Abstract
INTRODUCTION. Metabolic dysregulation, e.g. obesity and diabetes, affects plasticity-dependent cognitive functions. Recent data indicate that sensory plasticity is similarly affected, and negatively correlated with BMI. So far, metabolic effects were studied in pathological conditions and/or in the long term. We asked whether metabolic factors also modulate plasticity continuously and physiologically, for example every time we have breakfast (or skip it). METHODS. In 11 adult volunteers, we indexed sensory plasticity by measuring binocular rivalry before and after 2 hours of monocular deprivation. We repeated measurements on three mornings: 1) after overnight fasting; 2) with a controlled meal; 3) with an infusion of glucagon-like-peptide-1 (GLP-1). GLP-1 is an incretin released with every meal; it triggers the insulin response that reduces blood glycemia (we counteracted the would-be-hypoglycemia with titrated glucose infusions). RESULTS. Monocular deprivation transiently shifted ocular dominance in favor of the deprived eye. This form of plasticity was systematically stronger upon meal consumption than after overnight fasting (paired t-test, t = 2.407, p < 0.05). Although the GLP-1 infusion did not mimic meal consumption, plasticity upon GLP-1 infusion was tightly correlated with GLP-1 blood concentrations (variable across participants and slightly higher than upon meal consumption) and with an index of insulin sensitivity (HOMA-IR). Correlation coefficients were > 0.9 (p<0.001) even after factoring out the associations with infused glucose. CONCLUSIONS. Having breakfast enhances sensory plasticity as measured by short-term monocular deprivation, and sensory plasticity correlates with the incretins-insulin pathway activation achieved through GLP-1 infusion. The incretins-insulin pathway activation is one of the many (peripheral, autonomic and central) consequences of meal consumption, and our data suggest that GLP-1 is not the only mediator of its impact on neural dynamics. These findings strongly indicate that metabolic factors modulate neural dynamics even in low-level sensory cortex such as implicated in the monocular deprivation effect.