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Food restriction modifies ultrastructure of hippocampal synapses
Author(s) -
Babits Réka,
Szőke Balázs,
Sótonyi Péter,
Rácz Bence
Publication year - 2016
Publication title -
hippocampus
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.767
H-Index - 155
eISSN - 1098-1063
pISSN - 1050-9631
DOI - 10.1002/hipo.22533
Subject(s) - neuroscience , hippocampal formation , dendritic spine , postsynaptic density , hippocampus , synaptic plasticity , postsynaptic potential , synapse , neuropil , metaplasticity , biology , long term potentiation , inhibitory postsynaptic potential , excitatory postsynaptic potential , central nervous system , biochemistry , receptor
Consumption of high‐energy diets may compromise health and may also impair cognition; these impairments have been linked to tasks that require hippocampal function. Conversely, food restriction has been shown to improve certain aspects of hippocampal function, including spatial memory and memory persistence. These diet‐dependent functional changes raise the possibility that the synaptic structure underlying hippocampal function is also affected. To examine how short‐term food restriction (FR) alters the synaptic structure of the hippocampus, we used quantitative electron microscopy to analyze the organization of neuropil in the CA1 stratum radiatum of the hippocampus in young rats, consequent to reduced food. While four weeks of FR did not modify the density, size, or shape of postsynaptic spines, the synapses established by these spines were altered, displaying increased mean length, and more frequent perforations of postsynaptic densities. That the number of perforated synapses (believed to be an indicator of synaptic enhancement) increased, and that the CA1 spine population had on average significantly longer PSDs suggests that synaptic efficacy of axospinous synapses also increased in the CA1. Taken together, our ultrastructural data reveal previously unrecognized structural changes at hippocampal synapses as a function of food restriction, supporting a link between metabolic balance and synaptic plasticity. © 2015 Wiley Periodicals, Inc.