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Chapter 16

Chapter 16 notes

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Ryerson University
Health Services Management
HSM 330
Daolun Chen

Chapter 16: Motivation  Voluntary movements are incited to occur (motivate) in order to satisfy a need  Motivation can be very abstract (e.g. the need to go sailing on a warm and breezy summer) or very concrete (e.g. going to the bathroom because your bladder is full)  Motivation can be thought of as a driving force on behaviour The Hypothalamus, Homeostasis, and Motivated Behaviour  Homeostasis is the processes that maintain the internal environment of the body within a narrow physiological range  The hypothalamus plays a key role in the regulation of body temperature, fluid balance, and energy balance  Hypothalamic regulation of homeostasis starts with sensory transduction  A regulated parameter is measured by specialized sensory neurons and deviations from the optimal range are detected by neurons in the periventricular zone of the hypothalamus  The response generally has three components: o Humoral response: Hypothalamic neurons respond to sensory signals by stimulating or inhibiting the release of pituitary hormones into the bloodstream o Visceromotor response: Neurons in the hypothalamus respond to sensory signals by adjusting the balance of sympathetic and parasympathetic outputs of the ANS o Somatic motor response: Hypothalamic neurons (within lateral hypothalamus) respond to sensory signals by inciting an appropriate somatic motor behavioural response EXAMPLE o You are cold, dehydrate, and depleted of energy. The appropriate humoral and visceromotor responses kick in automatically. You shiver, blood is shunted away from the body surface, urine production is inhibited, and body fat reserves are mobilized. o However, the fastest and most effective way to correct these disturbances of brain homeostasis is to actively seek or generate warmth by moving, to drink water, and to eat. These are examples of motivated behaviours generated by the somatic motor system. The Long-Term Regulation of Feeding Behaviour  One primary reason we are motivated to eat is to keep these reserves at a level sufficient to ensure that there will not be an energy shortfall  Energy Balance o The body’s energy stores are replenished during and immediately after consuming a meal  This condition (i.e. blood filled with nutrients) is the prandial state.  Here, energy is stored as glycogen and triglycerides  Glycogen reserves have a finite capacity and found mainly in the liver and skeletal muscle  Triglyceride reserves are found in adipose (fat) tissue have an unlimited capacity  Assembly of macromolecules is called anabolism  During the fasting condition, postabsorptive, the stored glycogen and triglycerides are broken down to provide the body with a continuous supply of the molecules used as fuel for cellular metabolism (glucose for all cells; fatty acids and ketones for all cells other than neurons)  Breaking down of macromolecules is catabolism o The system is in balance when energy reserves are replenished at the same rate they are spent  If intake is greater than usage, the amount of fat (adiposity) increase  obesity  If intake is less than usage required, loss of fat tissues occurs  starvation  Hormonal and Hypothalamic Regulation of Body Fat and Feeding o Feeding is stimulated when neurons in the hypothalamus detect a drop in the level of a hormone released by fat cells  These neurons are in the periventricular zone and those that incite feeding behaviour are in the lateral hypothalamus o Body Fat and Food Consumption  The idea that the brain monitors the amount of body fat and acts to “defend” this energy store against perturbations, proposed in 1953 by Gordon Kennedy, is called the lipostatic hypothesis  The connection between body fat and feeding behaviour suggest there must be communication from adipose tissue to the brain  A bloodborne hormonal signal was confirmed in the 1960s by Douglas Coleman  Read how Coleman confirmed this on page 513.  The protein encode by the ob gene was called leptin  Leptin is released by adipocytes and regulates body mass by acting directly on neurons of the hypothalamus that decrease appetite and increase energy expenditure  Leptin deficiency stimulates hunger and feeding suppresses energy expenditure, and inhibits reproductive competence o The Hypothalamus and Feeding  Bilateral lesions of the lateral hypothalamus causes anorexia  lateral hypothalamic syndrome  Bilateral lesions of the ventromedial hypothalamus causes the animals to overeat and become obese  ventromedial hypothalamic syndrome o The Effects of Elevated Leptin Levels on the Hypothalamus Consider the response when leptin levels are high  Circulating leptin molecules, released into the bloodstream by adipocytes, activate leptin receptors on neurons of the arcuate nucleus of the hypothalamus (near 3 ventricle) o Arcuate neurons are activated by a rise in blood leptin levels are characterized by a distinctive mix of peptide neurotransmitter αMSH and CART.  