The role of the electrogenic sodium pump in the glutamate afterhyperpolarization of frog spinal cord.

Drug responses of isolated hemisected frog spinal cords were examined by means of the sucrose-gap technique. The glutamate-induced depolarizations (glu-d) of motoneurones (recorded from ventral roots), and primary afferents (recorded from dorsal roots), were followed by an afterhyperpolarization (glu-a.h.). The depolarization induced by DL-homocysteic acid (DLH) was only occasionally followed by an afterhyperpolarization (DLH-a.h.). The glu-a.h. on both roots persisted in the presence of tetrodotoxin (TTX, 0.1-1 microM), or Ringer solution containing 10 mM-Mg2+; 0.1 mM-Ca2+ or 2 mM-Mn2+; 0.2 mM-Ca2+. This indicated that the response was neither due to the release of endogenous neurally active substances nor to the activation of a Ca2+-sensitive K+ conductance. The glu-a.h. was reduced or blocked by K+-free Ringer solution, 3-acetylstrophanthin (3-Ac-Str; 1 microM) or Li+ ions, and was therefore attributed to the activity of the electrogenic Na+ pump. The duration of depolarization induced by glu or DLH was increased in the presence of K+-free Ringer solution, 1 microM 3-Ac-Str or Li ions. It is therefore suggested that the electrogenic Na+ pump may play a role in limiting the duration of depolarization induced by the action of excitatory amino acids. The re-admission of K+ ions to preparations which had been incubated in K+-free Ringer solution produced a transient hyperpolarization (K-a.h.) of the membrane potential of ventral roots which is also attributable to the activation of the electrogenic Na+ pump. Both the K-a.h. and the glu-a.h. were enhanced in Ca2+-free Ringer solution. It is therefore suggested that the Ca2+ ions may modulate the activity of the electrogenic pump in central nervous tissue.