Hippocampal oxytocin is involved in spatial memory and synaptic plasticity deficits following acute high-fat diet intake in juvenile rats.

The hippocampus undergoes maturation during juvenility, a period of increased vulnerability to environmental challenges. We recently found that acute high-fat diet (HFD) impaired hippocampal long-term potentiation (LTP) and hippocampal-dependent spatial memory. We also recently reported that similar HFD exposure affected prefrontal plasticity and social memory through decreased oxytocin levels in the prefrontal cortex.

Acute exposure to a high-fat diet in juvenile male rats disrupts hippocampal-dependent memory and plasticity through glucocorticoids.

The limbic circuit is still undergoing maturation during juvenility and adolescence, explaining why environmental and metabolic challenges during these developmental periods can have specific adverse effects on cognitive functions. We have previously shown that long-term exposure (8-12 weeks) to high-fat diet (HFD) during adolescence (from weaning to adulthood), but not at adulthood, was associated with altered amygdala and hippocampal functions. Moreover, these HFD effects were normalized by treatment with glucocorticoid receptor (GR) antagonists.

Different mechanisms underlie stress-induced changes in plasticity and metaplasticity in the prefrontal cortex of juvenile and adult animals: Emotional-induced metaplasticity in the prefrontal cortex.

Metaplasticity is the dynamic regulation of the ability to induce activity-dependent synaptic plasticity and is governed by the prior history of the synapses. Previous reports by others and us have shown that behavioral stress induces a form of emotional metaplasticity that affects the ability to induce LTP in the subiculum-medial prefrontal cortex pathway, which depends on NMDA receptors (NMDAr). However, studies addressing the effects of stress on LTP and metaplasticity have mainly focused on the adult animal.