Region-specific changes in the distribution of transient receptor potential vanilloid 4 channel (TRPV4) in the central nervous system of Alzheimer’s disease model mice

2016 ◽  
Vol 38 (7) ◽  
pp. 629-637 ◽  
Author(s):  
Jae Chul Lee ◽  
Soo Young Choe
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Central Nervous System ◽  
Nervous System ◽  
Transient Receptor Potential ◽  
Disease Model ◽  
Receptor Potential ◽  
Transient Receptor Potential Vanilloid ◽  
The Central Nervous System ◽  
Transient Receptor

scholarly journals Osmoregulatory thirst in mice lacking the transient receptor potential vanilloid type 1 (TRPV1) and/or type 4 (TRPV4) receptor

2014 ◽  
Vol 307 (9) ◽  
pp. R1092-R1100 ◽  
Author(s):  
Brian Kinsman ◽  
James Cowles ◽  
Jennifer Lay ◽  
Sarah S. Simmonds ◽  
Kirsteen N. Browning ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Transient Receptor Potential Vanilloid ◽  
Consistent Finding ◽  
Cellular Dehydration ◽  
Genes Encoding ◽  
The Central Nervous System ◽  
Transient Receptor

Recent studies suggest the ability of the central nervous system to detect changes in osmolality is mediated by products of the genes encoding the transient receptor potential vanilloid-1 (TRPV1) or vanilloid-4 (TRPV4) channel. The purpose of the present study was to determine whether deletion of TRPV1 and/or TRPV4 channels altered thirst responses to cellular dehydration in mice. Injection of 0.5 or 1.0 M NaCl produced dose-dependent increases in cumulative water intakes of wild-type (WT), TRPV1−/−, TRPV4−/−, and TRPV1−/−V4−/− mice. However, there were no differences in cumulative water intakes between WT versus any other strain despite similar increases in plasma electrolytes and osmolality. Similar results were observed after injection of hypertonic mannitol. This was a consistent finding regardless of the injection route (intraperitoneal vs. subcutaneous) or timed access to water (delayed vs. immediate). There were also no differences in cumulative intakes across strains after injection of 0.15 M NaCl or during a time-controlled period (no injection). Chronic hypernatremia produced by sole access to 2% NaCl for 48 h also produced similar increases in water intake across strains. In a final set of experiments, subcutaneous injection of 0.5 M NaCl produced similar increases in the number of Fos-positive nuclei within the organum vasculosum of the lamina terminalis and median preoptic nucleus across strains but significantly smaller number in the subfornical organ of WT versus TRPV1−/−V4−/− mice. Collectively, these findings suggest that TRPV1 and/or TRPV4 channels are not the primary mechanism by which the central nervous system responds to cellular dehydration during hypernatremia or hyperosmolality to increase thirst.

scholarly journals Potential Links between Cytoskeletal Disturbances and Electroneurophysiological Dysfunctions Induced in the Central Nervous System by Inorganic Nanoparticles

2016 ◽  
Vol 40 (6) ◽  
pp. 1487-1505 ◽  
Author(s):  
Yiyuan Kang ◽  
Jia Liu ◽  
Bin Song ◽  
Xiaoli Feng ◽  
Lingling Ou ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Transient Receptor Potential Channels ◽  
Inorganic Nanoparticles ◽  
The Central Nervous System ◽  
Inorganic Nanomaterials ◽  
Potential Channels ◽  
Transient Receptor

Inorganic nanomaterials have been widely applied in biomedicine. However, several studies have noted that inorganic nanoparticles can enter the brain and induce cytoskeletal remodeling, as well as electrophysiological alterations, which are related to neurodevelopmental disorders and neurodegenerative diseases. The toxic effects of inorganic nanomaterials on the cytoskeleton and electrophysiology are summarized in this review. The relationships between inorganic NPs-induced cytoskeletal and electrophysiological alterations in the central nervous system remain obscure. We propose several potential relationships, including those involving N-methyl-D-aspartate receptor function, ion channels, transient receptor potential channels, and the Rho pathway.

