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Ionic changes induced by excitatory amino acids in the rat cerebral cortex.
Canadian Journal of Physiology and Pharmacology
|May 1, 1987
Summary
Excitatory amino acids like glutamate alter ion concentrations in the rat motor cortex. N-methyl-D-aspartate (NMDA) receptors specifically allow calcium influx, impacting neuronal function.
Area of Science:
- Neuroscience
- Neurophysiology
- Molecular Neuroscience
Background:
- Excitatory amino acids are key neurotransmitters in the central nervous system.
- Understanding their ionic mechanisms is crucial for comprehending neuronal signaling and excitotoxicity.
Purpose of the Study:
- To investigate the ionic mechanisms of excitatory amino acids in the rat motor cortex.
- To differentiate the ionic effects of glutamate and its agonists, particularly NMDA, quisqualate, and kainate.
Main Methods:
- Utilized ion-selective microelectrodes and micropipettes for precise measurements.
- Performed ionophoretic applications of glutamate and its agonists.
- Measured local changes in extracellular sodium ([Na+]o), calcium ([Ca2+]o), and potassium ([K+]o).
Main Results:
- Glutamate agonists caused moderate [K+]o increases and significant tetrodotoxin-insensitive [Na+]o decreases.
- NMDA-induced Na+ responses were blocked by manganese, unlike quisqualate and kainate.
- NMDA triggered substantial [Ca2+]o decreases, while quisqualate and kainate caused [Ca2+]o increases or biphasic changes.
- All tested amino acids reduced extracellular space volume.
Conclusions:
- All tested excitatory amino acids increase neuronal permeability to sodium and potassium ions.
- NMDA-operated channels exhibit significant calcium permeability, though calcium contributes minimally to NMDA-induced inward currents.
- NMDA-specific ionic effects are layer-dependent and linked to pyramidal tract neurons.