De novo expression of calretinin in trimethyltin-induced degeneration of developing rat hippocampus

Brain Res Mol Brain Res. 2002 Jan 31;98(1-2):141-4. doi: 10.1016/s0169-328x(01)00334-5.

Abstract

In the model of trimethyltin (TMT)-induced neurodegeneration in developing rat hippocampus, calretinin (CR)-immunoreactive neurons are selectively spared and even more numerous than in controls. We investigated the possibility of an additional synthesis of CR using RT-PCR. The amount of CR mRNA increased significantly after TMT treatment. CR mRNA production after TMT treatment could hypothetically be regarded as a compensatory phenomenon in developing rats.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Calbindin 2
  • Calcium / metabolism
  • DNA, Complementary / genetics
  • Hippocampus / drug effects*
  • Hippocampus / growth & development
  • Hippocampus / metabolism
  • Nerve Degeneration / chemically induced*
  • Nerve Degeneration / genetics
  • Nerve Degeneration / metabolism
  • Nerve Tissue Proteins / biosynthesis*
  • Nerve Tissue Proteins / genetics
  • Neurotoxins / toxicity*
  • RNA, Messenger / genetics
  • Rats
  • Reverse Transcriptase Polymerase Chain Reaction
  • S100 Calcium Binding Protein G / biosynthesis*
  • S100 Calcium Binding Protein G / genetics
  • Trimethyltin Compounds / toxicity*

Substances

  • Calb2 protein, rat
  • Calbindin 2
  • DNA, Complementary
  • Nerve Tissue Proteins
  • Neurotoxins
  • RNA, Messenger
  • S100 Calcium Binding Protein G
  • Trimethyltin Compounds
  • trimethyltin
  • Calcium