Immunological characterization of T-type voltage-dependent calcium channel CaV3.1 (alpha1G) and CaV3.3 (alpha1I) isoforms reveal differences in their localization, expression, and neural development

Yunker, Anne Marie R.; Sharp, Alan H.; SundarRaj, Swathi; Ranganathan, Vaishnavi; Copeland, Terry D.; McEnery, Maureen W.

doi:10.1016/s0306-4522(02)00936-3

Cited by 74 publications

(77 citation statements)

References 57 publications

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“…The dendritic calcium transients require Na + -dependent action potentials and are strongly dependent on the membrane potential, decreasing with depolarization and increasing with hyperpolarization from rest, which is consistent with the properties of T-type calcium channels (Egger et al 2003). T-type calcium channels are known to be expressed in GCs of the AOB (Yunker et al 2003). Taken together, the action of NA on the spike fidelity could enhance the dendritic calcium entry through NMDA receptors and possibly T-type calcium channels, boosting 10-Hz synaptic inputs and consequently shifting the threshold for LTP induction from 400 to 200 stimuli.…”

Section: Discussionsupporting

confidence: 75%

α₂-Adrenergic receptor activation promotes long-term potentiation at excitatory synapses in the mouse accessory olfactory bulb

et al. 2018

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The formation of mate recognition memory in mice is associated with neural changes at the reciprocal dendrodendritic synapses between glutamatergic mitral cell (MC) projection neurons and GABAergic granule cell (GC) interneurons in the accessory olfactory bulb (AOB). Although noradrenaline (NA) plays a critical role in the formation of the memory, the mechanism by which it exerts this effect remains unclear. Here we used extracellular field potential and whole-cell patchclamp recordings to assess the actions of bath-applied NA (10 µM) on the glutamatergic transmission and its plasticity at the MC-to-GC synapse in the AOB. Stimulation (400 stimuli) of MC axons at 10 Hz but not at 100 Hz effectively induced N-methyl-D-aspartate (NMDA) receptor-dependent long-term potentiation (LTP), which exhibited reversibility. NA paired with subthreshold 10-Hz stimulation (200 stimuli) facilitated the induction of NMDA receptor-dependent LTP via the activation of α 2 -adrenergic receptors (ARs). We next examined how NA, acting at α 2 -ARs, facilitates LTP induction. In terms of acute actions, NA suppressed GC excitatory postsynaptic current (EPSC) responses to single pulse stimulation of MC axons by reducing glutamate release from MCs via G-protein coupled inhibition of calcium channels. Consequently, NA reduced recurrent inhibition of MCs, resulting in the enhancement of evoked EPSCs and spike fidelity in GCs during the 10-Hz stimulation used to induce LTP. These results suggest that NA, acting at α 2 -ARs, facilitates the induction of NMDA receptor-dependent LTP at the MC-to-GC synapse by shifting its threshold through disinhibition of MCs.

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Section: Discussionsupporting

confidence: 75%

α₂-Adrenergic receptor activation promotes long-term potentiation at excitatory synapses in the mouse accessory olfactory bulb

et al. 2018

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“…First, T-type channel synthesis might increase because of impaired synaptic transmission caused by deficient SNAP25 expression or phosphorylation (Boschert et al, 1996;Genoud et al, 1999). Presynaptic release defects may lead to developmental differences in the transcriptional regulation of a heterogeneous population of T-type channel isoforms (Bertolesi et al, 2003;Yunker et al, 2003), which in turn have been shown to influence patterns of neuritogenesis during neuronal differentiation (Chemin et al, 2002). Although a minor increase in expression of Ca v 3.1/␣1G and Ca v 3.2/␣1H has been reported in adult GAERS (genetic absence epilepsy rats from Strasbourg) rats, a genetically undefined absence model (Talley et al, 2000), no alteration in the thalamic expression pattern of any of the three Ca v 3.1-3 genes that closely resemble the Cm/ϩ model or evidence for abnormal modulation have been detected (Zhang et al, 2002).…”

Section: Mechanisms For Enhanced Lva Currentmentioning

confidence: 99%

Elevated Thalamic Low-Voltage-Activated Currents Precede the Onset of Absence Epilepsy in the SNAP25-Deficient Mouse MutantColoboma

