• Homeostatic Plasticity
• Ocular Dominance Plasticity
• Monocular Deprivation
• Short-term effects of food intake
• Metabolism

Neuroplasticity is a fundamental property of the nervous system that is maximal in early life, within the so called “critical period”, but with residual potential in the adult human cortex. The visual system is a paradigmatic model for studying experience-dependent plasticity both during development and in adulthood. Work in animal models has established that plasticity is strongly influenced by peripheral physiological signals, such as those accompanying physical activity and weight gain/loss. For example, plasticity is enhanced by caloric restriction and suppressed by high-fat diets. An open question remains as to whether these metabolic effects are observed only in the long term, or dynamically at every meal. Multiple factors that are dysregulated in obesity are also acutely released during a meal; among these, Glucagon-like peptide-1 (GLP-1), a potent insulinotropic hormone, acts on brain cortical synapses and their plasticity. Here we test the effects of GLP-1 and meal ingestion, by measuring whether they induce transient changes of plasticity (compared to a small fasting regime) in human adult participants.

A recent but well established line of research has demonstrated a form of homeostatic plasticity in the adult human visual cortex, which can be induced by a short period of monocular deprivation (MD), and consists of a shift of ocular dominance. In line with these observations, we found that 2 hours of MD shift the dynamics of binocular rivalry to promote dominance of the deprived eye and that the effect is accurately tracked by an alternative, completely objective index: the spontaneous oscillations of the diameter of the eye pupil at rest. In a first pilot experiment, we repeated the protocol twice on the same 10 participants (on different days, at the same time), and found that the MD effect is stronger after a meal than in a small fasting regime (~12h fast). We are in the process of extending these observations with a second more controlled study, performed in collaboration with the U.O. of Endocrinology of Cisanello, where we measure the effects of MD under three experimental conditions: 1) in a small fasting regime; 2) after a controlled meal; 3) with an infusion of GLP-1 and no meal. Preliminary results in 5 participants confirm that MD effects are stronger after a meal than in the small fasting regime, and suggest that GLP-1 infusion alone is not sufficient to reproduce the plasticity enhancement produced by a meal.

Our observations clearly indicate that at every meal there is a small but measurable boost of the plasticity potential of the human adult visual cortex – similar to that recently observed by engaging adult human participants in moderate physical exercise. Although we have no direct information as to their neural underpinnings, we suggest that the two effects might rely on similar GABAergic cortical circuits.