Aims

To support the free and open dissemination of research findings and information on alcoholism and alcohol-related problems. To encourage open access to peer-reviewed articles free for all to view.

For full versions of posted research articles readers are encouraged to email requests for "electronic reprints" (text file, PDF files, FAX copies) to the corresponding or lead author, who is highlighted in the posting.

___________________________________________

Monday, December 17, 2012

Imbalanced Synaptic Plasticity Induced Spatial Cognition Impairment in Male Offspring Rats Treated with Chronic Prenatal Ethanol Exposure


As chronic prenatal ethanol (EtOH) exposure (CPEE) may cause deficiencies in a variety of behavioral and cognitive functions, the aim of present study is to investigate the effects of CPEE on spatial learning and memory and examine the action of CPEE on synaptic plasticity balance in the hippocampus of adolescent male rats.
 
The animal model was produced by EtOH exposure throughout gestational period with 4 g/kg bodyweight, while the male offspring rats were used in the study. Morris water maze (MWM) test was performed, and then, long-term potentiation (LTP) and depotentiation were recorded from Schaffer collaterals to CA1 region in the hippocampus.
 
It was shown that escape latencies in learning period and re-acquisition period were prolonged in CPEE-treated group compared with that in control group. Furthermore, LTP was drastically inhibited, and depotentiation was distinctly enhanced in CPEE-treated group compared with that in control group.

It is suggested that the balance between cognitive stability and flexibility was broken by the bidirectional effects of long-term synaptic plasticity. In addition, the spatial cognition was attenuated by the alteration of synaptic plasticity balance in CPEE-treated male adolescent rats.


Read Full Abstract

Request Reprint E-Mail:    zhangtao@nankai.edu.cn
at