Zhang¹,

Vilaythong²,

Yoshor³

et al. 2004

J. Neurosci.

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Recessive mutations in genes encoding voltage-gated Ca 2ϩ channel subunits alter high-voltage-activated (HVA) calcium currents, impair neurotransmitter release, and stimulate thalamic low-voltage-activated (LVA) currents that contribute to a cortical spike-wave epilepsy phenotype in mice. We now report thalamic LVA current elevations in a non-Ca 2ϩ channel mutant. EEG analysis of Coloboma (Cm/؉), an autosomal dominant mutant mouse lacking one copy of the gene for a synaptosomal-associated protein (SNAP25) that interacts with HVA channels, reveals abnormal spike-wave discharges (SWDs) in the behaving animal. We compared the biophysical properties of both LVA and HVA currents in Cm/؉ and wild-type thalamic neurons and observed a 54% increase in peak current density of LVA currents evoked at Ϫ50 mV from Ϫ110 mV in Cm/؉ before the developmental onset of seizures relative to control. The midpoint voltage for steady-state inactivation of LVA currents in Cm/؉ was shifted in a depolarized direction by 8 mV before epilepsy onset, and the mean time constant for decay of LVA Ca 2ϩ currents at Ϫ50 mV was also prolonged. No significant differences were found in recovery from inactivation of LVA currents or in HVA current densities and kinetics. Our data demonstrate that a non-Ca 2ϩ channel subunit gene mutation leads to potentiated thalamic LVA currents that precede the appearance of SWDs and that altered somatodendritic HVA currents are not required for abnormal thalamocortical oscillations. We suggest that presynaptic release defects shared by these mutants lead to postsynaptic LVA excitability increases in thalamic pacemaker neurons that favor rebound bursting and absence epilepsy.

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“…Thus, a modest reduction in the levels of surface or total expression of Ca v 3.3 was observed when co-expressed with CatSper1 (although this did not achieve statistical significance p Ͻ 0.05). (17). Western blot analysis revealed that this antibody not only recognize cloned Ca v 3.3 expressed in HEK cells but also detected Ca v 3.3 expressed in human sperm and cerebral cortex (Fig.…”

Section: Identification Of Ca V 33 As a Catsper1-and Catsper2-associmentioning

confidence: 90%

Association of Catsper1 or -2 with Cav3.3 Leads to Suppression of T-type Calcium Channel Activity

Zhang

Saraf

Cassar

et al. 2006

Journal of Biological Chemistry

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Sperm-specific CatSper1 and CatSper2 proteins are critical to sperm-hyperactivated motility and male fertility. Although architecturally resembling voltage-gated ion channels, neither CatSper1 nor CatSper2 alone forms functional ion channels in heterologous expression systems, which may be related to the absence of yet unidentified accessory subunits. Here we isolated CatSper1-and CatSper2-associated protein (

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Immunological characterization of T-type voltage-dependent calcium channel CaV3.1 (alpha1G) and CaV3.3 (alpha1I) isoforms reveal differences in their localization, expression, and neural development

Cited by 74 publications

References 57 publications

α₂-Adrenergic receptor activation promotes long-term potentiation at excitatory synapses in the mouse accessory olfactory bulb

α₂-Adrenergic receptor activation promotes long-term potentiation at excitatory synapses in the mouse accessory olfactory bulb

Elevated Thalamic Low-Voltage-Activated Currents Precede the Onset of Absence Epilepsy in the SNAP25-Deficient Mouse MutantColoboma

Association of Catsper1 or -2 with Cav3.3 Leads to Suppression of T-type Calcium Channel Activity

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Immunological characterization of T-type voltage-dependent calcium channel CaV3.1 (alpha1G) and CaV3.3 (alpha1I) isoforms reveal differences in their localization, expression, and neural development

Cited by 74 publications

References 57 publications

α2-Adrenergic receptor activation promotes long-term potentiation at excitatory synapses in the mouse accessory olfactory bulb

α2-Adrenergic receptor activation promotes long-term potentiation at excitatory synapses in the mouse accessory olfactory bulb

Elevated Thalamic Low-Voltage-Activated Currents Precede the Onset of Absence Epilepsy in the SNAP25-Deficient Mouse MutantColoboma

Association of Catsper1 or -2 with Cav3.3 Leads to Suppression of T-type Calcium Channel Activity

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α₂-Adrenergic receptor activation promotes long-term potentiation at excitatory synapses in the mouse accessory olfactory bulb

α₂-Adrenergic receptor activation promotes long-term potentiation at excitatory synapses in the mouse accessory olfactory bulb