Functional Interaction of Neuronal Cav1.3 L-type Calcium Channel with Ryanodine Receptor Type 2 in the Rat Hippocampus

Kim, Sunoh; Yun, Hyung-Mun; Baik, Ja-Hyun; Chung, Kwang Chul; Nah, Seung‐Yeol; Rhim, Hyewhon

doi:10.1074/jbc.m701418200

Cited by 81 publications

(94 citation statements)

References 57 publications

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“…On the other hand, we have reported that there are significant increases of RyR-1 and -2 in the frontal cortex, significant increases of RyR-1 in the limbic forebrain, and no changes in RyR-3 in both regions of mice treated with methamphetamine, which are very similar to those in mice with cocaine-induced place preference (21). Recent investigations also reported nicotine-mediated RyR-2 up-regulation in the ventral tegmental area (43) and N-methyl-D-aspartate receptorsmediated and L-type calcium channel activator-mediated increase of RyR-2 in the rat hippocampus (44). Modification of RyR-2 and -3 expressions has been demonstrated under conditions of cerebral ischemia (46).…”

Section: Sal Cocamentioning

confidence: 66%

Dopamine D1 Receptors Participate in Cocaine-Induced Place Preference via Regulation of Ryanodine Receptor Expression

et al. 2011

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Abstract. Ryanodine receptors (RyRs) with three different isoforms in the brain play a role to facilitate Ca 2+ release from the intracellular Ca 2+ pool. Although cocaine is a strongly addictive psychostimulant that dramatically affects the central nervous system function, the role of RyRs and regulation of their expression by cocaine-induced place preference have not yet been defined well. The present study investigated the regulation of RyR expression in mice under intermittent cocaine treatment using the place preference procedure. The cocaine-induced place preference was inhibited by intracerebroventricular pretreatment with dantrolene, a RyRs antagonist, in a dosedependent manner. The levels of RyR-1 and -2 in the limbic forebrain and frontal cortex significantly increased in the cocaine-conditioned mice, whereas that of RyR-3 in these two brain regions showed no changes. Although the up-regulation of RyRs was not affected by blockade of L-type voltage-gated calcium channels, the increase of RyR-1 and -2 in the limbic forebrain and frontal cortex was completely abolished by SCH23390, a selective antagonist of dopamine D 1 receptors, but not by sulpiride, a selective antagonist of dopamine D 2 receptors. These findings indicate that RyRs play a critical role in the development of cocaine-induced place preference and that the upregulation of RyRs in the brain of a mouse showing cocaine-induced place preference is regulated by dopamine D 1 receptors.

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Section: Sal Cocamentioning

confidence: 66%

Dopamine D1 Receptors Participate in Cocaine-Induced Place Preference via Regulation of Ryanodine Receptor Expression

et al. 2011

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“…Our data first show, however, that in motor nerve ter minals the L type calcium channels are functionally coupled with ryanodine sensitive intracellular cal cium stores and calcium release from the intracellular stores. The coupling of the L type calcium channels with RyR calcium stores and the release of the intrac ellular calcium was described not only for muscle but also for nerve cells [30]. The RyR activation and the release of the stored calcium upon entry of the external calcium through the N type calcium channels trigger ing the vesicle exocytosis was described in frog motor nerve terminals [31,32].…”

Section: Discussionmentioning

confidence: 98%

The role of adenosine receptors and L-type calcium channels in the regulation of the mediator secretion in mouse motor synapses

Tarasova

Miteva

Gaidukov

et al. 2015

Biochem. Moscow Suppl. Ser. A

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The changes in spontaneous and evoked neurotransmitter release caused by agonists and antago nists of the A1 and A2A subtypes of adenosine receptors combined with inhibition of some enzymes and voltage dependent calcium channels of L type were studied in mouse diaphragm motor synapses using intra cellular microelectrode recordings of miniature endplate potentials (MEPPs) and evoked endplate potentials (EPPs). Simultaneous activation of presynaptic A1 and A2A receptors by endogenous adenosine during short term rhythmic activity of motor synapses was shown for the first time. Activation of receptors A1 pre vails and is followed by downregulation of the ACh release due to inhibition of intracellular cascade, which involves protein kinase A (PKA) and L type voltage dependent calcium channels. Activation of receptors A2A with their agonist CGS 21680 caused upregulation of the ACh secretion due to enhancement of PKA activity followed by activation of L type voltage dependent calcium channels. The mechanism of the evoked release potentiation, when A1 receptors are blocked or the activity of A2A receptors prevails over that of A1 receptors, involves calcium release from ryanodine sensitive intracellular calcium stores coupled with PKA and activation of L type voltage dependent calcium channels. It was found that protein phosphatase cal cineurin participates in downregulation of the L type voltage dependent calcium channels irrespective of the A1 receptors. It was shown for the first time that disinhibition of L type voltage dependent calcium channels caused by the calcineurin inhibition requires participation of the activity of A2A receptors and PKA. In con clusion, reciprocal interactions between presynaptic receptors A1 and A2A and their effect on the ACh release were shown in motor synapses. These interactions are mediated by the following cascade: PKA → L type volt age dependent calcium channels → ryanodine receptors of calcium stores. Final effect on the neurotrans mitter release depends on conditions of coactivation of these receptors and interplay of enzymes and L type voltage dependent calcium channels within synaptic terminals.

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“…Such an interaction is biologically feasible given that the proteins encoded by CACNA1C and RYR3 interact to maintain calcium homeostasis necessary for normal brain function (Ouardouz et al 2003; Kim et al 2007) and that many studies outlined below have shown a relationship between calcium homeostasis and amyloidigenesis, whereby increased intracellular calcium levels lead to increased Aβ deposition. An increase in Aβ is considered a key event in AD etiology (e.g., Jack et al 2013), and calcium dysregulation is thought to assist in amyloid formation and deposition and has been hypothesized to be very important in the etiology of AD (Berridge 2010).…”

Section: Discussionmentioning

confidence: 99%

Genetic interactions found between calcium channel genes modulate amyloid load measured by positron emission tomography

2013

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Late-onset Alzheimer’s disease (LOAD) is known to have a complex, oligogenic etiology, with considerable genetic heterogeneity. We investigated the influence of genetic interactions between genes in the Alzheimer’s disease (AD) pathway on amyloid-beta (Aβ) deposition as measured by PiB or AV-45 ligand positron emission tomography (PET) to aid in understanding LOAD’s genetic etiology. Subsets of the Alzheimer’s Disease Neuroimaging Initiative (ADNI) cohorts were used for discovery and for two independent validation analyses. A significant interaction between RYR3 and CACNA1C was confirmed in all three of the independent ADNI datasets. Both genes encode calcium channels expressed in the brain. The results shown here support previous animal studies implicating interactions between these calcium channels in amyloidigenesis and suggest that the pathological cascade of this disease may be modified by interactions in the amyloid-calcium axis. Future work focusing on the mechanisms of such relationships may inform targets for clinical intervention.

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Functional Interaction of Neuronal Cav1.3 L-type Calcium Channel with Ryanodine Receptor Type 2 in the Rat Hippocampus

Cited by 81 publications

References 57 publications

Dopamine D1 Receptors Participate in Cocaine-Induced Place Preference via Regulation of Ryanodine Receptor Expression

Dopamine D1 Receptors Participate in Cocaine-Induced Place Preference via Regulation of Ryanodine Receptor Expression

The role of adenosine receptors and L-type calcium channels in the regulation of the mediator secretion in mouse motor synapses

Genetic interactions found between calcium channel genes modulate amyloid load measured by positron emission tomography

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