Yasuhisa Nakayama

Anti‐prolactin (PRL) autoantibodies suppress PRL bioactivity in patients with macroprolactinaemia

Objectiveu2002 Macroprolactinaemia, mainly caused by anti‐prolactin (PRL) autoantibodies, is frequently found in patients with hyperprolactinaemia. Characteristically, these patients lack clinical symptoms of hyperprolactinaemia, but the serum bioactive PRL concentrations in vitro measured by the Nb2 bioassay are usually high. In this study, we investigated the causes of the discrepancy and the true biological features of macroprolactin.

Down-regulation of Cl− pump ClP55 subunit induced enhancement of glutamate neurotoxicity in cultured rat hippocampal neurons

To test whether the increased intracellular Cl- concentration ([Cl-]i) is responsible for the enhanced glutamate toxicity, antisense oligonucleotide of ClP55, a Cl- -ATPase/pump associated protein, was transfected in cultured rat hippocampal neurons. Neuronal [Cl-]i in the antisense oligonucleotide-transfected culture increased to a level 3- to 4-fold higher than that in control. Glutamate exposure (10 microM, 10 min) increased neuronal apoptosis and decreased Akt-pS473 level in the antisense oligonucleotide-transfected neurons, but not in control or sense oligonucleotide-transfected ones, suggesting the responsibility of elevated [Cl-]i in the enhancement of glutamate neurotoxicity.