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Acidosis leads to neurological disorders through overexciting cortical pyramidal neurons.
- Source :
-
Biochemical and biophysical research communications [Biochem Biophys Res Commun] 2011 Nov 18; Vol. 415 (2), pp. 224-8. Date of Electronic Publication: 2011 Aug 12. - Publication Year :
- 2011
-
Abstract
- The patients suffering from acidosis usually sign psychological deficits. The cerebral dysfunction is reportedly caused by an acid-induced functional impairment of GABAergic neurons; however, the role of pyramidal neurons in this process remains unclear. By using electrophysiological method and changing extracellular pH, we investigated the influence of acidic environment on pyramidal neurons in the cortical slices, such as their ability of firing spikes and response to synaptic inputs. A low pH of artificial cerebral spinal fluid elevates the responses of pyramidal neurons to excitatory synaptic inputs and their ability of encoding digital spikes, as well as reduces the signal transmission at GABAergic synapses. The elevated ability of neuronal spiking is associated with the decreases of refractory periods and threshold potentials. Therefore, acidosis deteriorates brain functions through making the activities between cortical pyramidal neurons and GABAergic neurons imbalanced toward the overexcitation of neural networks, a process similar to neural excitotoxicity.<br /> (Copyright © 2011 Elsevier Inc. All rights reserved.)
- Subjects :
- Action Potentials
Animals
Cells, Cultured
Humans
Hydrogen-Ion Concentration
Ion Channel Gating
Mice
Mice, Inbred Strains
Sodium Channels physiology
Synapses physiology
Acidosis complications
Acidosis physiopathology
Nervous System Diseases etiology
Nervous System Diseases physiopathology
Pyramidal Cells physiopathology
Subjects
Details
- Language :
- English
- ISSN :
- 1090-2104
- Volume :
- 415
- Issue :
- 2
- Database :
- MEDLINE
- Journal :
- Biochemical and biophysical research communications
- Publication Type :
- Academic Journal
- Accession number :
- 21856290
- Full Text :
- https://doi.org/10.1016/j.bbrc.2011.08.008