Susceptibility of striatal neurons to excitotoxic injury correlates with basal levels of Bcl-2 and the induction of P53 and c-Myc immunoreactivity

Neurobiol Dis. 2005 Nov;20(2):562-73. doi: 10.1016/j.nbd.2005.04.011.

Abstract

The present studies evaluated the potential contribution of Bcl-2, p53, and c-Myc to the differential vulnerability of striatal neurons to the excitotoxin quinolinic acid (QA). In normal rat striatum, Bcl-2 immunoreactivity (Bcl-2-i) was most intense in large aspiny interneurons including choline acetyltransferase positive (CAT+) and parvalbumin positive (PARV+) neurons, but low in a majority of medium-sized neurons. In human brain, intense Bcl-2-i was seen in large striatal neurons but not in medium-sized spiny projection neurons. QA produced degeneration of numerous medium-sized neurons, but not those enriched in Bcl-2-i. Many Bcl-2-i-enriched interneurons including those with CAT+ and PARV+ survived QA injection, while medium-sized neurons labeled for calbindin D-28K (CAL D-28+) did not. In addition, proapoptotic proteins p53-i and c-Myc-i were robustly induced in medium-sized neurons, but not in most large neurons. The selective vulnerability of striatal medium spiny neurons to degeneration in a rodent model of Huntington's disease appears to correlate with their low levels of Bcl-2-i and high levels of induced p53-i and c-Myc-i.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Aged, 80 and over
  • Animals
  • Calbindins
  • Choline O-Acetyltransferase / metabolism
  • Corpus Striatum / metabolism*
  • Corpus Striatum / pathology
  • Corpus Striatum / physiopathology
  • Disease Models, Animal
  • Disease Susceptibility / metabolism
  • Disease Susceptibility / physiopathology
  • Humans
  • Huntington Disease / metabolism*
  • Huntington Disease / pathology
  • Huntington Disease / physiopathology
  • Immunohistochemistry
  • Male
  • Middle Aged
  • Nerve Degeneration / metabolism*
  • Nerve Degeneration / pathology
  • Nerve Degeneration / physiopathology
  • Neurons / drug effects
  • Neurons / metabolism*
  • Neurons / pathology
  • Neurotoxins / pharmacology
  • Parvalbumins / metabolism
  • Proto-Oncogene Proteins c-bcl-2 / metabolism*
  • Proto-Oncogene Proteins c-myc / metabolism*
  • Quinolinic Acid / pharmacology
  • Rats
  • Rats, Sprague-Dawley
  • Reference Values
  • S100 Calcium Binding Protein G / metabolism
  • Tumor Suppressor Protein p53 / metabolism*

Substances

  • Calbindins
  • Neurotoxins
  • Parvalbumins
  • Proto-Oncogene Proteins c-bcl-2
  • Proto-Oncogene Proteins c-myc
  • S100 Calcium Binding Protein G
  • Tumor Suppressor Protein p53
  • Choline O-Acetyltransferase
  • Quinolinic Acid