Abstract
Since the introduction of ion-selective microelectrodes (SME) by Walker [19], a wealth of evidence has been accumulated indicating that the transmembrane Cl− gradient is not in equilibrium with the membrane potential E m . Depending upon the preparation, both higher (e.g., sheep heart Purkinje fibers [18]; guinea pig vas deferens [1]) and lower intracellular Cl− levels (e.g., crayfish stretch receptor [7,9a]) than those expected from a passive distribution have been measured. A low intracellular Cl− activity a cl i , maintained by Cl− extrusion, appears to be of particular significance in those neurons where the driving force for inhibitory postsynaptic potentials (i. p. s. p.) is provided by the Cl− gradient.
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