Course 12: Neuroscience of Stress and Feeding Behavior PDF

Introduction in Neuroscience Course 12 – The neuroscience of stress and feeding behavior 20 December 2024 Lect. Dr. Michael-Bogdan Mărgineanu  What to expect from the courses Morphology of the Morphology of the Neurons and Glia:...

Introduction in Neuroscience Course 12 – The neuroscience of stress and feeding behavior 20 December 2024 Lect. Dr. Michael-Bogdan Mărgineanu  What to expect from the courses Morphology of the Morphology of the Neurons and Glia: human nervous system human nervous system morphological and Introductory course I: The central nervous II: The peripheral functional system (CNS) nervous system (PNS) characteristics The motor system, the Synaptic transmission, The visual, gustatory, Methods for studying somatic sensory system neural activity and olfactory, and auditory the nervous system and integration of energetic demands systems sensory information The second brain: the The limbic system and The molecular enteric nervous system brain mechanisms of mechanisms of and the gut-brain emotion and addiction learning and memory connection The neuroscience of Neurodegeneration Mental illnesses: stress and feeding and neural cellular and molecular Written exam behavior regeneration insights Long-term regulation of feeding behavior Bear, M., Connors, B., & Paradiso, M. A. (2016). Neuroscience: Exploring the Brain. 4th edition. Wolters Kluwer.  Glucostatic and lipostatic theories Glucostatic theory Eating is regulated by a system that is designed to maintain a blood glucose set point the idea being that we become hungry when our blood glucose levels drop significantly below their set point and that we become satiated when eating returns our blood glucose levels to their set point. Lipostatic theory every person has a set point for body fat, and deviations from this set point produce compensatory adjustments in the level of eating that return levels of body fat to their set point. Challenges to the theories: Reductions in blood glucose of the magnitude needed to reliably induce eating rarely occur naturally. Set-point theories of hunger and eating are deficient because they fail to recognize the major influences on hunger and eating of such important factors as taste, learning, and social influences. Any human ancestor that stopped feeling hungry as soon as immediate energy needs were met would not have survived the first hard winter or prolonged drought. Pinel, J. P., & Barnes, S. (2011). Biopsychology.8 th edition. Pearson.  Appetite, eating, and digestion The positive incentive perspective These include the following: the flavor of the food you are likely to consume, what you have learned about the effects of this food either from eating it previously or from other people, the amount of time since you last ate, the type and quantity of food in your gut, whether or not other people are present and eating, whether or not your blood glucose levels are within the normal range. Digestion phases: 1. Cephalic phase: The sight and smell of food trigger a number of physiological processes that anticipate the arrival of breakfast. The parasympathetic and enteric divisions of the ANS are activated, causing the secretion of saliva into your mouth and digestive juices into your stomach. 2. Gastric phase: These responses grow much more intense, when you start chewing, swallowing, and filling your stomach with food. 3. Substrate phase: As your stomach fills and the partially digested pancakes move into your intestines, nutrients begin to be absorbed into your bloodstream. Pinel, J. P., & Barnes, S. (2011). Biopsychology.8 th edition. Pearson.  THC, olfaction and appetite Activation of CB1 receptors by THC, the psychoactive ingredient in marijuana, enhances olfaction by suppressing the release of glutamate from corticofugal inputs to inhibitory granule cells in the olfactory bulb. Bear, M., Connors, B., & Paradiso, M. A. (2016). Neuroscience: Exploring the Brain. 4th edition. Wolters Kluwer. When, what and how much we eat: Factors What we eat: - learned taste preferences and aversions - learning to eat vitamins and minerals If we are capable of learning to select diets that are rich in the vitamins and minerals we need, why are dietary deficiencies so prevalent in our society? Manufacturers produce foods that have the tastes we prefer but lack many of the nutrients we need to maintain our health. The number of different substances, both nutritious and not, consumed each day by most people in industrialized societies is immense, and this makes it difficult, if not impossible, for their bodies to learn which foods are beneficial and which are not. When we eat: - premeal hunger The strong, unpleasant feelings of hunger that you may experience at mealtimes are not cries from your body for food; they are the sensations of your body s preparations for the expected homeostasis-disturbing