Optical imaging reveals cation–Cl− cotransporter-mediated transient rapid decrease in intracellular Cl− concentration induced by oxygen–glucose deprivation in rat neocortical slices
| Autor: | Atsuo Fukuda, Masaki Tanaka, Hitoo Nishino, Yasumasa Yamada, Yoshiro Wada, Hajime Togari, Kanji Muramatsu, Yasunobu Shimano |
|---|---|
| Rok vydání: | 2001 |
| Předmět: |
medicine.medical_specialty
Sodium-Potassium-Chloride Symporters Iodide Chlorides Internal medicine medicine Animals RNA Messenger Rats Wistar Fluorescent Dyes chemistry.chemical_classification Ion Transport Chemistry Pyramidal Cells Quinolinium Compounds General Neuroscience Sodium Furosemide Somatosensory Cortex General Medicine Fluorescence Cell Hypoxia Rats Glucose Endocrinology Potassium Biophysics Oxygen glucose deprivation Efflux Carrier Proteins Cotransporter Bumetanide Intracellular medicine.drug |
| Zdroj: | Neuroscience Research. 39:269-280 |
| ISSN: | 0168-0102 |
| Popis: | In brain slices from young (postnatal day (P) 10–15) rat somatosensory cortex, real-time neuronal intracellular Cl − concentration ([Cl − ] i ) recordings were made by an optical technique measuring 6-methoxy- N -ethlquinolinium iodide (MEQ) fluorescence. Oxygen–glucose deprivation (in vitro model of ischemia) induced a long-lasting [Cl − ] i increase preceded by a rapid, transient [Cl − ] i decrease that could not be inhibited by blockers of Cl − pumps, Cl − channels, or Cl − antiporters, but was sensitive to cation–Cl − cotransporter inhibitors (bumetanide and furosemide). Use of low external Na + or high external K + revealed that the Na + ,K + –2Cl − cotransporter was inhibited by bumetanide and furosemide, whereas the K + –Cl − cotransporter was preferentially inhibited by furosemide under our experimental conditions. With a reduced inward driving force for Na + (reducing Na + ,K + –2Cl − cotransport), the transient [Cl − ] i decrease was only rarely induced by oxygen–glucose deprivation. In contrast, with a reduced outward driving force for K + (reducing K + –Cl − cotransport), the transient [Cl − ] i decrease still occurred. These results suggest that the transient [Cl − ] i decrease was primarily mediated by a rapid inhibition of the inwardly directed Na + ,K + –2Cl − cotransporter. Reverse transcriptase-polymerase chain reaction (RT-PCR) experiments suggested that the isoform involved is NKCC1. We hypothesize that the initial rapid Cl − efflux might effectively delay the irreversible Cl − influx that mediates neuronal injury. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|
Full Text from ScienceDirect