Neurochemical and electrophysiological deficits in the ventral hippocampus and selective behavioral alterations caused by high-fat diet in female C57BL/6 mice

Apr 8, 2015Neuroscience

Brain chemical and electrical changes in the emotion area and specific behavior changes caused by high-fat diet in female mice

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Abstract

High-fat diet (HFD) consumption for 11-12 weeks in female mice led to multiple behavioral alterations and impaired brain function.

HFD-fed female mice showed increased locomotor activity, anxiety-like behavior, and altered emotional responses during various behavioral tests.
Despite these changes, memory performance, as assessed by novel object recognition, remained unaffected.
Neurochemical analysis indicated decreased norepinephrine and dopamine turnover in specific brain regions, including the prefrontal cortex and ventral hippocampus.
HFD consumption resulted in significant reductions in synaptic plasticity in the ventral hippocampus, as evidenced by changes in paired-pulse ratio and long-term potentiation magnitude.
These findings suggest that HFD intake preferentially affects anxiety-related behaviors and specific brain areas in female mice.

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Mounting experimental evidence, predominantly from male rodents, demonstrates that high-fat diet (HFD) consumption and ensuing obesity are detrimental to the brain. To shed additional light on the neurological consequences of HFD consumption in female rodents and to determine the relatively early impact of HFD in the likely continuum of neurological dysfunction in the context of chronic HFD intake, this study investigated effects of HFD feeding for up to 12weeks on selected behavioral, neurochemical, and electrophysiological parameters in adult female C57BL/6 mice; particular focus was placed on the ventral hippocampus (vHIP). Selected locomotor, emotional and cognitive functions were evaluated using behavioral tests after 5weeks on HFD or control (low-fat diet) diets. One week later, mice were sacrificed and brain regional neurochemical (monoamine) analysis was performed. Behaviorally naïve mice were maintained on their respective diets for an additional 5-6weeks at which time synaptic plasticity was determined in ex vivo slices from the vHIP. HFD-fed female mice exhibited increased: (i) locomotor activity in the open field testing, (ii) mean turn time on the pole test, (iii) swimming time in the forced swim test, and (iv) number of marbles buried in the marble burying test. In contrast, the novel object recognition memory was unaffected. Mice on HFD also had decreased norepinephrine and dopamine turnover, respectively, in the prefrontal cortex and the vHIP. HFD consumption for a total of 11-12weeks altered vHIP synaptic plasticity, evidenced by significant reductions in the paired-pulse ratio and long-term potentiation (LTP) magnitude. In summary, in female mice, HFD intake for several weeks induced multiple behavioral alterations of mainly anxiety-like nature and impaired monoamine pathways in a brain region-specific manner, suggesting that in the female, certain behavioral domains (anxiety) and associated brain regions, i.e., the vHIP, are preferentially targeted by HFD.

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Neurochemical and electrophysiological deficits in the ventral hippocampus and selective behavioral alterations caused by high-fat diet in female C57BL/6 mice

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