A brain-to-blood carrier-mediated transport system for small, N-tyrosinated peptides

Pharmacol Biochem Behav. 1984 Dec;21(6):943-6. doi: 10.1016/s0091-3057(84)80077-5.

Abstract

Recently, we found that lipophilicity is a good predictor of the degree to which most peptides cross the blood-brain-barrier. Small (MW less than 1000) peptides with an N-terminal tyrosine, however, penetrated to a much smaller degree than was predicted by their measurements of lipophilicity. We show here that two such peptides, N-Tyr-MIF-1 and Met-enkephalin, can significantly inhibit transport of 125I-N-Tyr-MIF-1 out of the rat brain in vivo in a saturable, dose-dependent way. The half-time disappearance of injected 125I-N-Tyr-MIF-1 from the rat brain was 12.4 min but when injected with 200 nmol/animal of unlabeled N-Tyr-MIF-1 was 23.6 min (p less than 0.01). The Km was calculated to be 0.123 nmol. At higher doses, leucine, but not tyrosine, alanine, glutamine, MIF-1, or the dipeptide Gly-Gly, also significantly inhibited transport out of the brain.

Publication types

  • Comparative Study
  • Research Support, U.S. Gov't, Non-P.H.S.

MeSH terms

  • Amino Acids / pharmacology
  • Animals
  • Blood-Brain Barrier* / drug effects
  • Depression, Chemical
  • Enkephalin, Methionine / pharmacology
  • Glycylglycine / pharmacology
  • MSH Release-Inhibiting Hormone / analogs & derivatives*
  • MSH Release-Inhibiting Hormone / metabolism
  • MSH Release-Inhibiting Hormone / pharmacology
  • Rats

Substances

  • Amino Acids
  • Glycylglycine
  • Enkephalin, Methionine
  • tyrosyl-prolyl-leucyl-glycinamide
  • MSH Release-Inhibiting Hormone