Subcellular distribution of L-type calcium channel subtypes in rat hippocampal neurons

Leitch, Beulah; Szostek, A.; Lin, R.C.S.; Shevtsova, Olga

doi:10.1016/j.neuroscience.2009.08.006

Cited by 67 publications

(51 citation statements)

References 50 publications

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“…This is the major subunit in the brain and plays an important role in synaptic plasticity, dendritic structure, learning, and memory [22]. Ca v 1.2 proteins are concentrated near the cell body, proximal dendrites, and dendritic tree in the neurons, modulating gene transcription and signaling pathways and thereby altering neuronal excitability [22,33,34,35]. The CACNA1D gene maps to chromosome 3p14.3; this gene codes for the alpha 1 delta subunit of the L-type voltage-gated calcium channel Ca v 1.3 [30].…”

Section: Calcium Ank3 and Potassium Channel Genes And Proteinsmentioning

confidence: 99%

Variants in Ion Channel Genes Link Phenotypic Features of Bipolar Illness to Specific Neurobiological Process Domains

2015

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Recent advances in genome-wide association studies are pointing towards a major role for voltage-gated ion channels in neuropsychiatric disorders and, in particular, bipolar disorder (BD). The phenotype of BD is complex, with symptoms during mood episodes and deficits persisting between episodes. We have tried to elucidate the common neurobiological mechanisms associated with ion channel signaling in order to provide a new perspective on the clinical symptoms and possible endophenotypes seen in BD patients. We propose a model in which the multiple variants in genes coding for ion channel proteins would perturb motivational circuits, synaptic plasticity, myelination, hypothalamic-pituitary-adrenal axis function, circadian neuronal rhythms, and energy regulation. These changes in neurobiological mechanisms would manifest in endophenotypes of aberrant reward processing, white matter hyperintensities, deficits in executive function, altered frontolimbic connectivity, increased amygdala activity, increased melatonin suppression, decreased REM latency, and aberrant myo-inositol/ATP shuttling. The endophenotypes result in behaviors of poor impulse control, motivational changes, cognitive deficits, abnormal stress response, sleep disturbances, and energy changes involving different neurobiological process domains. The hypothesis is that these disturbances start with altered neural circuitry during development, following which multiple environmental triggers may disrupt the neuronal excitability balance through an activity-dependent molecular process, resulting in clinical mood episodes.

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Section: Calcium Ank3 and Potassium Channel Genes And Proteinsmentioning

confidence: 99%

Variants in Ion Channel Genes Link Phenotypic Features of Bipolar Illness to Specific Neurobiological Process Domains

2015

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“…Although a presynaptic location cannot be excluded (Tippens et al, 2008;Leitch et al, 2009), they have been localized predominantly to the somatic and dendritic compartments (Hell et al, 1993;Lima and Marrion, 2007;Sukiasyan et al, 2009). Here, they mediate persistent Ca 2ϩ influx, sustain plateau potentials, and support pacemaking (Puopolo et al, 2007;Guzman et al, 2009).…”

Section: Introductionmentioning

confidence: 99%

Ca_v1.3 Calcium Channels Are Required for Normal Development of the Auditory Brainstem

Hirtz

Boesen²,

Braun³

et al. 2011

J. Neurosci.

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Within the Ca v 1 family of voltage-gated calcium channels, Ca v 1.2 and Ca v 1.3 channels are the predominant subtypes in the brain. Whereas specific functions for each subtype were described in the adult brain, their role in brain development is poorly understood. Here we assess the role of Ca v 1.3 subunits in the activity-dependent development of the auditory brainstem. We used Ca v 1.3-deficient (Ca v 1.3 Ϫ/Ϫ ) mice because these mice lack cochlea-driven activity that deprives the auditory centers from peripheral input. We found a drastically reduced volume in all auditory brainstem centers (range 25-59%, total 35%), which was manifest before hearing onset. A reduction was not obvious outside the auditory system. The lateral superior olive (LSO) was strikingly malformed in Ca v 1.3 Ϫ/Ϫ mice and had fewer neurons (1/3 less). The remaining LSO neurons displayed normal dendritic trees and received functional glutamatergic input, yet they fired action potentials predominantly with a multiple pattern upon depolarization, in contrast to the single firing pattern prevalent in controls. The latter finding appears to be due to a reduction of dendrototoxin-sensitive potassium conductances, presumably mediated through the K v 1.2 subtype. Fura2 imaging provided evidence for functional Ca v 1.3 channels in the LSO of wild-type mice. Our results imply that Ca v 1.3 channels are indispensable for the development of the central auditory system. We propose that the unique LSO phenotype in Ca v 1.3 Ϫ/Ϫ mice, which hitherto was not described in other hereditary deafness models, is caused by the synergistic contribution of two factors: on-site loss of Ca v 1.3 channels in the neurons plus lack of peripheral input.

