Neuroscience of Stress & Feeding Behavior - Quiz

Course Information

• Course: Neuroscience of stress and feeding behavior
• Course number: 12
• Date: 20 December 2024
• Lecturer: Dr. Michael-Bogdan Mărgineanu

Course Content Overview

• Introductory course covers the morphology of the human nervous system (both central and peripheral), methods for studying the nervous system, neurons and glia, the motor system, somatic sensory system, and sensory information integration.
• Neuroscience of stress and feeding behavior explores neurodegeneration and neural regeneration, examines mental illnesses from a cellular and molecular perspective, and investigates long-term feeding behavior regulation.

Long-Term Feeding Behavior

• Energy balance is crucial to maintaining health, where intake and expenditure of energy are critical factors.
• Intake greater than expenditure (consuming more than needed) leads to obesity.
• Intake lower than expenditure (consuming less than needed) results in starvation.

Glucostatic and Lipostatic Theories

• Eating is regulated by a system designed to maintain a blood glucose set point.
• Hungry when glucose levels fall below set point. Filled when back to set point.
• Set point for body fat also exists and has related compensatory mechanisms.
• Set point theories are deficient in fully explaining eating behavior and needs.

Appetite, Eating and Digestion

• Appetite is influenced by flavor, learned experiences, time since last meal, presence of others eating, blood glucose levels etc. This impacts food choices.
• Digestion has three phases (cephalic, gastric, substrate):
  • Cephalic phase: anticipation of food (saliva and gastric juice production) triggered by smell or sight.
  • Gastric phase: intense responses when chewing/swallowing as stomach fills.
  • Substrate phase: nutrients are absorbed into the bloodstream as partially digested food is carried through the intestines.

THC, Olfaction, and Appetite

• THC (psychoactive component of marijuana) enhances olfaction by suppressing the release of glutamate.

When, What, and How Much We Eat

• Food preferences and aversions are learned.
• Dietary deficiencies exist despite our ability to learn what to eat.
• The amount of food consumed is related to many factors:
• Pre-meal hunger is the expectation to eat, not necessarily a direct need for food.
• Meal size is influenced by variety of flavors available.

When, What, and How Much We Eat: Factors - Detail

• Satiety signals include various peptides regulating food intake, including cholecystokinin, bombesin, glucagon, alpha-melanocyte-stimulating hormone, and somatostatin.
• Gastric distension is also a satiety signal.
• Previous eating experience impacts future meal size.
• Serving size and social interactions impact portions.
• "Sensory-specific satiety" exists: the more flavors available, the larger the meal.
• Hunger peptides such as neuropeptide Y, galanin, orexin-A, and ghrelin also play a role.
• The hormone leptin regulates body mass by decreasing appetite and increasing energy expenditure.

Leptin and the Hypothalamus

• Leptin levels impact feeding behavior in the hypothalamus: increased leptin inhibits, decreased leptin activates.
• Signals regulate metabolic rate.

Summary of Responses to Leptin

• Blood leptin level, and activity of MSH/CART and NPY/AgRP neurons in the hypothalamus are related to responses of the body to increase or decrease feeding.

Serotonin, Food and Mood

• Serotonin levels are low between meals, rise before meals, and spike after eating.
• Particularly associated with carbohydrates.
• Serotonin has influences on food intake.
• Tryptophan is an amino acid that is essential to the production of serotonin.

The Stress Response

• The stress response is coordinated to threats.
• Avoidance, vigilance, and arousal are aspects of the stress response.
• Stress activates the sympathetic nervous system and increases epinephrine and norepinephrine.
• Brief stressors boost cytokine production.
• Glucocorticoids are released from the adrenal cortex (in response to ACTH from anterior pituitary).

Control of Stress Response by the Amygdala and Hippocampus

• The amygdala relays sensory and neocortex information regarding stress to the central nucleus, activating the stress response.
• The hippocampus can regulate the stress response through negative feedback by inhibiting CRH release.

Effects of Childhood Stress

• Childhood stress impacts brain development through changes in monoamine and glutamate metabolism affecting function and neuroactivity.
• Related effects include reduced monoamine synthesis and availability, increased glutamate release and availability.
• Stress impacts brain function, development, and reactivity over long periods.

Brain Reward System and Anti-Tumor Immunity

• The brain reward system affects anti-tumor immunity demonstrating a potential biological link.
• VTA-activated (reward related) signaling impacts tumor development.