meal. - Pavlovian conditioning Hunger is often caused by an expectation of food not by an energy deficit. Pinel, J. P., & Barnes, S. (2011). Biopsychology.8 th edition. Pearson. When, what and how much we eat: Factors How much we eat: - satiety signals: satiety peptides (cholecystokinin, bombesin, glucagon, alpha-melanocyte-stimulating hormone, and somatostatin) that are released in the gut and bind to receptors in the brain (hypothalamus) to reduce food intake; gastric distension. - sham eating: the amount we eat is influenced largely by our previous experience with the particular food’s physiological effects. - appetizer effect. - serving size. - social influences. - sensory-specific satiety: the number of different tastes available at each meal has a major effect on meal size. There are also hunger peptides: neuropeptide Y, galanin, orexin-A, and ghrelin. The hormone leptin, released by adipocytes (fat cells), regulates body mass by acting directly on neurons of the hypothalamus that decrease appetite and increase energy expenditure. Pinel, J. P., & Barnes, S. (2011). Biopsychology.8 th edition. Pearson. Bear, M., Connors, B., & Paradiso, M. A. (2016). Neuroscience: Exploring the Brain. 4th edition. Wolters Kluwer.  Leptin and the hypothalamus A rise in leptin levels in the blood is A reduction in blood levels of detected by neurons in the arcuate leptin is detected by neurons in nucleus that contain the peptides the arcuate nucleus that contain MSH and CART. the peptides NPY and AgRP. Metabolic rate of cells Feeding behavior Feeding behavior Bear, M., Connors, B., & Paradiso, M. A. (2016). Neuroscience: Exploring the Brain. 4th edition. Wolters Kluwer. Summary of responses to leptin Bear, M., Connors, B., & Paradiso, M. A. (2016). Neuroscience: Exploring the Brain. 4th edition. Wolters Kluwer.  Serotonin, food and mood Serotonin levels are low during the postabsorptive period, rise in anticipation of food, and spike during a meal, especially in response to carbohydrates. The particular case of serotonin (studies in rats): - reduces the amount of food consumed during a meal. - can help resist the attraction of highly palatable diets. - associated with a shift in food preferences away from fatty foods. In humans, serotonin agonists can reduce hunger, eating and body weight. Serotonin is derived from the dietary amino acid tryptophan, and tryptophan levels in the blood vary with the amount of carbohydrate in the diet. This effect of “carbs” on mood is particularly evident during periods of stress. Pinel, J. P., & Barnes, S. (2011). Biopsychology.8 th edition. Pearson. Bear, M., Connors, B., & Paradiso, M. A. (2016). Neuroscience: Exploring the Brain. 4th edition. Wolters Kluwer. The stress response The stress response is the coordinated reaction to threatening stimuli. It is characterized by the following: Avoidance behavior Increased vigilance and arousal Activation of the sympathetic division of the ANS Release of cortisol from the adrenal glands Stressors acting on neural circuits stimulate the release of adrenocorticotropic hormone (ACTH) from the anterior pituitary, ACTH in turn triggers the release of glucocorticoids from the adrenal cortex, and glucocorticoids produce many of the components of the stress response. Stressors activate the sympathetic nervous system, thereby increasing the amounts of epinephrine and norepinephrine released from the adrenal medulla. Brief stressors also produce an increase in blood levels of cytokines, a group of peptide hormones that are released by many cells and participate in a variety of physiological and immunological responses, causing inflammation and fever. Pinel, J. P., & Barnes, S. (2011). Biopsychology.8 th edition. Pearson. Bear, M., Connors, B., & Paradiso, M. A. (2016). Neuroscience: Exploring the Brain. 4th edition. Wolters Kluwer. Control of stress response by the amygdala and hippocampus The amygdala receives ascending sensory information from the thalamus as well as descending inputs from the neocortex. This information is integrated by the basolateral nuclei and is relayed to the central nucleus. Activation of the central nucleus leads to the stress response. The hippocampus contains numerous glucocorticoid receptors that respond to the cortisol released from the adrenal gland in response to HPA system activation. Thus, the hippocampus normally participates in the feedback regulation of the HPA axis by inhibiting CRH release (and the subsequent release of ACTH and cortisol) when circulating cortisol levels get too high. Bear, M., Connors, B., & Paradiso, M. A. (2016). Neuroscience: Exploring the Brain. 4th edition. Wolters Kluwer. Effects of childhood stress Neuropsychopharmacology Reviews (2017) 42, 99-114; doi:10.1038/npp.2016.198 The brain reward system and anti-tumor immunity Ben-Shaanan et al, Nature Communications, 2018 Questions? Contact: michael.margineanu@e- uvt.ro