Paroxysmal afterpotentials and role of calcium-dependent potassium conductivity in neuronal activity of strychninized neocortex

AbstractCalcium-dependent secretion activator 2 (CAPS2) regulates the trafficking and exocytosis of neuropeptide-containing dense-core vesicles (DCVs). CAPS2 is prominently expressed in the medial habenula (MHb), which is related to depressive behavior; however, how MHb neurons cause depressive symptoms and the role of CAPS2 remains unclear. We hypothesized that dysfunction of MHb CAPS neurons might cause defects in neuropeptide secretion and the activity of monoaminergic centers, resulting in depressive-like behaviors. In this study, we examined (1) CAPS2 expression in the habenula of depression animal models and major depressive disorder patients and (2) the effects of down-regulation of MHb CAPS2 on the animal behaviors, synaptic transmission in the interpeduncular nucleus (IPN), and neuronal activity of monoamine centers. Habenular CAPS2 expression was decreased in the rat chronic restraint stress model, mouse learned helplessness model, and showed tendency to decrease in depression patients who died by suicide. Knockdown of CAPS2 in the mouse habenula evoked despair-like behavior and a reduction of the release of DCVs in the IPN. Neuronal activity of IPN and monoaminergic centers was also reduced. These results implicate MHb CAPS2 as playing a pivotal role in depressive behavior through the regulation of neuropeptide secretion of the MHb-IPN pathway and the activity of monoaminergic centers.

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The emerging role of calcium-dependent exocytosis in ATP release from nonexcitable cells

10.36866/pn.60.21 ◽

2005 ◽

pp. 21-22 ◽

Cited By ~ 1

Author(s):

Ryszard Grygorczyk ◽

Francis Boudreault

Keyword(s):

Atp Release ◽

Calcium Dependent

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Effect of Annexins Translocated in Extracellular Vesicles on Tumorigenesis

Current Molecular Medicine ◽

10.2174/1566524020666200825163512 ◽

2020 ◽

Vol 20 ◽

Author(s):

Qionghui Wu ◽

Haidong Wei ◽

Wenbo Meng ◽

Xiaodong Xie ◽

Zhenchang Zhang ◽

...

Keyword(s):

Tumor Cells ◽

Extracellular Vesicles ◽

Immune Cell ◽

Epithelial Mesenchymal Transition ◽

Main Role ◽

Tumor Cell Adhesion ◽

Mesenchymal Transition ◽

Calcium Dependent ◽

Tumor Neovascularization

: Annexin, a calcium-dependent phospholipid binding protein, can affect tumor cell adhesion, proliferation, apoptosis, invasion and metastasis, as well as tumor neovascularization in different ways. Recent studies have shown that annexin exists not only as an intracellular protein in tumor cells, but also in different ways to be secret outside the cell as a “crosstalk” tool for tumor cells and tumor microenvironment, thus playing an important role in the development of tumors, such as participating in epithelial-mesenchymal transition, regulating immune cell behavior, promoting neovascularization and so on. The mechanism of annexin secretion in the form of extracellular vesicles and its specific role is still unclear. This paper summarizes the main role of annexin secreted into the extracellular space in the form of extracellular vesicles in tumorigenesis and drug resistance and analyzes its possible mechanism.

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A CACNA1A variant associated with trigeminal neuralgia alters the gating of Cav2.1 channels

Molecular Brain ◽

10.1186/s13041-020-00725-y ◽

2021 ◽

Vol 14 (1) ◽

Author(s):

Eder Gambeta ◽

Maria A. Gandini ◽

Ivana A. Souza ◽

Laurent Ferron ◽

Gerald W. Zamponi

Keyword(s):

