Nutrients and foods that are beneficial for the brain are currently the focus of much attention. However, their precise roles in brain function and the mechanisms involved remain unclear. State-of-the-art technologies for analyzing the mechanisms of brain function, such as imaging, electrophysiology, molecular biology, and behavioral studies, have recently been established and applied for clarifying the roles of essential nutrients in brain function, especially learning and memory. In this review, I present our findings on the effects of magnesium or vitamin B₁ deficiency on memory performance in mice. We found that magnesium or vitamin B₁ deficiency impairs hippocampus-dependent memory at the behavioral level and induces neuroinflammation in the brain at the molecular level. In particular, vitamin B₁ deficiency leads to strong neuroinflammation and neurodegeneration in the hippocampus. These results, in combination with other findings, suggest common mechanisms by which abnormal nutritional intake induces neuroinflammation and impairs memory performance.

Feeding is an essential type of behavior for maintenance of life activities. Regulation of feeding is necessary for the control of body energy balance, and its dysfunction leads to obesity and malnutrition. Recent studies have identified multiple neural circuits that contribute to homeostatic feeding and hedonic feeding, these circuits acting in a coordinated manner to regulate feeding overall. The hypothalamus and brainstem play important roles in homeostatic regulation. Hedonic feeding, which is regulated by the reward system including dopaminergic neurons in the ventral tegmental area, manifests as hyperphagia for palatable diets rather than for control of body energy balance. In this review article, we first review the mechanism of food intake regulation including homeostatic and hedonic feeding. Food intake alters peripheral energy status, hormones and metabolites in the body. These associated peripheral factors send information to the brain via two distinct routes: the blood‐brain barrier (humoral pathway) and the vagal afferents (neural pathway). Finally, we review the functions of the vagal afferent nerves that transmit meal-associated peripheral factors to the brain.

Appetite is one of the most important instincts for survival in both humans and animals. The brain plays a central role in appetite regulation. Impairment of this regulation leads to overeating or low food intake, which can ultimately increase the risk of obesity or sarcopenia, respectively. Appropriate control of appetite with proper nutrient intake is thus the key to maintaining or improving health. Appetite is categorized as homeostatic for appropriate nutrient intake and hedonic for taste and smell. There is accumulated evidence to suggest a complex brain mechanism for sensing and evaluating diverse food factors. In this review, I summarize recent progress and perspectives in our understanding of the neural mechanism underlying appetite.

The human brain controls various phenomena essential for life, such as sensation, thought, learning, emotion, and behavior, and these have been investigated in a wide variety of studies. Recently, it has been shown that non-neuronal tissues such as the gut support the function of the nervous system. The nervous system of the nematode Caenorhabditis elegans is composed of a small number of neurons, unlike the complex nervous system of mammals, thereby making it possible to study information processing in the entire brain at single-cell resolution. C. elegans exhibits behavioral responses to various stimuli such as chemicals and temperature, and these behavioral changes are dependent on memory, feeding status, or nutritional status. Such responses are mediated by signal transduction molecules such as the RAS/MAPK pathway, TOR, insulin, and monoamine signaling, which are also evolutionarily conserved in humans. Here, we describe how analysis of the nervous system of C. elegans can help clarify the molecular mechanisms involved in learning behavior, and the regulation of behavioral plasticity by sensory responses and trophic state.