BDNF regains function in hippocampal long-term potentiation deficits caused by diencephalic damage
- Department of Psychology, Behavioral Neuroscience Program, Binghamton University, State University of New York, Binghamton, New York 13902, USA
- Corresponding author: lsavage{at}binghamton.edu
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.
Footnotes
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Article is online at http://www.learnmem.org/cgi/doi/10.1101/lm.043927.116.
- Received August 28, 2016.
- Accepted November 2, 2016.
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