Vedder Lindsey C, Savage Lisa M
Department of Psychology, Behavioral Neuroscience Program, Binghamton University, State University of New York, Binghamton, New York 13902, USA.
Learn Mem. 2017 Jan 17;24(2):81-85. doi: 10.1101/lm.043927.116. Print 2017 Feb.
Thiamine deficiency (TD), commonly associated with chronic alcoholism, leads to diencephalic damage, hippocampal dysfunction, and spatial learning and memory deficits. We show a decrease in the magnitude of long-term potentiation (LTP) and paired-pulse facilitation (PPF) at CA3-CA1 synapses, independent of sex, following diencephalic damage induced by TD in rats. Thus, despite a lack of extensive hippocampal cell loss, diencephalic brain damage down-regulates plastic processes within the hippocampus, likely contributing to impaired hippocampal-dependent behaviors. However, both measures of hippocampal plasticity (LTP, PPF) were restored with brain-derived neurotrophic factor (BDNF), revealing an avenue for neural and behavioral recovery following diencephalic damage.
硫胺素缺乏症（TD）通常与慢性酒精中毒有关，会导致间脑损伤、海马功能障碍以及空间学习和记忆缺陷。我们发现，在大鼠中，由TD诱导的间脑损伤后，CA3-CA1突触处的长期增强（LTP）和双脉冲易化（PPF）幅度降低，且与性别无关。因此，尽管海马细胞没有大量损失，但间脑损伤会下调海马内的可塑性过程，这可能导致依赖海马的行为受损。然而，海马可塑性的两种测量指标（LTP、PPF）都通过脑源性神经营养因子（BDNF）得以恢复，这揭示了间脑损伤后神经和行为恢复的一条途径。
