Activation of γ-aminobutyric Acid (A) Receptor Protects Hippocampus from Intense Exercise-induced Synapses Damage and Apoptosis in Rats

Chinese Medical Journal
Yi DingHua Ai

Abstract

Our previous study has confirmed that one bout of exhaustion (Ex) can cause hippocampus neurocyte damage, excessive apoptosis, and dysfunction. Its initial reason is intracellular calcium overload in hippocampus triggered by N-methyl-D-aspartic acid receptor (NMDAR) over-activation. NMDAR activation can be suppressed by γ-aminobutyric acid (A) receptor (GABAAR). Whether GABAAR can prevent intense exercise-induced hippocampus apoptosis, damage, or dysfunction will be studied in this study. According to dose test, rats were randomly divided into control (Con), Ex, muscimol (MUS, 0.1 mg/kg) and bicuculline (BIC, 0.5 mg/kg) groups, then all rats underwent once swimming Ex except ones in Con group only underwent training. Intracellular free calcium concentration ([Ca2+]i) was measured by Fura-2-acetoxymethyl ester; glial librillary acidic protein (GFAP) and synaptophysin (SYP) immunofluorescence were also performed; apoptosis were displayed by dUTP nick end labeling (TUNEL) stain; endoplasmic reticulum stress-induced apoptosis pathway was detected by Western blotting analysis; Morris water maze was used to detect learning ability and spatial memory. The appropriate dose was 0.1 mg/kg for MUS and 0.5 mg/kg for BIC. Ex group showed si...Continue Reading

References

Aug 1, 1988·International Journal of Sports Medicine·D P Thomas, K I Marshall
May 1, 1984·Journal of Neuroscience Methods·R Morris
Feb 1, 1994·Japanese Journal of Pharmacology·S OhkumaK Kuriyama
Jun 12, 2001·Current Opinion in Neurobiology·S Cull-CandyM Farrant
Jun 23, 2001·Pharmacology, Biochemistry, and Behavior·M ZarrindastM Sadeghi-Hariri
Jan 17, 2002·Proceedings of the National Academy of Sciences of the United States of America·Leila Tarsa, Yukiko Goda
Oct 5, 2002·Cellular and Molecular Neurobiology·Hidetoshi Ishibashi
Jan 22, 2003·Trends in Neurosciences·Giles E Hardingham, Hilmar Bading
Apr 23, 2005·Glia·Milos Pekny, Michael Nilsson
Dec 3, 2005·Philosophical Transactions of the Royal Society of London. Series B, Biological Sciences·Laura BerliocchiPierluigi Nicotera
Sep 6, 2006·EMBO Reports·Eva SzegezdiAfshin Samali
Nov 4, 2006·Cell Death and Differentiation·S Kumar
Oct 20, 2007·Neuroscience Letters·Seong Shoon YoonChae Ha Yang
May 20, 2009·Psychonomic Bulletin & Review·Teal S Eich, Janet Metcalfe
Jul 7, 2009·International Journal of Developmental Neuroscience : the Official Journal of the International Society for Developmental Neuroscience·Andreia Oliveira-da-SilvaYael Abreu-Villaça
Feb 16, 2011·Behavioral Neuroscience·Abigail L Kerr, Rodney A Swain
Nov 23, 2011·International Journal of Sports Medicine·G L WuL X Zhang
Mar 23, 2012·Brain Research·Radha ArasChristian J Pike
Aug 14, 2012·Neurobiology of Aging·Inês Tomás PereiraPeter R Rapp

❮ Previous
Next ❯

Methods Mentioned

BETA
MDA
Protein Assay

Software Mentioned

SPSS

Related Concepts

Related Feeds

B-Cell Lymphoma

B-cell lymphomas include lymphomas that affect B cells. This subtype of cancer accounts for over 80% of non-Hodgkin lymphomas in the US. Here is the latest research.

Apoptosis

Apoptosis is a specific process that leads to programmed cell death through the activation of an evolutionary conserved intracellular pathway leading to pathognomic cellular changes distinct from cellular necrosis

BCL-2 Family Proteins

BLC-2 family proteins are a group that share the same homologous BH domain. They play many different roles including pro-survival signals, mitochondria-mediated apoptosis and removal or damaged cells. They are often regulated by phosphorylation, affecting their catalytic activity. Here is the latest research on BCL-2 family proteins.