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“…Cav1.2 intensely expressed in the CA1-CA4 pyramidal cell layer and the DG granule cell layer (Leitch et al, 2009), and also in the entorhinal coratex (Kelly et al, 2001). It has Page 15 of 28 Synapse also been shown that most inhibitory interneurons located in the hilar region of dentate gyrus express both Cav1.2 and Cav1.3 channels (Vinet and Sik, 2006).…”

Section: Discussionmentioning

confidence: 99%

Calcium channel blockade attenuates abnormal synaptic transmission in the dentate gyrus elicited by entorhinal amyloidopathy

Pourbadie

Naderi

Janahmadi

et al. 2016

Synapse

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Entorhinal-hippocampal network is one of the earliest circuits which is affected by Alzheimer's disease (AD). There are numerous data providing the evidence of synaptic deficit in the dentate gyrus (DG) of AD animal model. However, there is little known about how entorhinal cortex (EC) amyloidophaty affects each excitatory and/or inhibitory transmission in the early stage of AD. On the other hand, it is believed that calcium dyshomeostasis has a critical role in the etiology of AD. Here, the effect of the EC amyloid pathogenesis on excitatory or inhibitory post synaptic currents (EPSC and IPSC, respectively) in the DG granule cells and then the possible neuroprotective action of L-type calcium channel blockers (CCBs), nimodipine and isradipine, were examined. The amyloid beta (Aβ) 1-42 was injected bilaterally into the EC of male rats and one week later, synaptic currents in the DG granule cells were assessed by whole cell patch clamp. EPSCs were evoked by stimulating the perforant pathway. Voltage clamp recording showed profound decrease of evoked EPSC amplitude and paired pulse facilitation in the DG granule cells of Aβ treated rats. Furthermore, AMPA/NMDA ratio was significantly decreased in the Aβ treated animals. On the other hand, amplitude of IPSC currents was significantly increased in the DG granule cells of these animals. These modifications of synaptic currents were partially reversed by daily intracerebroventricular administration of isradipine or nimodipine. In conclusion, our results suggest that Aβ in the EC triggers decreased excitatory transmission in the DG with substantial decrement in AMPA currents, leading to a prominent activity of inhibitory circuits and increased inhibition of granule cells which may contribute to the development of AD-related neurological deficits in AD and treatment by CCBs could preserve normal synaptic transmission against Aβ toxicity.

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Subcellular distribution of L-type calcium channel subtypes in rat hippocampal neurons

Cited by 67 publications

References 50 publications

Variants in Ion Channel Genes Link Phenotypic Features of Bipolar Illness to Specific Neurobiological Process Domains

Variants in Ion Channel Genes Link Phenotypic Features of Bipolar Illness to Specific Neurobiological Process Domains

Ca_v1.3 Calcium Channels Are Required for Normal Development of the Auditory Brainstem

Calcium channel blockade attenuates abnormal synaptic transmission in the dentate gyrus elicited by entorhinal amyloidopathy

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Subcellular distribution of L-type calcium channel subtypes in rat hippocampal neurons

Cited by 67 publications

References 50 publications

Variants in Ion Channel Genes Link Phenotypic Features of Bipolar Illness to Specific Neurobiological Process Domains

Variants in Ion Channel Genes Link Phenotypic Features of Bipolar Illness to Specific Neurobiological Process Domains

Cav1.3 Calcium Channels Are Required for Normal Development of the Auditory Brainstem

Calcium channel blockade attenuates abnormal synaptic transmission in the dentate gyrus elicited by entorhinal amyloidopathy

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Ca_v1.3 Calcium Channels Are Required for Normal Development of the Auditory Brainstem