Visceral Homeostasis - Body Temperature, Metabolism, and Weight

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1 Visceral Homeostasis - Body Temperature, Metabolism, and Weight Hypothalamus: General Principles 1. The specific homeostatic mechanisms discussed in the previous lecture (baroreceptor reflex, basic respiratory rhythm, micturation) were largely controlled by the brainstem. It was also mentioned that chronic control of blood pressure requires coordination of several mechanisms, and involves the hypothalamus as well as the brainstem 2. The functions discussed today (body temperature, metabolism, and weight) are largely controlled by the hypothalamus and illustrate the coordination of several mechanisms. a. How does the hypothalamus do these things? i. It functions like a thermostat: 1. It maintains a set point to which it compares the current state of the body, and then effects changes in the body to correct any deviations from the set point. ii. It should be obvious that hypothalamus needs 2 things to do what it does: 1. Inputs about the current state of the body: a. Temp from spino-reticulo-hypothalamic tract (see later). b. Vision from retinal ganglion cells c. Blood chemistry from circumventricular organs which allow chemicals to cross the BBB. d. Stress/Emotion from periaqueductal gray and limbic structures 2. Outputs to effectors that can correct deviations from the set point: a. The many nuclei of the hypothalamus do this and will be discussed later. i. Very generally, they operate in three general ways: 1. Activate cerebral cortex to modulate behavior. 2. Engage the autonomic nervous system. 3. Alter endocrine output. Review of Pituitary Function 1. We said that the hypothalamus can alter endocrine output. How? a. The hypothalamus is intimately related to the two divisions of the pituitary gland (see diagram): i. Posterior pituitary 1. Axons from hypothalamic neurons travel into the posterior pituitary and release hormones (vasopressin and oxytocin) directly into the systemic circulation. a. The axons come from two places in the hypothalamus: i. Supraoptic nucleus. ii. Lateral part of the paraventricular nucleus (PVN). ii. Anterior pituitary 1. Hypothalamic cells secrete releasing hormones into the hypophyseal portal system, which make their way to the anterior pituitary to stimulate endocrine cells, which secrete hormones into the systemic circulation. a. The hypothalamic cells that secrete releasing hormones live in two places: i. Arcuate nucleus. ii. Medial part of the paraventricular nucleus (PVN). 2. Hypothalamus/anterior pituitary/periphery triplets include: a. CRH ACTH Cortisol b. TRH TSH Thyroxin c. GnRH FSH/LH Testosterone/estrogen d. Dopamine (a negative releasing hormone) Prolactin Milk e. GHRH GH Tissue growth

2 Thermoregulation 1. To effectively regulate body temperature, the hypothalamus needs to do 2 things: a. Be attuned to the current body temperature: i. The hypothalamus has intrinsic temperature-sensing cells in the pre-optic nucleus. ii. The hypothalamus receives information about skin temperature from the spino-reticulohypothalamic tract (see diagram). 1. (FYI) For those who remember Dr. Snyder s pain lecture from the 1 st half of the course, you might remember the spinoreticular tract, which goes spinal cord reticular formation VPL somatosensory cortex. a. The spino-reticulo-hypothalamic tract is just an offshoot of this pathway. b. Send outputs to effectors to correct deviations from the body temperature set point: i. Activate cerebral cortex to modulate behavior (seek shade, build a fire, etc). ii. Alter endocrine output (to increase or decrease metabolism). 1. Occurs via action of the arcuate nucleus and medial PVN on anterior pituitary : a. CRH ACTH Cortisol b. TRH TSH Thyroxin iii. Engage the autonomic nervous system (sweat, shiver, metabolize brown fat, etc): 1. Mediated by two nuclei in the hypothalamus: a. Lateral hypothalamic area b. Dorsal & ventral parts of the paraventricular nucleus 2. These nuclei can activate sympathetics: a. Project directly to IML neurons. b. Project to ventrolateral medulla neurons, which themselves project to IML 3. These nuclei can activate parasympathetics: a. Project to dorsal nucleus of the vagus (to modulate non-heart organs). b. Project to nucleus ambiguus (to modulate heart). 2. Fever is when our temperature set point is raised in an effort to fry pathogenic bacteria. Here s how: a. Bacterial membranes cause the endothelial cells of our vessels to make prostaglandin E2 (PGE2) i. This activates PGE3 receptors in the pre-optic nucleus. 1. This raises the temperature set point through unknown mechanisms.

