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Chapter 16 Motivation
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Introduction Types of behavior Unconscious reflexes and Voluntary Movements Motivation Driving force on behavior Analogy– ionic driving force dependent upon many factors Probability and direction of behavior Vary with the driving force needed to perform the behavior
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The Hypothalamus, Homeostasis, And Motivated Behavior
Maintains the internal environment within a narrow physiological range Role of Hypothalamus Regulates homeostasis Three components of neuronal response Humoral response Visceromotor response Somatic motor response
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The Hypothalamus, Homeostasis, And Motivated Behavior (Cont’d)
Example of motivated behaviors Response when body is cold Body shivers, blood shunted away from the body surface, urine production inhibited, body fat reserves - mobilized Lateral hypothalamus Initiates motivation to actively seek or generate warmth - Homeostasis
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The Long-term Regulation of Feeding Behavior
Energy Balance Prandial state - Anabolism: Energy storage as glycogen and triglycerides Postabsorptive state - Catabolism: Breaking down complex macromolecules
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The Long-term Regulation of Feeding Behavior
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Hormonal and Hypothalamic Regulation of Body Fat and Feeding
Body Fat and Food Consumption Lipostatic hypothesis Parabiosis: e.g., Siamese twins Leptin Regulates body mass Decreases appetite Increases energy expenditure Leptin depletion Incites adaptive responses to fight starvation
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Hormonal and Hypothalamic Regulation of Body Fat and Feeding
The Hypothalamus and Feeding Anorexia: lateral hypothalamic syndrome Obesity: ventromedial hypothalamic syndrome Both related to leptin signaling
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Hormonal and Hypothalamic Regulation of Body Fat and Feeding
The Hypothalamus and Feeding Hypothalamic nuclei important for the control of feeding
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Hormonal and Hypothalamic Regulation of Body Fat and Feeding
Response to Elevated Leptin Levels Activation of arcuate neurons that release αMSH and CART peptides Anorectic peptides- diminish appetite Activation of arcuate neurons that release αMSH and CART peptides (Cont’d) Project to regions that orchestrate coordinated response of humoral, visceromotor, and somatic responses Paraventricular nucleus (humoral response) Intermediolateral gray matter of spinal cord Lateral hypothalamus
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Hormonal and Hypothalamic Regulation of Body Fat and Feeding
Response to Elevated Leptin Levels
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Hormonal and Hypothalamic Regulation of Body Fat and Feeding
Response to Decreased Leptin Levels Activation of arcuate neurons that release NPY and AgRP Effects on energy balance: Opposite to the effects of αMSH and CART Orexigenic peptides– increase appetite NPY and AgRP inhibit secretion of TSH and ACTH Activate parasympathetic division of ANS Stimulate feeding behavior
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Hormonal and Hypothalamic Regulation of Body Fat and Feeding
Response to Decreased Leptin Levels
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Hormonal and Hypothalamic Regulation of Body Fat and Feeding
The Control of Feeding by Lateral Hypothalamic Peptides LH neurons stimulating feeding behavior contain: Melanin-concentrating hormone (MCH) Orexin
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Harry Harlow – in 1967 received the National Medal of Science for his work on general human and child psychology. His work examined motivation in monkeys.
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The Short-Term Regulation of Feeding Behavior
Model for short-term regulation of feeding 3 phases: Cephalic; Gastric; Substrate
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The Short-Term Regulation of Feeding Behavior
Model for short-term regulation of feeding Cephalic: Hunger Ghrelin released when stomach is empty Activates NPY- and AgRP-containing neurons in arcuate nucleus
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The Short-Term Regulation of Feeding Behavior
Model for short-term regulation of feeding Gastric: Feeling full Gastric distension signals brain via vagus Works synergistically with CCK released in intestines in response to certain foods Insulin also released by B cells of the pancreas - important in anabolism
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The Short-Term Regulation of Feeding Behavior
Model for short-term regulation of feeding Changes in blood insulin levels before, during, and after a meal Highest during “substrate” phase
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Why Do We Eat? Reinforcement and Reward Liking: Hedonic Wanting: Drive reduction Electrical self-stimulation: Experiments to identify sites of reinforcement Effective sites for self-stimulation: Trajectory of dopaminergic axons in the ventral tegmental area projecting to the forebrain Drugs that block dopamine receptors: Reduce self-stimulation
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Why Do We Eat? Mesocorticolimbic dopamine system
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Why Do We Eat? The Role of Dopamine in Motivation Old belief: Dopamine projection served hedonic reward New understanding Dopamine-depleted animals “like” food but “do not want” food Lack motivation to seek food, but enjoy it when available Stimulation of the dopamine axons Craving for food without increasing the hedonic impact
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Why Do We Eat? Changes in hypothalamic serotonin levels Low:Postabsorptive period Rise: In anticipation of food Spike: During meals Mood elevation - Rise in blood tryptophan and brain serotonin
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Why Do We Eat? The Role of Dopamine in Motivation Serotonin, Food, and Mood (Cont’d) Drugs that elevate serotonin levels Example: Dexfenfluramine (Redux) Disorders: Anorexia nervosa; Bulimia nervosa both often accompanied by depression Treatment Antidepressant drugs—elevate brain serotonin levels Example: Fluoxetine (“Prozac”)
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Other Motivated Behaviors
Drinking: Pathway triggering osmotic thirst Hypertonicity: Increased concentration of dissolved substances in blood (salt)
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Other Motivated Behaviors
Drinking: Vasopressin - Antidiuretic hormone or ADH Acts on kidneys to increase water retention Inhibit urine production Diabetes insipidus - loss of vasopressin
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