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ELEVATED EXTRACELLULAR POTASSIUM AS A STIMULUS FOR RELEASING [<sup>3</sup>H]NOREPINEPHRINE AND [<sup>14</sup>C]<i>α</i>‐AMINOISOBUTYRATE FROM NEOCORTICAL SLICES. SPECIFICITY AND CALCIUM DEPENDENCY OF THE PROCESS
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Citations
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References
1976
Year
Synaptic TransmissionElevated Extracellular PotassiumNeuromodulation TherapiesNe ReleaseNeurotransmitterNeurotransmissionExtracellular Calcium IonsSocial SciencesNeurologyNeurochemistryThe ProcessSodium HomeostasisIon ChannelsNeuropharmacologyCalcium IonsNervous SystemPharmacologyPotassium HomeostasisSynaptic PlasticityNeurophysiologyCellular NeurosciencePhysiologyNeuroscienceBrain ElectrophysiologyCentral Nervous SystemElectrophysiologyMedicine
Abstract —The effect of short (4–6 min)‘pulses’ of elevated extracellular potassium ions K 0 , in the 10–50 m m range, on the efflux of [ 3 H]norepinephrine [ 3 H]NE) and [ 14 C]α‐aminoisobutyrate (AIB) has been studied in a superfused neocortical thin slice system. At all the concentrations tested high K 0 increases the efflux of both NE and AIB, although thc effects on the former are greater. In the absence of calcium ions, or in the presence of 8 m m ‐MnCl 2 , the potassium‐stimulated release of both NE and AIB is severely depressed. However, potassium induced NE release is proportional to extracellular calcium ions in the 0–1.5 m m range, while that of AIB does not continue to increase above 0.2 m m ‐calcium. This permissive role of calcium in amino acid efflux is interpreted as due to changes in the inactivation of membrane sodium conductance.
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