; or ascorbic acid, known to inhibit Ca(v)3.2 selectively among three T-channel isoforms; and knockdown of Ca(v)3.2. In contrast, AP18 and knockdown of TRPA1 had no significant effect on the cerulein-induced referred hyperalgesia, although they significantly potentiated the antihyperalgesic effect of NNC at a subeffective dose. TRPA1 but not Ca(v)3.2 in the dorsal root ganglia was downregulated at a protein level in mice with cerulein-induced pancreatitis. The data indicate that TRPA1 and Ca(v)3.2 mediate the exogenous H(2)S-induced pancreatic nociception in naïve mice and suggest that, in the mice with pancreatitis, Ca(v)3.2 targeted by H(2)S primarily participates in the pancreatic pain, whereas TRPA1 is downregulated and plays a secondary role in pancreatic nociceptive signaling.

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Transcriptional Regulation of T-type Calcium Channel CaV3.2

Cited by 66 publications

References 53 publications

Synergy of Direct and Indirect Cholinergic Septo-Hippocampal Pathways Coordinates Firing in Hippocampal Networks

Synergy of Direct and Indirect Cholinergic Septo-Hippocampal Pathways Coordinates Firing in Hippocampal Networks

Modulation of Ca_v3.2 T-type calcium channel permeability by asparagine-linked glycosylation

Roles of Ca_v3.2 and TRPA1 channels targeted by hydrogen sulfide in pancreatic nociceptive processing in mice with or without acute pancreatitis

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Transcriptional Regulation of T-type Calcium Channel CaV3.2

Cited by 66 publications

References 53 publications

Synergy of Direct and Indirect Cholinergic Septo-Hippocampal Pathways Coordinates Firing in Hippocampal Networks

Synergy of Direct and Indirect Cholinergic Septo-Hippocampal Pathways Coordinates Firing in Hippocampal Networks

Modulation of Cav3.2 T-type calcium channel permeability by asparagine-linked glycosylation

Roles of Cav3.2 and TRPA1 channels targeted by hydrogen sulfide in pancreatic nociceptive processing in mice with or without acute pancreatitis

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Modulation of Ca_v3.2 T-type calcium channel permeability by asparagine-linked glycosylation

Roles of Ca_v3.2 and TRPA1 channels targeted by hydrogen sulfide in pancreatic nociceptive processing in mice with or without acute pancreatitis