ANION TRANSPORT MECHANISMS IN NEURONS

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Abstract
Evidence has been presented and reviewed to show that chloride is often not in electrochemical equilibrium across neuronal cell membranes. An ATP- and sodium-dependent uptake mechanism has been described for the squid giant axon. Finally, the role of chloride in the maintenance of pH1 has been discussed. Present evidence favors a net chloride extrusion being involved in the acid extrusion process. Measurements of free, ionized chloride levels in several neuronal cells have suggested that the transmembrane distribution of chloride does not conform to thermodynamic equilibrium conditions. Net extrusion of Cl- against its electrochemical gradient has been measured in the giant neuron of the Aplysia abdominal ganglion. In the squid giant axon, cellular Cl- levels are higher than predicted from passive thermodynamic considerations. An ATP requirement as well as a dependence upon extracellular sodium has been demonstrated for chloride influx. Similarly, there is an ATP-, external Cl-dependent, Na+ influx. Thus, an ATP-requiring Na-Cl cotransport mechanism appears to account for the high cellular chloride content of the squid giant axon. Chloride efflux from several neurons appears to be involved in the regulation of intracellular pH (pHI). When pHi is made acidic, chloride efflux from the squid giant axon increases and this stimulation requires cellular ATP and external HCO3-. When pHi is measured following an acid load, it is found that pHi recovery toward normal values requires cellular Cl-, ATP and external HCO3-. Thus, an exchange process between cellular Cl- and extracellular HCO3- appears to play an important role in pH1 regulation. Such a process appears to be responsible for the lower-than-equilibrium levels of chloride found in certain neuronal cells.