In vitro studies on the putative function of N-acetylaspartate as an osmoregulator
Efflux and tissue content of N-acetylaspartate (NAA) and amino acids were evaluated from cultured and acutely prepared hippocampal slices in response to changes in osmolarity. The osmoregulator taurine, but not NAA, was lost from both types of slices after moderate reductions in extracellular osmola...
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Published in | Neurochemical research Vol. 32; no. 7; pp. 1248 - 1255 |
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Main Authors | , , |
Format | Journal Article |
Language | English |
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Springer Nature B.V
01.07.2007
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Abstract | Efflux and tissue content of N-acetylaspartate (NAA) and amino acids were evaluated from cultured and acutely prepared hippocampal slices in response to changes in osmolarity. The osmoregulator taurine, but not NAA, was lost from both types of slices after moderate reductions in extracellular osmolarity (-60 mOsm) for 10-48 h. Hypoosmotic shock (-166 mOsm) for 5 min resulted in unselective efflux of several amino acids from acutely prepared slices. Notably, the efflux of taurine, but not NAA, was prominent also after the shock. Efflux of NAA was markedly enhanced by NMDA and high K(+), in particular after the stimulation period. The high K(+)-mediated efflux was decreased by high extracellular osmolarity and a NMDA-receptor antagonist. The results indicate that NAA efflux can be induced by a sudden non-physiological decrease in extracellular osmolarity but not by prolonged more moderate changes in osmolarity. The mechanisms behind the efflux of NAA by high K(+) are complex and may involve both swelling and activation of NMDA-receptors. |
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AbstractList | Efflux and tissue content of N-acetylaspartate (NAA) and amino acids were evaluated from cultured and acutely prepared hippocampal slices in response to changes in osmolarity. The osmoregulator taurine, but not NAA, was lost from both types of slices after moderate reductions in extracellular osmolarity (-60 mOsm) for 10-48 h. Hypoosmotic shock (-166 mOsm) for 5 min resulted in unselective efflux of several amino acids from acutely prepared slices. Notably, the efflux of taurine, but not NAA, was prominent also after the shock. Efflux of NAA was markedly enhanced by NMDA and high K super(+), in particular after the stimulation period. The high K super(+)-mediated efflux was decreased by high extracellular osmolarity and a NMDA-receptor antagonist. The results indicate that NAA efflux can be induced by a sudden non-physiological decrease in extracellular osmolarity but not by prolonged more moderate changes in osmolarity. The mechanisms behind the efflux of NAA by high K super(+) are complex and may involve both swelling and activation of NMDA-receptors. Efflux and tissue content of N-acetylaspartate (NAA) and amino acids were evaluated from cultured and acutely prepared hippocampal slices in response to changes in osmolarity. The osmoregulator taurine, but not NAA, was lost from both types of slices after moderate reductions in extracellular osmolarity (-60 mOsm) for 10-48 h. Hypoosmotic shock (-166 mOsm) for 5 min resulted in unselective efflux of several amino acids from acutely prepared slices. Notably, the efflux of taurine, but not NAA, was prominent also after the shock. Efflux of NAA was markedly enhanced by NMDA and high K(+), in particular after the stimulation period. The high K(+)-mediated efflux was decreased by high extracellular osmolarity and a NMDA-receptor antagonist. The results indicate that NAA efflux can be induced by a sudden non-physiological decrease in extracellular osmolarity but not by prolonged more moderate changes in osmolarity. The mechanisms behind the efflux of NAA by high K(+) are complex and may involve both swelling and activation of NMDA-receptors. Efflux and tissue content of N-acetylaspartate (NAA) and amino acids were evaluated from cultured and acutely prepared hippocampal slices in response to changes in osmolarity. The osmoregulator taurine, but not NAA, was lost