3 Body Weight and Metabolism 1. Leptin is a hormone released from fat cells (adipocytes). a. It activates POMC cells in the arcuate nucleus (and to a lesser degree, the dorsomedial & ventromedial nuclei). i. These cells, either directly or indirectly, effect actions to make us lose weight: 1. Activate cerebral cortex to modulate behavior (reduce appetite). 2. Alter endocrine output (to increase metabolism). a. Occurs via action of arcuate nucleus & medial PVN on anterior pituitary: i. CRH ACTH Cortisol ii. TRH TSH Thyroxin 3. Engage the autonomic nervous system (sweat, metabolize brown fat): a. Mediated by two nuclei in the hypothalamus: i. Lateral hypothalamus ii. Dorsal & ventral parts of paraventricular nucleus b. Sympathetics are activated. c. Parasympathetics are deactivated. b. Interestingly, chronic obesity raises our leptin setpoint. i. In other words, we become tolerant of the high levels of leptin circulating in the blood. 1. Thus, there is no leptin drive to lose weight, and we remain obese. ii. This resetting of the setpoint makes leptin supplements ineffective as weight loss agents. 2. Ghrelin is a hormone released by the gut. a. It activates NPY cells in the arcuate nucleus (and to a lesser degree, the dorsomedial & ventromedial nuclei). i. These cells effect actions that are the complete opposite of leptin-activated POMC cells, causing us to gain weight. 3. Orexin is a peptide made by some hypothalamic cells, which project all over the forebrain and release orexin onto target neurons. a. The orexin neurons have two roles: i. Increase appetite. ii. Maintain stable sleep/wake behavior. iii. Also other metabolic functions, as yet poorly understood.

4 1. It maintains a balance between wakefulness neurons (locus ceruleus, raphe, PPT) and sleepiness neurons (VLPO) (to be discussed in the upcoming sleep lecture). 2. A lack of orexin neurons has been associated with narcolepsy (a disease in which patients fall asleep randomly and without warning). 4. Summary: a. Leptin = lose weight (raise metabolism & lower appetite). b. Ghrelin = gain weight (lower metabolism & raise appetite). c. Orexin = gain weight (raise appetite) AND keep sleep/wake balance (and other metabolic functions). Miscellaneous Topic: Stress 1. The periqueductal grey (PAG) is a coordinating center for reactions to stress. The role of the PAG in pain modification is part of this reaction,, but it also involves visceral and behavioral components. a. To perform this function, the PAG needs to do 2 things: b. Be attuned to the current stress state of the body: i. It gets ascending input about pain via the spinomesencephalic tract, and descending input about emotional state from hypothalamus, amygdala, and medial prefrontal cortex. c. Send outputs to effectors to correct stress: i. It can do this directly: 1. Project to the spinal cord to modulate pain sensitivity. 2. Engage sympathetics: a. Project directly to IML neurons. b. Project to ventrolateral medulla neurons, which themselves project to IML 3. Engage parasympathetics: a. Project to dorsal nucleus of the vagus (to modulate non-heart organs). b. Project to nucleus ambiguus (to modulate heart). ii. It can do this indirectly: 1. Activate hypothalamus to engage coordinated visceral modulation 2. Activate midline thalamus with relays to amygdala, cortex. d. It turns out that the lateral PAG activates effectors that give the fight or flight response. i. This is good if we are facing acute pain (stress), like from a predator, and must stop it. e. It turns out that the ventrolateral PAG activates effectors that give a quiescent response. i. This is good if we have internal injuries (stress) that require rest to heal. ii. Interestingly, it has been found that this response may be overactive in depressed people. 2. The hypothalamic-pituitary-adrenal axis (HPA axis) is another way we deal with stress (see diagram). a. Stress causes the hypothalamus to release CRH, which leads to release of ACTH from the anterior pituitary, which leads to release of cortisol from the adrenal gland. i. Cortisol can help us deal with stressors: 1. It increases glucose levels in the blood so we can have a fight-or-flight response. b. Normally, there is negative feedback of cortisol onto the hypothalamus and pituitary that keeps the system from running out of control. i. Chronic stress (such as obesity, addiction, or depression) seems to prevent cortisol from having a strong negative feedback effect, by deceasing cortisol receptors in brain. 1. In other words, we have consistently higher cortisol levels in the blood. 2. This is bad because constantly being in stress response mode harms the body.

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