Their levels in the brain vary in proportion to the level of leptin in the blood Consider the body’s integrated response to excessive adiposity (and high leptin levels)  Humoral response: increase secretion of thyroid-stimulating hormone (TSH) and adrenocorticotropic hormone (ACTH) o Act on thyroid and adrenal glands and raise the metabolic rate of cells throughout the body  Visceromotor response: increases the tone of the sympathetic division of the ANS o Also raises the metabolic rate and in part, raises the body temperature  Somatic motor response: decreases feeding behaviour o αMSH and Cart orchestrate this coordinated response  The humoral response is triggered by the activation in the paraventricular nucleus of the hypothalamus which causes the release of the hormones that regulate the secretion of TSH and ACTH from the anterior pituitary o The paraventricular nucleus controls the activity of the sympathetic division of the ANS  There is also a directive path for arcuate control of the sympathetic response o The αMSH and CART neurons project axons directly down to the intermediolateral gray matter of the spinal cord  Feeding behaviour is inhibited via connections of the arcuate nucleus neurons with cells in the lateral hypothalamus  Injection of αMSH or CART into the brain mimics the response to elevated leptin levels and are called anorectic peptides – they diminish appetite o The Effects of Decreased Leptin Levels on the Hypothalamus  A fall in in leptin levels actually stimulates another type of arcuate nucleus neuron which contains their own mix of peptides: NPY and AgRP.  These neurons have connections with the paraventricular nucleus and the lateral hypothalamus  The effects of these neuropeptides on energy balance are the opposite of the effects of αMSH and CART.  NPY and AgRP inhibit the secretion of TSH and ACTH, activate the parasympathetic division of the ANS, stimulate feeding behaviour  orexigenic peptides  AgRP and αMSH are antagonistic  Both bind to the same receptor  MC4 receptor  αMSH is the receptor agonist and AgRP in a antagonist that blocks the stimulation of αMSH  Activation of MC4 receptors inhibits feeding; blocking the receptors stimulates feeding o The Control of Feeding by Lateral Hypothalamic Peptides  This region of the brain is not organized into well-defined nuclei lateral hypothalamic area We will now concentrate on the role of the neurons within the lateral hypothalamic area  One group of neurons receives direct input from the leptin-sensitive cells and has another peptide neurotransmitter called MCH  These cells have extremely widespread connections in the brain (including most of the cerebral cortex). o Cortex is involved in organized and initiating goal-directed behaviours  The MCH system informs the cortex of leptin levels in the blood and could contribute to motivating the search for food o Mutant mice that lack this peptide exhibit reduced feeding behaviour, have elevated metabolic rate, and are lean  A second population of neurons were identified and contain orexin. They also receive direct inputs from the arcuate nucleus. o Orexin is a orexigenic peptide (stimulates feeding behaviour) o Levels of MCH and orexin rise in the brain when leptin levels in the blood fall The Short-Term Regulation of Feeding Behaviour  Satiety signals occur when we eat and begin the process of digestion o These signals terminate the meal and inhibit feeding for some time afterward o During this postabsorptive (fasting) period, the satiety signals slowly dissipate and the orexigenic signals build, until the drive to eat again takes over  Appetite, Eating, Digestion, and Satiety o EXAMPLE: You have awakened in the morning after a long night’s slumber. You come to the kitchen to find pancakes cooking on the stove; when they are ready, you enthusiastically eat them until you are satiated. o Your body’s reactions during this process can be divided into three phases: cephalic, gastric, and substrate  Cephalic Phase: the sight and smell of pancakes triggers physiological process that anticipate breakfast.The parasympathetic and enteric divisions of the ANS are activated: saliva is secreted into your mouth and digestive juices into your stomach  Gastric Phase: grow much more intense when you start chewing, swallowing and filling your stomach with food  Substrate Phase: as your stomach fills, partially digested food move into your intestines and nutrients beg
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