ArticleJournal of neurotrauma2013
Hypothermia and pharmacological regimens that prevent overexpression and overactivity of the extracellular calcium-sensing receptor protect neurons against traumatic brain injury.
Article in Journal of neurotrauma, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 25 citations in OpenAlex.
- Article
- Article
- Danger-Sensing/Patten Recognition Receptors and Neuroinflammation in Alzheimer's Disease.International journal of molecular sciences · 2020Review
- International Union of Basic and Clinical Pharmacology. CVIII. Calcium-Sensing Receptor Nomenclature, Pharmacology, and Function.Pharmacological reviews · 2020Review
- Combined network pharmacology and virtual reverse pharmacology approaches for identification of potential targets to treat vascular dementia.Scientific reports · 2020Article
- Microglial Calcium Release-Activated Calcium Channel Inhibition Improves Outcome from Experimental Traumatic Brain Injury and Microglia-Induced Neuronal Death.Journal of neurotrauma · 2019Article
- Neuroprotective and neuroregenerative potential of pharmacologically-induced hypothermia with D-alanine D-leucine enkephalin in brain injury.Neural regeneration research · 2018Review
- Changes in Posttraumatic Brain Edema in Craniectomy-Selective Brain Hypothermia Model Are Associated With Modulation of Aquaporin-4 Level.Frontiers in neurology · 2018Article
- Hydroxysafflor yellow A exerts antioxidant effects in a rat model of traumatic brain injury.Molecular medicine reports · 2016Article
- Calcium-Sensing Receptor: A Key Target for Extracellular Calcium Signaling in Neurons.Frontiers in physiology · 2016Review
- Calcium-sensing receptor (CaSR) as a novel target for ischemic neuroprotection.Annals of clinical and translational neurology · 2014Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Traumatic brain injury (TBI) leads to acute functional deficit in the brain. Molecular events underlying TBI remain unclear. In mouse brains, we found controlled cortical impact (CCI) injury induced overexpression of the extracellular calcium-sensing receptor (CaSR), which is known to stimulate neuronal activity and accumulation of intracellular Ca(2+) and concurrent down-regulation of type B or metabotropic GABA receptor 1 (GABA-B-R1), a prominent inhibitory pathway in the brain. These changes in protein expression preceded and were closely associated with the loss of brain tissue, as indicated by the increased size of cortical cavity at impact sites, and the development of motor deficit, as indicated by the increased frequency of right-biased swing and turn in the CCI mice. Mild hypothermia, an established practice of neuroprotection for brain ischemia, partially but significantly blunted all of the above effects of CCI. Administration of CaSR antagonist NPS89636 mimicked hypothermia to reduce loss of brain tissue and motor functions in the CCI mice. These data together support the concept that CaSR overexpression and overactivity play a causal role in potentiating TBI potentially by stimulating excitatory neuronal responses and by interfering with inhibitory GABA-B-R signaling and that the CaSR could be a novel target for neuroprotection against TBI.
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Registered trials
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