NDLI: PGF$_{2α}$ FP Receptor Contributes to Brain Damage Following Transient Focal Brain Ischemia

Please wait, while we are loading the content...

1-Benzyl-1,2,3,4-Tetrahydroisoquinoline, an Endogenous Parkinsonism-Inducing Toxin, Strongly Potentiates MAO-Dependent Dopamine Oxidation and Impairs Dopamine Release: Ex vivo and In vivo Neurochemical Studies

Protective Effect of Memantine Against Doxorubicin Toxicity in Primary Neuronal Cell Cultures: Influence a Development Stage

Molecular Determinants of Multiple Effects of Nickel on NMDA Receptor Channels

Substance P Upregulates LTB$_{4}$ in Rat Adherent Macrophages from Granuloma Induced by KMnO$_{4}$

Disubstituted Diaryl Diselenides Inhibit [$^{3}$H]-Serotonin Uptake in Rats

PGF$_{2α}$ FP Receptor Contributes to Brain Damage Following Transient Focal Brain Ischemia

Diabetic Hyperglycemia Aggravates Seizures and Status Epilepticus-induced Hippocampal Damage

The Mitochondrial ATP-Sensitive Potassium Channel Blocker 5-Hydroxydecanoate Inhibits Toxicity of 6-Hydroxydopamine on Dopaminergic Neurons

Neurotoxicity Research : Volume 14

Neurotoxicity Research : Volume 13

Neurotoxicity Research : Volume 12

Neurotoxicity Research : Volume 11

Neurotoxicity Research : Volume 10

Neurotoxicity Research : Volume 9

Neurotoxicity Research : Volume 8

Neurotoxicity Research : Volume 7

Neurotoxicity Research : Volume 6

Neurotoxicity Research : Volume 5

Neurotoxicity Research : Volume 4

Neurotoxicity Research : Volume 3

Neurotoxicity Research : Volume 2

Neurotoxicity Research : Volume 1

PGF$_{2α}$ FP Receptor Contributes to Brain Damage Following Transient Focal Brain Ischemia

Content Provider	Springer Nature Link
Author	Saleem, Sofiyan Ahmad, Abdullah Shafique Maruyama, Takayuki Narumiya, Shuh Doré, Sylvain
Copyright Year	2009
Abstract	Although some of the COX-2 metabolites and prostaglandins have been implicated in stroke and excitotoxicity, the role of prostaglandin F$_{2α}$ (PGF$_{2α}$) and its FP receptor have not been elucidated in the pathogenesis of ischemic-reperfusion (I/R) brain injury. Here we investigated the FP receptor’s contribution in a unilateral middle cerebral artery (MCA) occlusion model of focal cerebral ischemia in mice. The MCA in wild type (WT) and FP knockout (FP$^{−/−}$) C57BL/6 male mice was transiently occluded with a monofilament for 90 min. After 96 h of reperfusion, the FP$^{−/−}$ mice had 25.3% less neurological deficit (P < 0.05) and 34.4% smaller infarct volumes (P < 0.05) than those of the WT mice. In a separate cohort, physiological parameters were monitored before, during, and after ischemia, and the results revealed no differences between the groups. Because excitotoxicity is an acute mediator of stroke outcome, the effect of acute NMDA-induced neurotoxicity was also tested. Forty-eight hours after unilateral intrastriatal NMDA injection, excitotoxic brain damage was 20.8% less extensive in the FP$^{−/−}$ mice (P < 0.05) than in the WT counterparts, further supporting the toxic contribution of the FP receptor in I/R injury. Additionally, we investigated the effect of post-treatment with the FP agonist latanoprost in mice subjected to MCA occlusion; such treatment resulted in an increase in neurological deficit and infarct size in WT mice (P < 0.05), though no effects were observed in the latanoprost-treated FP$^{−/−}$ mice. Together, the results suggest that the PGF$_{2α}$ FP receptor significantly enhances cerebral ischemic and excitotoxic brain injury and that these results are of importance when planning for potential development of therapeutic drugs to treat stroke and its acute and/or long term consequences.
Starting Page	62
Ending Page	70
Page Count	9
File Format	PDF
ISSN	10298428
Journal	Neurotoxicity Research
Volume Number	15
Issue Number	1
e-ISSN	14763524
Language	English
Publisher	Springer-Verlag
Publisher Date	2009-02-11
Publisher Place	New York
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	13,14-Dihydro-17-phenyl-18,19,20-trinor-PGF$_{2α}$-isopropyl ester Excitotoxicity Latanoprost Middle cerebral artery occlusion Mouse Neurodegeneration Prostaglandin Neurobiology Pharmacology/Toxicology Neurochemistry Neurology Pharmaceutical Sciences/Technology Neurosciences
Content Type	Text
Resource Type	Article
Subject	Neuroscience Toxicology

