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.
D000818:Animals; D002118:Calcium / Q000502:physiology; D004305:Dose-Response Relationship, Drug; D005971:Glutamates / Q000494:pharmacology*; D006710:Homocysteine / Q000031:analogs & derivatives / Q000494:pharmacology; D066298:In Vitro Techniques; D007473:Ion Channels; D008094:Lithium / Q000494:pharmacology; D008564:Membrane Potentials / Q000187:drug effects; D011188:Potassium / Q000502:physiology; D011894:Rana pipiens; D012964:Sodium / Q000378:metabolism*; D012970:Sodium Glutamate / Q000494:pharmacology*; D013116:Spinal Cord / Q000378:metabolism / Q000502:physiology*; D013126:Spinal Nerve Roots / Q000378:metabolism; D013328:Strophanthins / Q000494:pharmacology; D013696:Temperature
D005971:Glutamates; D007473:Ion Channels; D013328:Strophanthins; D006710:Homocysteine; C007956:homocysteic acid; C038677:3-acetylstrophanthin; D008094:Lithium; D012964:Sodium; D011188:Potassium; D002118:Calcium; D012970:Sodium Glutamate