PMID- 24810836
OWN - NLM
STAT- MEDLINE
DCOM- 20151110
LR  - 20211021
IS  - 1590-3478 (Electronic)
IS  - 1590-1874 (Linking)
VI  - 35
IP  - 11
DP  - 2014 Nov
TI  - Downregulation of dopamine D(1) receptors and increased neuronal apoptosis upon 
      ethanol and PTZ exposure in prenatal rat cortical and hippocampal neurons.
PG  - 1681-8
LID - 10.1007/s10072-014-1812-7 [doi]
AB  - The objective of this study was to evaluate the effect of ethanol and 
      pentylenetetrazol (PTZ) on the expression of dopamine receptors (D1R) and to 
      observe the apoptotic neurodegeneration in prenatal rat cortical and hippocampal 
      neurons at gestational days (GD) 17.5. In the present study, ethanol (100 mM) and 
      PTZ (15 mM) were exposed to the prenatal rat cortical and hippocampal neuronal 
      cell cultures for 1 h. For mRNA RT-PCR and for protein Western blot analysis was 
      done to elucidate D1R, Bax, Bak, Bcl-2 and cleaved caspase-3 expression upon 
      ethanol and PTZ exposure in neuronal cell cultures. Furthermore, ethanol and 
      PTZ-induced apoptotic neurodegeneration was also observed using TUNEL staining 
      and propidium iodide (PI) used as counter stain under confocal microscopy. The 
      results of present study showed that ethanol and PTZ exposure significantly 
      decreased D1R expression and induced neuronal death by significantly increasing 
      the expression of pro-apoptotic Bax, Bak and decreasing anti-apoptotic protein 
      Bcl-2 leading to the apoptosis by increasing cleaved caspase-3 expression in 
      cortical and hippocampal primary neuronal cell cultures. Our findings indicated 
      that ethanol and PTZ exposure to the prenatal neurons showed not only 
      downregulation of D1R but also causes neuronal apoptosis in the developing rat 
      brain. Further, this explains the possibility of higher risk of developmental 
      disturbances and malformations during early developmental stage.
FAU - Naseer, Muhammad Imran
AU  - Naseer MI
AD  - Center of Excellence in Genomic Medicine and Research (CEGMR), King Abdulaziz 
      University, Jeddah, 21589, Saudi Arabia, mimrannaseer@yahoo.com.
FAU - Ullah, Ikram
AU  - Ullah I
FAU - Rasool, Mahmood
AU  - Rasool M
FAU - Ansari, Shakeel Ahmed
AU  - Ansari SA
FAU - Sheikh, Ishfaq Ahmed
AU  - Sheikh IA
FAU - Bibi, Fehmida
AU  - Bibi F
FAU - Chaudhary, Adeel Gulzar
AU  - Chaudhary AG
FAU - Al-Qahtani, Mohammed H
AU  - Al-Qahtani MH
FAU - Kim, Myeong Ok
AU  - Kim MO
LA  - eng
PT  - Journal Article
DEP - 20140509
PL  - Italy
TA  - Neurol Sci
JT  - Neurological sciences : official journal of the Italian Neurological Society and 
      of the Italian Society of Clinical Neurophysiology
JID - 100959175
RN  - 0 (Convulsants)
RN  - 0 (Receptors, Dopamine D1)
RN  - 3K9958V90M (Ethanol)
RN  - WM5Z385K7T (Pentylenetetrazole)
SB  - IM
EIN - Neurol Sci. 2014 Nov;35(11):1689. Kim, Myeong Ok [added]
MH  - Animals
MH  - Apoptosis/*drug effects
MH  - Blotting, Western
MH  - Cells, Cultured
MH  - Cerebral Cortex/drug effects/metabolism/pathology
MH  - Convulsants/toxicity
MH  - Down-Regulation
MH  - Ethanol/*toxicity
MH  - Female
MH  - Hippocampus/*drug effects/metabolism/pathology
MH  - In Situ Nick-End Labeling
MH  - Neurons/*drug effects/metabolism/pathology
MH  - Pentylenetetrazole/toxicity
MH  - Pregnancy
MH  - Prenatal Exposure Delayed Effects/*metabolism/pathology
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Receptors, Dopamine D1/*biosynthesis
MH  - Reverse Transcriptase Polymerase Chain Reaction
EDAT- 2014/05/09 06:00
MHDA- 2015/11/11 06:00
CRDT- 2014/05/10 06:00
PHST- 2013/11/08 00:00 [received]
PHST- 2014/04/23 00:00 [accepted]
PHST- 2014/05/10 06:00 [entrez]
PHST- 2014/05/09 06:00 [pubmed]
PHST- 2015/11/11 06:00 [medline]
AID - 10.1007/s10072-014-1812-7 [doi]
PST - ppublish
SO  - Neurol Sci. 2014 Nov;35(11):1681-8. doi: 10.1007/s10072-014-1812-7. Epub 2014 May 
      9.