PMID- 20175221
OWN - NLM
STAT- MEDLINE
DCOM- 20100719
LR  - 20151119
IS  - 1098-2396 (Electronic)
IS  - 0887-4476 (Linking)
VI  - 64
IP  - 6
DP  - 2010 Jun
TI  - Neuroprotective effect of vitamin C against the ethanol and nicotine modulation 
      of GABA(B) receptor and PKA-alpha expression in prenatal rat brain.
PG  - 467-77
LID - 10.1002/syn.20752 [doi]
AB  - Prenatal ethanol exposure has various deleterious effects on neuronal development 
      and can induce various defects in developing brain, resulting in fetal alcohol 
      syndrome (FAS). gamma-Aminobutyric acid (GABA(B)) receptor (R) is known to play 
      an important role during the development of the central nervous system (CNS). Our 
      study was designed to investigate the effect of ethanol (100 mM), nicotine (50 
      microM) (for 30 min and 1 h), vitamin C (vitC, 0.5 mM), ethanol plus vitC, and 
      nicotine plus vitC on expression level of GABA(B1), GABA(B2)R, and protein kinase 
      A-alpha (PKA) in prenatal rat cortical and hippocampal neurons at gestational 
      days (GD) 17.5. The results showed that, upon ethanol and nicotine exposure, 
      GABA(B1) and GABA(B2)R protein expression increased significantly in the cortex 
      and hippocampus for a short (30 min) and long term (1 h), whereas only GABA(B2)R 
      subunit was decreased upon nicotine exposure for a long term in the cortex. 
      Furthermore, PKA expression in cortex and hippocampus increased with ethanol 
      exposure during short term, whereas long-term exposure results increased in 
      cortex and decreased in hippocampus. Moreover, the cotreatment of vitC with 
      ethanol and nicotine showed significantly decreased expression of GABA(B1), 
      GABA(B2)R, and PKA in cortex and hippocampus for a long-term exposure. 
      Mitochondrial membrane potential, Fluoro-jade-B, and propidium iodide staining 
      were used to elucidate possible neurodegeneration. Our results suggest the 
      involvement of GABA(B)R and PKA in nicotine and ethanol-mediated 
      neurodevelopmental defects and the potential use of vitC as a effective 
      protective agent for FAS-related deficits.
FAU - Naseer, M I
AU  - Naseer MI
AD  - Division of Life Science, College of Natural Sciences and Applied Life Science 
      (Brain Korea 21), Gyeongsang National University, Chinju 660-701, South Korea.
FAU - Lee, H Y
AU  - Lee HY
FAU - Kim, M O
AU  - Kim MO
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Synapse
JT  - Synapse (New York, N.Y.)
JID - 8806914
RN  - 0 (Antioxidants)
RN  - 0 (Central Nervous System Depressants)
RN  - 0 (Neuroprotective Agents)
RN  - 0 (Receptors, GABA-B)
RN  - 3K9958V90M (Ethanol)
RN  - 6M3C89ZY6R (Nicotine)
RN  - EC 2.7.11.11 (Cyclic AMP-Dependent Protein Kinases)
RN  - PQ6CK8PD0R (Ascorbic Acid)
SB  - IM
MH  - Alcohol-Induced Disorders, Nervous System/*drug 
      therapy/metabolism/physiopathology
MH  - Animals
MH  - Antioxidants/pharmacology/therapeutic use
MH  - Ascorbic Acid/*pharmacology/therapeutic use
MH  - Cells, Cultured
MH  - Central Nervous System Depressants/antagonists & inhibitors/toxicity
MH  - Cyclic AMP-Dependent Protein Kinases/drug effects/metabolism
MH  - Ethanol/*antagonists & inhibitors/toxicity
MH  - Female
MH  - Neuroprotective Agents/*pharmacology/therapeutic use
MH  - Nicotine/antagonists & inhibitors/toxicity
MH  - Pregnancy
MH  - Prenatal Exposure Delayed Effects/chemically induced/*drug 
      therapy/physiopathology
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Receptors, GABA-B/drug effects/metabolism
EDAT- 2010/02/23 06:00
MHDA- 2010/07/20 06:00
CRDT- 2010/02/23 06:00
PHST- 2010/02/23 06:00 [entrez]
PHST- 2010/02/23 06:00 [pubmed]
PHST- 2010/07/20 06:00 [medline]
AID - 10.1002/syn.20752 [doi]
PST - ppublish
SO  - Synapse. 2010 Jun;64(6):467-77. doi: 10.1002/syn.20752.