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Learn Mem. 2017 Jan 17;24(2):81-85. doi: 10.1101/lm.043927.116. Print 2017 Feb.

BDNF regains function in hippocampal long-term potentiation deficits caused by diencephalic damage.

Author information

1
Department of Psychology, Behavioral Neuroscience Program, Binghamton University, State University of New York, Binghamton, New York 13902, USA.

Abstract

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.

PMID:
28096497
PMCID:
PMC5238722
DOI:
10.1101/lm.043927.116
[Indexed for MEDLINE]
Free PMC Article

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