Glutamate is transported across the rat blood-brain barrier by a sodium-independent system

Neurosci Lett. 1996 May 24;210(1):9-12. doi: 10.1016/0304-3940(96)12635-5.

Abstract

Transport of L-glutamate from blood to brain in equithesin-anesthetized rats was examined using in situ brain perfusion combined with multiple-time/graphical analysis. In situ perfusion allowed precise control of the composition of the perfusate, which was necessary for a detailed investigation of glutamate transport, while multiple time/graphical analysis permitted evaluation of the rapidly reversible volume and the period when the influx was unidirectional. Glutamate had no reversible volume and efflux from brain occurred after 30 s of perfusion. The in situ transfer coefficient (Kin) ranged from 0.74 +/- 0.07 mul/s per g in parietal cortex to 0.44 +/- 0.07 mul/s per g in hippocampus. L-Glutamate uptake was unaffected by removal of sodium from the perfusate, reduced by 5 mM L-glutamate, L-homocysteate, L-aspartate, plasma and 0.1 mM L-glutamate, while L-cystine did not reduce its uptake. These results suggest that the transport system for glutamate is saturated mainly by L-glutamate at physiological conditions and that it is not the sodium-independent x-C system since glutamate transport was not reduced by L-cystine except in hippocampus and that it was responsive to L-aspartate.

MeSH terms

  • ATP-Binding Cassette Transporters / physiology
  • Amino Acid Transport System X-AG
  • Animals
  • Aspartic Acid / pharmacology
  • Biological Transport / physiology
  • Blood-Brain Barrier / drug effects
  • Blood-Brain Barrier / physiology*
  • Cystine / metabolism
  • Glutamic Acid / analogs & derivatives
  • Glutamic Acid / metabolism*
  • Glutamic Acid / pharmacology
  • Perfusion
  • Rats
  • Rats, Sprague-Dawley
  • Sodium / metabolism*
  • Time Factors

Substances

  • ATP-Binding Cassette Transporters
  • Amino Acid Transport System X-AG
  • Aspartic Acid
  • Glutamic Acid
  • Cystine
  • Sodium