Intermittent ethanol exposure in adolescent rats: dose-dependent impairments in trace conditioning.
Intermittent ethanol exposure in adolescent rats: dose-dependent impairments in trace conditioning.
复制标题
青春期大鼠间歇性乙醇暴露:微量调节的剂量依赖性损伤。
DOI:
10.1097/01.alc.0000147657.51745.a7
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发表时间:
2004
期刊:
影响因子:
--
通讯作者:
Hunt,PamelaS
中科院分区:
文献类型:
--
作者:
Yttri,EricA;Burk,JoshuaA;Hunt,PamelaS
Background:Recent studies have revealed that the adolescent brain may be especially vulnerable to ethanol‐induced toxicity. Corticolimbic regions are more severely damaged following ethanol exposure during adolescence than during adulthood. The consequences of adolescent ethanol exposure on cognition however, have only recently begun to be explored.Methods:Male and female rats were administered 0, 1.5, 2.5 or 4.5 g/kg ethanol (20% v/v) by acute intragastric gavage during adolescence (postnatal days [PD] 28, 30, 32 and 34). On PD 40, half of the subjects in each dose group were given 5 pairings of a 10‐sec flashing light (CS; conditioned stimulus) immediately followed by mild footshock (US; unconditioned stimulus), a procedure known as delay conditioning. The other half were also given 5 CS‐US pairings, but the US was presented 10 sec after CS offset, a procedure known as trace conditioning. All subjects were tested for CS‐elicited freezing 24 h later.Results:There was no effect of adolescent ethanol exposure on delay conditioned responding, with all subjects demonstrating comparable levels of CS‐elicited freezing. In contrast, the amount of freezing in the trace conditioned subjects was negatively correlated with prior ethanol dose. Specifically, exposure to 2.5 or 4.5 g/kg during adolescence resulted in a deficit in trace conditioned responding.Conclusions:These data indicate that intermittent exposure to ethanol during adolescence results in impairment in hippocampal‐dependent trace conditioning that persists beyond the period of ethanol exposure. Delay conditioning was unaffected by prior ethanol treatment, indicating that there was no difficulty in detecting the CS or US, or in the ability to engage in freezing behavior. These results suggest that the adolescent brain may be particularly vulnerable to the effects of repeated exposure to ethanol that can have consequences for nonspatial, hippocampal‐dependent cognitive abilities.
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DOI:
--
发表时间:
1988
期刊:
Journal of immunology (Baltimore, Md. : 1950)
影响因子:
--
作者:
Koller,BH;Geraghty,DE;Shimizu,Y;DeMars,R;Orr,HT
通讯作者:
Orr,HT
影响因子:
--
作者:
Sarmiento,UM;Storb,RF
通讯作者:
Storb,RF
影响因子:
--
作者:
K. Krumbacher;M. J. van der Feltz;M. Happel;C. Gerlach;L. K. Lösslein;H. Grosse
通讯作者:
H. Grosse
影响因子:
6.2
作者:
R. W. Bull;H. Vriesendorp;R. Cech;H. Grosse;A. Bijma;W. Ladiges;K. Krumbacher;I. Doxiadis;H. Ejima;J. Templeton;E. Albert;R. Storb;H. Deeg
通讯作者:
H. Deeg
影响因子:
4.4
作者:
T. Kindt;D. Singer
通讯作者:
D. Singer