scholarly journals Functions of the Alzheimer’s Disease Protease BACE1 at the Synapse in the Central Nervous System

2016 ◽  
Vol 60 (3) ◽  
pp. 305-315 ◽  
Author(s):  
Kathryn M. Munro ◽  
Amelia Nash ◽  
Martina Pigoni ◽  
Stefan F. Lichtenthaler ◽  
Jenny M. Gunnersen
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Central Nervous System ◽  
Nervous System ◽  
The Central Nervous System

Roles of Cannabidiol in the treatment and prevention of Alzheimer’s disease by multi-target actions

2021 ◽  
Vol 21 ◽  
Author(s):  
Xiao- Bei Zhang ◽  
Jintao Li ◽  
Juanhua Gu ◽  
Yue-Qin Zeng
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Transient Receptor Potential ◽  
Senile Plaques ◽  
Memory Loss ◽  
Receptor Potential ◽  
Transient Receptor Potential Vanilloid ◽  
Peroxisome Proliferator ◽  
Protective Effects ◽  
Peroxisome Proliferator Activated Receptor

: Alzheimer’s disease (AD) is one of the most common neurodegenerative diseases with chronic, progressive, and irreversible characteristics, affecting nearly 50 million older adults worldwide. The pathogenesis of AD includes the formation of senile plaques, the abnormal aggregation of tau protein and the gradual degeneration and death of cerebral cortical cells. The main symptoms are memory loss, cognitive decline and behavioral disorders. Studies indicate that cannabidiol(CBD) possesses various pharmacological activities including anti-inflammatory, anti-oxidation and neuroprotective activities. It has been suggested as a potential multi-target medicine for treatment of AD. In this review, we aim to summarize the underlying mechanisms and protective effects of CBD on signaling pathways and central receptors involved in the pathogenesis of AD, including the endocannabinoid system（eCBs）, the Transient receptor potential vanilloid type 1(TRPV1) receptor, and the Peroxisome proliferator-activated receptor (PPAR) receptor.

Nerve Growth Factor (NGF) in the Central Nervous System: Implications for the Treatment of Alzheimer’s Disease

Brain Repair ◽  
1990 ◽  
pp. 99-112
Author(s):  
Dan Lindholm ◽  
Christine Bandtlow ◽  
Matthias Spranger ◽  
Bastian Hengerer ◽  
Michael Meyer ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Central Nervous System ◽  
Nervous System ◽  
Nerve Growth Factor ◽  
Growth Factor ◽  
Nerve Growth ◽  
The Central Nervous System

scholarly journals CX3CL1/CX3CR1 in Alzheimer’s Disease: A Target for Neuroprotection

2016 ◽  
Vol 2016 ◽  
pp. 1-9 ◽  
Author(s):  
Peiqing Chen ◽  
Wenjuan Zhao ◽  
Yanjie Guo ◽  
Juan Xu ◽  
Ming Yin
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Central Nervous System ◽  
Nervous System ◽  
Early Diagnosis ◽  
Vital Role ◽  
Therapeutic Interventions ◽  
Chemokine Ligand ◽  
The Central Nervous System ◽  
Receptor Cx3cr1

CX3C chemokine ligand 1 (CX3CL1) is an intriguing chemokine belonging to the CX3C family. CX3CL1 is secreted by neurons and plays an important role in modulating glial activation in the central nervous system after binding to its sole receptor CX3CR1 which mainly is expressed on microglia. Emerging data highlights the beneficial potential of CX3CL1-CX3CR1 in the pathogenesis of Alzheimer’s disease (AD), a common progressive neurodegenerative disease, and in the progression of which neuroinflammation plays a vital role. Even so, the importance of CX3CL1/CX3CR1 in AD is still controversial and needs further clarification. In this review, we make an attempt to present a concise map of CX3CL1-CX3CR1 associated with AD to find biomarkers for early diagnosis or therapeutic interventions.

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