PMID- 3558895
OWN - NLM
STAT- MEDLINE
DCOM- 19870521
LR  - 20151119
IS  - 0021-9967 (Print)
IS  - 0021-9967 (Linking)
VI  - 257
IP  - 3
DP  - 1987 Mar 15
TI  - Effect of prenatal exposure to alcohol on the distribution and time of origin of 
      corticospinal neurons in the rat.
PG  - 372-82
AB  - The distribution and the time of origin of corticospinal neurons were examined in 
      rats prenatally exposed to ethanol and in control rats. The distribution of 
      corticospinal neurons was determined by tracing the retrograde transport of 
      horseradish peroxidase (HRP) from an injection site in the cervical spinal cord. 
      In control rats, HRP-positive neurons were distributed in layer Vb throughout 
      motor area 4, rostral motor area 6/8, dorsal somatosensory area 3, caudal 
      somatosensory area 2, and various "association" regions including parietal areas 
      14, 39, and 40, occipital areas 18a and 18b, cingulate areas 24a and 24b, and 
      prefrontal area 32. In ethanol-exposed rats, the distribution of retrogradely 
      labeled neurons was similar to control animals with three notable exceptions: (1) 
      HRP-positive neurons were evident throughout the rostrocaudal extent of area 6/8; 
      (2) occasionally ectopic labeled neurons were identified in the supragranular 
      layers, layers Va and Vc, and superficial layer VI; and (3) the density of 
      HRP-labeled neurons and the ratio of labeled neurons to the total number of 
      neurons in areas 4, 6/8, 3 and 2 were significantly greater (20-48%) in 
      ethanol-exposed rats than in controls. There was, however, no intergroup 
      difference in the area of the cell bodies of HRP-positive neurons. Taken 
      together, these findings indicate that ethanol exposure resulted in an increased 
      number of corticospinal neurons. The time of origin of corticospinal neurons was 
      determined by using a technique that combined tritiated thymidine autoradiography 
      and retrograde transport of HRP. In control animals, HRP-positive neurons were 
      double labeled by an injection of tritiated thymidine on gestational day (GD) 15, 
      16, or 17. In ethanol-exposed rats, corticospinal neurons were generated on GD 
      16, 17, and 18, the late-generated ones being distributed in caudal area 6/8. 
      These intergroup differences represent a persisting ethanol-induced alteration of 
      cortical structure that may underlie motor dysfunction and mental retardation in 
      fetal alcohol-affected offspring. Moreover, the increase in the number and the 
      delay in the time of origin of corticospinal neurons suggest that the normal 
      process of paring down exuberant corticospinal projections may be affected by 
      prenatal exposure to ethanol.
FAU - Miller, M W
AU  - Miller MW
LA  - eng
GR  - AA 06916/AA/NIAAA NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Comp Neurol
JT  - The Journal of comparative neurology
JID - 0406041
RN  - 3K9958V90M (Ethanol)
RN  - EC 1.11.1.- (Horseradish Peroxidase)
RN  - VC2W18DGKR (Thymidine)
SB  - IM
MH  - Animals
MH  - Cell Count
MH  - Cell Division
MH  - Cerebral Cortex/*drug effects/growth & development/pathology
MH  - Ethanol/*toxicity
MH  - Female
MH  - Fetus/*drug effects
MH  - Horseradish Peroxidase
MH  - Neurons/pathology
MH  - Pregnancy
MH  - Rats
MH  - Rats, Inbred Strains
MH  - Spinal Cord/*drug effects/growth & development/pathology
MH  - Thymidine
EDAT- 1987/03/15 00:00
MHDA- 1987/03/15 00:01
CRDT- 1987/03/15 00:00
PHST- 1987/03/15 00:00 [pubmed]
PHST- 1987/03/15 00:01 [medline]
PHST- 1987/03/15 00:00 [entrez]
AID - 10.1002/cne.902570306 [doi]
PST - ppublish
SO  - J Comp Neurol. 1987 Mar 15;257(3):372-82. doi: 10.1002/cne.902570306.