Paper Information

Title: 

MATERNAL ORAL CONSUMPTION OF MORPHINE INCREASES BAX/BCL-2 RATIO AND CASPASE-3 ACTIVITY DURING EARLY DEVELOPMENT OF NEURAL SYSTEM IN RAT EMBRYOS

Type: POSTER
Author(s): NASIRI MOGHADAM H.*,KAZEMINEZHAD B.,DARGAHI L.,AHMADIAN ABOU ALHASAN
 
 *NEUROSCIENCE RESEARCH CENTER, SAHHID BEHESHTI UNIVERSITY OF MEDICAL SCIENCES, TEHRAN, IRAN
 
Name of Seminar: IRANIAN CONGRESS OF PHYSIOLOGY AND PHARMACOLOGY
Type of Seminar:  CONGRESS
Sponsor:  PHYSIOLOGY AND PHARMACOLOGY SOCIETY, MASHHAD UNIVERSITY OF MEDICAL SCIENCE
Date:  2009Volume 19
 
 
Abstract: 

Maternal morphine consumption has shown defects in fetus and offspring, but the underlying molecular mechanisms of these defects remain unclear. Regarding the critical role of apoptosis in normal development of the central nervous system, we investigated the effect of intrauterine morphine exposure on programmed cell death of neuroblasts during the early development of neural system. Pregnant Wistar rats received morphine sulfate in drinking water (0.01 mg/ml) from the first day of gestation up to the time of sampling. Control group received tap water. Pregnant rats in gestational days 9.5 to 13.5 and embryos were taken out, fixed and embedded in paraffin. Immunohistochemical assay was used to investigate the protein expression of Bax, Bcl2 and activation of caspase3. The results showed a significant increase in Bax immunoreactivity at all of the mentioned embryonic days and a significant decrease in Bcl-2 immunoreactivity at days E10.5 to E13.5 in morphine-treated groups compared with control. Data analysis revealed that Bax/Bcl2 ratio was increased in all of the morphine-exposed groups. Consistent with these results, immunostaining of cleaved caspase3 showed a significant increase in the activity of this effector protease at days E11.5 to E13.5. These finding suggests that morphine exposure during the first embryonic days enhances neuroblasts apoptosis by upregulating the Bax/Bcl-2 gene expression, and increasing downstream caspase-3 activity in the developing neural system. The increased apoptosis of neuroblasts may be the cause of morphine induced-defects in the central nervous system development.

 
Keyword(s): EARLY DEVELOPMENT, MORPHINE, BAX, BCL-2, CASPASE3
 
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