Ionic mechanisms associated with the depolarization by glutamate and aspartate on human and rat spinal neurones in tissue culture.
The action of glutamate and aspartate was studied on the membrane potential of human and rat spinal neurones in tissue culture. Both amino acids caused a depolarization of the cell membrane, the size of which was dependent on the concentration of the amino acids in the bathing fluid. In order to study ionic mechanisms associated with the amino acid depolarization, the ionic composition of the extracellular fluid was altered. Removal of sodium ions from the bathing solution reversibly reduced or abolished the depolarization produced by glutamate and aspartate suggesting that the action of these amino acids is associated with an increased sodium permeability. Substituting lithium for sodium ions also reversibly abolished the depolarization by glutamate indicating that in contrast to the effect of lithium on the action potential, this ion cannot replace sodium for the glutamate depolarization. These experiments show that the method of tissue culture is a suitable model to study ionic mechanisms underlying the action of neurotransmitters in the mammalian and especially in the human CNS.
D000818:Animals; D001224:Aspartic Acid / Q000494:pharmacology*; D002794:Choline / Q000494:pharmacology; D046508:Culture Techniques; D005971:Glutamates / Q000494:pharmacology*; D006801:Humans; D008094:Lithium / Q000494:pharmacology; D008564:Membrane Potentials / Q000187:drug effects; D009474:Neurons / Q000187:drug effects* / Q000502:physiology; D051381:Rats; D012964:Sodium / Q000378:metabolism*; D013127:Spinal Nerves / Q000187:drug effects / Q000502:physiology*
D005971:Glutamates; D001224:Aspartic Acid; D008094:Lithium; D012964:Sodium; D002794:Choline