![[Feedback]](/icons/banner/feedbackACT.gif){kind=icon}
![[For Subscribers]](/icons/banner/subscriberACT.gif){kind=icon}
![[Archive]](/icons/banner/archiveACT.gif){kind=icon}
![[Search]](/icons/banner/searchACT.gif){kind=icon}
![[Contents]](/icons/banner/tocACT.gif){kind=icon}
|
|
|
|
|
||
L Kiedrowski, JT Wroblewski and E Costa
Fidia-Georgetown Institute for the Neurosciences, Georgetown University, Washington D.C. 20007.
We monitored simultaneously the changes in the intracellular sodium concentration ([Na+]i) and intracellular calcium concentration ([Ca2+]i) in individual neurons from primary cultures of cerebellar granule cells loaded with sodium-binding benzofuran isophthalate and fluo-3. An application of glutamate (50 microM) in Mg(2+)-free medium containing 10 microM glycine evoked [Na+]i and [Ca2+]i increases that exceeded 60 mM and 1 microM, respectively. The kinetics of [Na+]i and [Ca2+]i decreases after the termination of the glutamate pulse were different. [Na+]i failed to decrease immediately after glutamate withdrawal and the delay in the onset of [Na+]i decrease after the glutamate pulse termination was proportional to the glutamate dose, the glutamate pulse duration, and the extent of [Ca2+]i elevation elicited by glutamate. The kinetics of [Ca2+]i decrease were biphasic, with the first phase occurring immediately after glutamate withdrawal and the second phase being correlated in time with a [Na+]i value lower than 15- 20 mM. These results were interpreted to indicate that the glutamate- evoked calcium influx may lead to sodium homeostasis destabilization. The delay in the restoration of the sodium gradient may in turn prolong the neuronal exposure to toxic [Ca2+]i values, due to the decrease in the efficiency of the Na+/Ca2+ exchanger to extrude calcium. The glutamate effects on [Na+]i and [Ca2+]i were potentiated by glycine. Glycine (10 microM) added alone also evoked [Na+]i and [Ca2+]i increases; this effect was inhibited by a competitive inhibitor of the N-methyl-D-aspartate receptor, 3-(2-carboxypiperazin-4-yl)propyl-1- phosphonic acid, indicating an involvement of endogenous glutamate.
This article has been cited by other articles:
|
|
 |
|
  T. A. Vander Jagt, J. A. Connor, and C. W. Shuttleworth Localized Loss of Ca2+ Homeostasis in Neuronal Dendrites Is a Downstream Consequence of Metabolic Compromise during Extended NMDA Exposures J. Neurosci., May 7, 2008; 28(19): 5029 - 5039. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 N. Shalbuyeva, T. Brustovetsky, A. Bolshakov, and N. Brustovetsky Calcium-dependent Spontaneously Reversible Remodeling of Brain Mitochondria J. Biol. Chem., December 8, 2006; 281(49): 37547 - 37558. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. Diarra, C. Sheldon, and J. Church In situ calibration and [H+] sensitivity of the fluorescent Na+ indicator SBFI Am J Physiol Cell Physiol, June 1, 2001; 280(6): C1623 - C1633. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. C. Rego, M. W. Ward, and D. G. Nicholls Mitochondria Control AMPA/Kainate Receptor-Induced Cytoplasmic Calcium Deregulation in Rat Cerebellar Granule Cells J. Neurosci., March 15, 2001; 21(6): 1893 - 1901. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. W. Ward, A. C. Rego, B. G. Frenguelli, and D. G. Nicholls Mitochondrial Membrane Potential and Glutamate Excitotoxicity in Cultured Cerebellar Granule Cells J. Neurosci., October 1, 2000; 20(19): 7208 - 7219. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. J. Gangemi, J. A. Kern, S. D. Ross, K. S. Shockey, I. L. Kron, and C. G. Tribble Retrograde perfusion with a sodium channel antagonist provides ischemic spinal cord protection Ann. Thorac. Surg., June 1, 2000; 69(6): 1744 - 1748. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. Chinopoulos, L. Tretter, A. Rozsa, and V. Adam-Vizi Exacerbated Responses to Oxidative Stress by an Na+ Load in Isolated Nerve Terminals: the Role of ATP Depletion and Rise of [Ca2+]i J. Neurosci., March 15, 2000; 20(6): 2094 - 2103. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. P. Blaustein and W. J. Lederer Sodium/Calcium Exchange: Its Physiological Implications Physiol Rev, July 1, 1999; 79(3): 763 - 854. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. F. Castilho, O. Hansson, M. W. Ward, S. L. Budd, and D. G. Nicholls Mitochondrial Control of Acute Glutamate Excitotoxicity in Cultured Cerebellar Granule Cells J. Neurosci., December 15, 1998; 18(24): 10277 - 10286. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 L. Tretter, C. Chinopoulos, and V. Adam-Vizi Plasma Membrane Depolarization and Disturbed Na+ Homeostasis Induced by the Protonophore Carbonyl Cyanide-p-trifluoromethoxyphenyl-hydrazon in Isolated Nerve Terminals Mol. Pharmacol., April 1, 1998; 53(4): 734 - 741. [Abstract] [Full Text]
|
|
|
|
 |
|
 F. Impagnatiello, A. Oberto, P. Longone, E. Costa, and A. Guidotti 7-Chloro-3-methyl-3,4-dihydro-2H-1,2,4-benzothiadiazine S,S-dioxide: A partial modulator of AMPA receptor desensitization devoid of neurotoxicity PNAS, June 24, 1997; 94(13): 7053 - 7058. [Abstract] [Full Text] [PDF]
|
|
 |
 |
 |
|
 |
 |
 |