Sl.	Authority	Responsibilities	Communication Details
1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
2	Indian Institute of Technology Kharagpur	Host Institute of the Project: The host institute of the project is responsible for providing infrastructure support and hosting the project	https://www.iitkgp.ac.in
3	National Digital Library of India Office, Indian Institute of Technology Kharagpur	The administrative and infrastructural headquarters of the project	Dr. B. Sutradhar bsutra@ndl.gov.in
4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
5	Website/Portal (Helpdesk)	Queries regarding NDLI and its services	support@ndl.gov.in
6	Contents and Copyright Issues	Queries related to content curation and copyright issues	content@ndl.gov.in
7	National Digital Library of India Club (NDLI Club)	Queries related to NDLI Club formation, support, user awareness program, seminar/symposium, collaboration, social media, promotion, and outreach	clubsupport@ndl.gov.in
8	Digital Preservation Centre (DPC)	Assistance with digitizing and archiving copyright-free printed books	dpc@ndl.gov.in
9	IDR Setup or Support	Queries related to establishment and support of Institutional Digital Repository (IDR) and IDR workshops	idr@ndl.gov.in

Prostaglandin EP1 Receptor Contributes to Excitotoxicity and Focal Ischemic Brain Damage

Low Doses of Carbon Monoxide Protect Against Experimental Focal Brain Ischemia

Selective blockade of PGE$^{2}$ EP1 receptor protects brain against experimental ischemia and excitotoxicity, and hippocampal slice cultures against oxygen-glucose deprivation

Women and Smokers Have Elevated Urinary F$_{2}$-Isoprostane Metabolites: A Novel Extraction and LC–MS Methodology

Sphingosine 1-phosphate receptor subtype 3 (S1P3) contributes to brain injury after transient focal cerebral ischemia via modulating microglial activation and their M1 polarization

Apelin-13 Protects the Brain Against Ischemic Reperfusion Injury and Cerebral Edema in a Transient Model of Focal Cerebral Ischemia

Elevated body swing test after focal cerebral ischemia in rodents: methodological considerations

Hydrogen Sulfide Protects the Brain Against Ischemic Reperfusion Injury in a Transient Model of Focal Cerebral Ischemia

Unconjugated TAT Carrier Peptide Protects Against Excitotoxicity

PGF$_{2α}$ FP Receptor Contributes to Brain Damage Following Transient Focal Brain Ischemia

Similar Documents

Prostaglandin EP1 Receptor Contributes to Excitotoxicity and Focal Ischemic Brain Damage

Low Doses of Carbon Monoxide Protect Against Experimental Focal Brain Ischemia

Selective blockade of PGE$^{2}$ EP1 receptor protects brain against experimental ischemia and excitotoxicity, and hippocampal slice cultures against oxygen-glucose deprivation

Women and Smokers Have Elevated Urinary F$_{2}$-Isoprostane Metabolites: A Novel Extraction and LC–MS Methodology

Sphingosine 1-phosphate receptor subtype 3 (S1P3) contributes to brain injury after transient focal cerebral ischemia via modulating microglial activation and their M1 polarization

Apelin-13 Protects the Brain Against Ischemic Reperfusion Injury and Cerebral Edema in a Transient Model of Focal Cerebral Ischemia

Elevated body swing test after focal cerebral ischemia in rodents: methodological considerations

Hydrogen Sulfide Protects the Brain Against Ischemic Reperfusion Injury in a Transient Model of Focal Cerebral Ischemia

Unconjugated TAT Carrier Peptide Protects Against Excitotoxicity

PGF$_{2α}$ FP Receptor Contributes to Brain Damage Following Transient Focal Brain Ischemia