from both types of slices after moderate reductions in extracellular osmolarity (-60 mOsm) for 10-48 h. Hypoosmotic shock (-166 mOsm) for 5 min resulted in unselective efflux of several amino acids from acutely prepared slices. Notably, the efflux of taurine, but not NAA, was prominent also after the shock. Efflux of NAA was markedly enhanced by NMDA and high K+, in particular after the stimulation period. The high K+-mediated efflux was decreased by high extracellular osmolarity and a NMDA-receptor antagonist. The results indicate that NAA efflux can be induced by a sudden non-physiological decrease in extracellular osmolarity but not by prolonged more moderate changes in osmolarity. The mechanisms behind the efflux of NAA by high K+ are complex and may involve both swelling and activation of NMDA-receptors. [PUBLICATION ABSTRACT] Efflux and tissue content of N-acetylaspartate (NAA) and amino acids were evaluated from cultured and acutely prepared hippocampal slices in response to changes in osmolarity. The osmoregulator taurine, but not NAA, was lost from both types of slices after moderate reductions in extracellular osmolarity (−60 mOsm) for 10–48 h. Hypoosmotic shock (−166 mOsm) for 5 min resulted in unselective efflux of several amino acids from acutely prepared slices. Notably, the efflux of taurine, but not NAA, was prominent also after the shock. Efflux of NAA was markedly enhanced by NMDA and high K+, in particular after the stimulation period. The high K+-mediated efflux was decreased by high extracellular osmolarity and a NMDA-receptor antagonist. The results indicate that NAA efflux can be induced by a sudden non-physiological decrease in extracellular osmolarity but not by prolonged more moderate changes in osmolarity. The mechanisms behind the efflux of NAA by high K+ are complex and may involve both swelling and activation of NMDA-receptors. |
Author | Sandberg, Mats Abbas, Abdul-Karim Tranberg, Mattias |
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BackLink | https://www.ncbi.nlm.nih.gov/pubmed/17401659$$D View this record in MEDLINE/PubMed https://gup.ub.gu.se/publication/60122$$DView record from Swedish Publication Index |
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CitedBy_id | crossref_primary_10_3389_fnmol_2017_00161 crossref_primary_10_1007_s00401_017_1784_9 crossref_primary_10_1016_j_pscychresns_2010_02_008 crossref_primary_10_1016_j_drudis_2022_05_019 crossref_primary_10_1038_jcbfm_2009_8 |
Cites_doi | 10.1016/0003-2697(80)90024-X 10.1002/glia.20174 10.1046/j.1471-4159.1994.62062349.x 10.1023/A:1020778832745 10.1042/bj2560251 10.1016/S0006-8993(03)02536-8 10.1016/0165-0270(91)90128-M 10.1016/j.ab.2005.03.004 10.1046/j.1471-4159.2001.00403.x 10.1111/j.1471-4159.1960.tb13458.x 10.1016/0736-5748(93)90065-L 10.1111/j.1471-4159.1986.tb02847.x 10.1111/j.1748-1716.2006.01537.x 10.1023/B:NERE.0000010434.06311.18 10.1152/physrev.2001.81.4.1415 10.1046/j.1471-4159.1995.65010275.x 10.1016/S0306-4522(96)00403-4 10.1152/ajpcell.1997.272.6.C1804 10.1016/j.neuint.2004.06.005 10.1016/S0197-0186(01)00095-X 10.1086/317749 10.1097/00001756-199103000-00005 10.1385/NMM:3:2:95 10.1097/00004647-199902000-00008 10.1016/0165-0270(95)00077-1 10.1007/s004240100604 10.1523/JNEUROSCI.16-23-07447.1996 10.1111/j.1460-9568.2005.04006.x 10.1016/S0021-9258(18)65008-2 10.1006/exnr.1996.6375 |
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SubjectTerms | Amino acids analogs & derivatives Animals Aspartic Acid Aspartic Acid - analogs & derivatives Aspartic Acid - metabolism cytology Efflux Excitatory Amino Acid Agonists Excitatory Amino Acid Agonists - metabolism Glutamic acid receptors (ionotropic) Hippocampus Hippocampus - cytology Hippocampus - metabolism MEDICAL AND HEALTH SCIENCES MEDICIN OCH HÄLSOVETENSKAP metabolism N-Acetylaspartate N-Methyl-D-aspartic acid receptors N-Methylaspartate N-Methylaspartate - metabolism Osmolar Concentration Osmolarity Potassium Potassium - metabolism Rats Rats, Sprague-Dawley Receptors Sprague-Dawley Taurine Taurine - metabolism Tissue Culture Techniques Water-Electrolyte Balance |
Title | In vitro studies on the putative function of N-acetylaspartate as an osmoregulator |
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