PMID- 23218665
OWN - NLM
STAT- MEDLINE
DCOM- 20130627
LR  - 20240323
IS  - 1873-6823 (Electronic)
IS  - 0741-8329 (Print)
IS  - 0741-8329 (Linking)
VI  - 47
IP  - 1
DP  - 2013 Feb
TI  - The role of cortisol in chronic binge alcohol-induced cerebellar injury: Ovine 
      model.
PG  - 53-61
LID - S0741-8329(12)00176-0 [pii]
LID - 10.1016/j.alcohol.2012.10.004 [doi]
AB  - Women who drink alcohol during pregnancy are at high risk of giving birth to 
      children with neurodevelopmental disorders. Previous reports from our laboratory 
      have shown that third trimester equivalent binge alcohol exposure at a dose of 
      1.75 g/kg/day results in significant fetal cerebellar Purkinje cell loss in fetal 
      sheep and that both maternal and fetal adrenocorticotropin (ACTH) and cortisol 
      levels are elevated in response to alcohol treatment. In this study, we 
      hypothesized that repeated elevations in cortisol from chronic binge alcohol are 
      responsible at least in part for fetal neuronal deficits. Animals were divided 
      into four treatment groups: normal control, pair-fed saline control, alcohol and 
      cortisol. The magnitude of elevation in cortisol in response to alcohol was 
      mimicked in the cortisol group by infusing pregnant ewes with hydrocortisone for 
      6 h on each day of the experiment, and administering saline during the first hour 
      in lieu of alcohol. The experiment was conducted on three consecutive days 
      followed by four days without treatment beginning on gestational day (GD) 109 
      until GD 132. Peak maternal blood alcohol concentration in the alcohol group was 
      239 +/- 7 mg/dl. The fetal brains were collected and processed for stereological 
      cell counting on GD 133. The estimated total number of fetal cerebellar Purkinje 
      cells, the reference volume and the Purkinje cell density were not altered in 
      response to glucocorticoid infusion in the absence of alcohol. These results 
      suggest that glucocorticoids independently during the third trimester equivalent 
      may not produce fetal cerebellar Purkinje cell loss. However, the elevations in 
      cortisol along with other changes induced by alcohol could together lead to brain 
      injury seen in the fetal alcohol spectrum disorders.
CI  - Published by Elsevier Inc.
FAU - Washburn, Shannon E
AU  - Washburn SE
AD  - Department of Veterinary Physiology and Pharmacology and Michael E. DeBakey 
      Institute, College of Veterinary Medicine and Biomedical Sciences, Texas A&M 
      University, College Station, TX 77843, USA. swashburn@cvm.tamu.edu
FAU - Tress, Ursula
AU  - Tress U
FAU - Lunde, Emilie R
AU  - Lunde ER
FAU - Chen, Wei-Jung A
AU  - Chen WJ
FAU - Cudd, Timothy A
AU  - Cudd TA
LA  - eng
GR  - K08 AA018166/AA/NIAAA NIH HHS/United States
GR  - R01 AA010940/AA/NIAAA NIH HHS/United States
GR  - K08AA18166/AA/NIAAA NIH HHS/United States
GR  - AA10940/AA/NIAAA NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
DEP - 20121205
PL  - United States
TA  - Alcohol
JT  - Alcohol (Fayetteville, N.Y.)
JID - 8502311
RN  - WI4X0X7BPJ (Hydrocortisone)
SB  - IM
MH  - Alcoholic Intoxication/complications/pathology/*physiopathology
MH  - Animals
MH  - Cerebellum/*drug effects/pathology
MH  - Disease Models, Animal
MH  - Female
MH  - Fetal Alcohol Spectrum Disorders/pathology
MH  - Hydrocortisone/blood/*pharmacology
MH  - Pregnancy
MH  - Purkinje Cells/drug effects
MH  - Sheep, Domestic
PMC - PMC3544992
MID - NIHMS427694
EDAT- 2012/12/12 06:00
MHDA- 2013/06/29 06:00
PMCR- 2014/02/01
CRDT- 2012/12/11 06:00
PHST- 2012/06/10 00:00 [received]
PHST- 2012/10/29 00:00 [revised]
PHST- 2012/10/31 00:00 [accepted]
PHST- 2012/12/11 06:00 [entrez]
PHST- 2012/12/12 06:00 [pubmed]
PHST- 2013/06/29 06:00 [medline]
PHST- 2014/02/01 00:00 [pmc-release]
AID - S0741-8329(12)00176-0 [pii]
AID - 10.1016/j.alcohol.2012.10.004 [doi]
PST - ppublish
SO  - Alcohol. 2013 Feb;47(1):53-61. doi: 10.1016/j.alcohol.2012.10.004. Epub 2012 Dec 
      5.