TY - JOUR
T1 - Prenatal exposure to alcohol in adult rats
T2 - Relationships between sleep and memory deficits, and effects of glucose administration on memory
AU - Stone, William S.
AU - Altman, Harvey J.
AU - Hall, Jeremy
AU - Arankowsky-Sandoval, Gloria
AU - Parekh, Priti
AU - Gold, Paul E.
N1 - Funding Information:
Supported by research grants from the National Institute on Aging (AG 07648), the National Institute of Neurological Disorders and Stroke (NS32914), the National Science Foundation (BNS-9012239 and BNS-8914941), and the Office of Naval Research (NOOO1489-J-1216). We are grateful to the Fetal Alcohol Research Center at Wayne State University (Detroit, MI) for supplying prenatally exposed rats.
PY - 1996/12/2
Y1 - 1996/12/2
N2 - Previous studies show that prenatal exposure to alcohol results in sleep deficits in rats, including reductions in paradoxical sleep. Little is known, however, about the extent or duration of sleep impairments beyond the neonatal period. The present experiment examined effects of prenatal exposure on sleep in young adulthood. Three-hour, daytime sleep EEGs were obtained in 6-month-old female rats prenatally exposed to alcohol. Compared to isocaloric pair-fed and ad libitum control groups, the alcohol-exposed group showed reduced paradoxical sleep. Non-paradoxical sleep did not differ between groups. Concurrent deficits were obtained in radial arm maze, but not inhibitory (passive) avoidance, performance. One year later, at the age of 18 months, alcohol-exposed rats showed deficits in spontaneous alternation behavior which were reversed by administration of glucose (100 mg/kg). Deficits in paradoxical sleep at 6 months of age were highly correlated with deficits in spontaneous alternation behavior at 18 months of age, in individual, alcohol-exposed animals. These results provide the first evidence that prenatal exposure to alcohol results in selective and persistent deficits in sleep. They also show that measures of paradoxical sleep can predict impaired memory over a large portion of the life span, and suggest that glucose can attenuate memory deficits in this population.
AB - Previous studies show that prenatal exposure to alcohol results in sleep deficits in rats, including reductions in paradoxical sleep. Little is known, however, about the extent or duration of sleep impairments beyond the neonatal period. The present experiment examined effects of prenatal exposure on sleep in young adulthood. Three-hour, daytime sleep EEGs were obtained in 6-month-old female rats prenatally exposed to alcohol. Compared to isocaloric pair-fed and ad libitum control groups, the alcohol-exposed group showed reduced paradoxical sleep. Non-paradoxical sleep did not differ between groups. Concurrent deficits were obtained in radial arm maze, but not inhibitory (passive) avoidance, performance. One year later, at the age of 18 months, alcohol-exposed rats showed deficits in spontaneous alternation behavior which were reversed by administration of glucose (100 mg/kg). Deficits in paradoxical sleep at 6 months of age were highly correlated with deficits in spontaneous alternation behavior at 18 months of age, in individual, alcohol-exposed animals. These results provide the first evidence that prenatal exposure to alcohol results in selective and persistent deficits in sleep. They also show that measures of paradoxical sleep can predict impaired memory over a large portion of the life span, and suggest that glucose can attenuate memory deficits in this population.
KW - glucose
KW - inhibitory avoidance
KW - memory
KW - prenatal alcohol exposure
KW - radial arm maze
KW - sleep
KW - spontaneous alternation
UR - http://www.scopus.com/inward/record.url?scp=0030566644&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0030566644&partnerID=8YFLogxK
U2 - 10.1016/S0006-8993(96)00976-6
DO - 10.1016/S0006-8993(96)00976-6
M3 - Article
C2 - 9117426
AN - SCOPUS:0030566644
SN - 0006-8993
VL - 742
SP - 98
EP - 106
JO - Brain Research
JF - Brain Research
IS - 1-2
ER -