Postischemic binding of [3H]phorbol 12,13-dibutyrate and [3H]inositol 1,4,5-trisphosphate in the gerbil brain: an autoradiographic study.

Abstract

Postischemic alteration of second messenger systems was investigated in the Mongolian gerbil, utilizing [3H]phorbol 12,13-dibutyrate and [3H]inositol 1,4,5-trisphosphate receptor autoradiography. Transient ischemia was induced for 10 min, and animals were allowed to survive for various recirculation periods of up to one month. [3H]Phorbol 12,13-dibutyrate binding in selectively vulnerable areas showed no significant change 1-24 h after ischemia except for a transient decline in a few regions. Thereafter, the binding in most of the selectively vulnerable areas showed significant alteration 48 h or seven days after ischemia. Interestingly, dentate molecular layer which was resistant to ischemia showed a significant elevation in the number of [3H]phorbol 12,13-dibutyrate binding sites. One month after ischemia, [3H]phorbol 12,13-dibutyrate binding showed significant reduction only in the striatum and the hippocampal CA1 sector where severe neuronal damage was seen morphologically. A significant elevation in the number of [3H]phorbol 12,13-dibutyrate binding sites was still seen in the dentate molecular layer one month after ischemia. In contrast, [3H]inositol 1,4,5-trisphosphate binding showed significant reduction in the selectively vulnerable regions 1-24 h after ischemia. Thereafter, [3H]inositol 1,4,5-trisphosphate binding in most of the selectively vulnerable areas markedly decreased up to one month after ischemia. In the dentate molecular layer, [3H]inositol 1,4,5-trisphosphate binding also showed significant reduction during recirculation except for a slight recovery 48 h and seven days after ischemia. One month after ischemia, the binding in all regions showed significant reduction. These results suggest that postischemic alteration of two second messenger (protein kinase C and inositol 1,4,5-trisphosphate) binding sites was produced with different processes in selectively vulnerable areas.(ABSTRACT TRUNCATED AT 250 WORDS)

• Authors: T Araki, H Kato, H Hara, K Kogure
• Journal: Neuroscience (Neuroscience) Vol. 46 Issue 4 Pg. 973-80 ( 1992) ISSN: 0306-4522 [Print] United States
• PMID: 1311818 (Publication Type: Journal Article)

Chemical References

• Caenorhabditis elegans Proteins
• Calcium Channels
• Carrier Proteins
• Inositol 1,4,5-Trisphosphate Receptors
• Receptors, Cell Surface
• Receptors, Cytoplasmic and Nuclear
• Receptors, Drug
• phorbol ester binding protein
• phorbol ester receptor
• Tritium
• Phorbol 12,13-Dibutyrate
• Inositol 1,4,5-Trisphosphate
• Protein Kinase C

Topics

• Animals
• Autoradiography
• Brain (metabolism)
• Caenorhabditis elegans Proteins
• Calcium Channels
• Carrier Proteins
• Gerbillinae
• Inositol 1,4,5-Trisphosphate (metabolism)
• Inositol 1,4,5-Trisphosphate Receptors
• Ischemic Attack, Transient (metabolism)
• Male
• Organ Specificity
• Phorbol 12,13-Dibutyrate (metabolism)
• Protein Kinase C
• Receptors, Cell Surface (metabolism)
• Receptors, Cytoplasmic and Nuclear
• Receptors, Drug (metabolism)
• Reference Values
• Reperfusion
• Time Factors
• Tritium