Trigeminal Neuralgia ◽

Missense Mutation ◽

Neurotransmitter Release ◽

Trigeminal System ◽

Wild Type ◽

Calcium Dependent ◽

Whole Cell Patch Clamp ◽

C Terminus ◽

Dependent Inactivation

AbstractA novel missense mutation in the CACNA1A gene that encodes the pore forming α1 subunit of the CaV2.1 voltage-gated calcium channel was identified in a patient with trigeminal neuralgia. This mutation leads to a substitution of proline 2455 by histidine (P2455H) in the distal C-terminus region of the channel. Due to the well characterized role of this channel in neurotransmitter release, our aim was to characterize the biophysical properties of the P2455H variant in heterologously expressed CaV2.1 channels. Whole-cell patch clamp recordings of wild type and mutant CaV2.1 channels expressed in tsA-201 cells reveal that the mutation mediates a depolarizing shift in the voltage-dependence of activation and inactivation. Moreover, the P2455H mutant strongly reduced calcium-dependent inactivation of the channel that is consistent with an overall gain of function. Hence, the P2455H CaV2.1 missense mutation alters the gating properties of the channel, suggesting that associated changes in CaV2.1-dependent synaptic communication in the trigeminal system may contribute to the development of trigeminal neuralgia.

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Role of Phosphopantetheinyl Transferase Genes in Antibiotic Production by Streptomyces coelicolor

Journal of Bacteriology ◽

10.1128/jb.00865-08 ◽

2008 ◽

Vol 190 (20) ◽

pp. 6903-6908 ◽

Cited By ~ 20

Author(s):

Ya-Wen Lu ◽

Adrianna K. San Roman ◽

Amy M. Gehring

Keyword(s):

Antibiotic Production ◽

Streptomyces Coelicolor ◽

Morphological Development ◽

Phosphopantetheinyl Transferase ◽

Calcium Dependent ◽

Actinorhodin Production

ABSTRACT The phosphopantetheinyl transferase genes SCO5883 (redU) and SCO6673 were disrupted in Streptomyces coelicolor. The redU mutants did not synthesize undecylprodigiosin, while SCO6673 mutants failed to produce calcium-dependent antibiotic. Neither gene was essential for actinorhodin production or morphological development in S. coelicolor, although their mutation could influence these processes.

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Modulation of acetylcholine release by cholecystokinin in striatum – receptor specificity; role of dopaminergic neuronal activity

Brain Research Bulletin ◽

10.1016/j.brainresbull.2012.08.009 ◽

2012 ◽

Vol 89 (5-6) ◽

pp. 177-184 ◽

Cited By ~ 1

Author(s):

Polina Petkova-Kirova ◽

Maria Grazia Giovannini ◽

Reni Kalfin ◽

Angelina Rakovska

Keyword(s):

Neuronal Activity ◽

Acetylcholine Release ◽

Receptor Specificity

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Dissociable roles of cortical excitation-inhibition balance during patch-leaving versus value-guided decisions

Nature Communications ◽

10.1038/s41467-020-20875-w ◽

2021 ◽

Vol 12 (1) ◽

Author(s):

Luca F. Kaiser ◽

Theo O. J. Gruendler ◽

Oliver Speck ◽

Lennart Luettgau ◽

Gerhard Jocham

Keyword(s):

Decision Making ◽

Prefrontal Cortex ◽

Neuronal Activity ◽

Ventromedial Prefrontal Cortex ◽

Anterior Cingulate ◽

Mutual Inhibition ◽

Dorsal Anterior Cingulate Cortex ◽

Cortical Excitation ◽

The Cost

AbstractIn a dynamic world, it is essential to decide when to leave an exploited resource. Such patch-leaving decisions involve balancing the cost of moving against the gain expected from the alternative patch. This contrasts with value-guided decisions that typically involve maximizing reward by selecting the current best option. Patterns of neuronal activity pertaining to patch-leaving decisions have been reported in dorsal anterior cingulate cortex (dACC), whereas competition via mutual inhibition in ventromedial prefrontal cortex (vmPFC) is thought to underlie value-guided choice. Here, we show that the balance between cortical excitation and inhibition (E/I balance), measured by the ratio of GABA and glutamate concentrations, plays a dissociable role for the two kinds of decisions. Patch-leaving decision behaviour relates to E/I balance in dACC. In contrast, value-guided decision-making relates to E/I balance in vmPFC. These results support mechanistic accounts of value-guided choice and provide evidence for a role of dACC E/I balance in patch-leaving decisions.

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