| Abstract: | Exposure to sodium-deficient (tris) saline caused an appreciable decline in the sodium content of intact connectives in the absence of equivalent reduction in the amplitude of the recorded action potentials. Return of sodium-depleted connectives to normal saline resulted in a rapid recovery of axonal function despite only a partial (less than 70%) recovery in sodium content. Replacement of sodium ions by those of lithium in the bathing medium resulted in a substantial accumulation of this cation. Lithium movements exhibited a marked asymetry, no significant decline in concentration being observed upon return to normal saline. These results are tentatively interpreted in terms of an exchangeable glial sodium fraction and are discussed in relation to extra-axonal sodium regulation. |
