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Week 7 Physiology Notes

by: Alesa Taylor

Week 7 Physiology Notes 3014

Marketplace > Mississippi State University > 3014 > Week 7 Physiology Notes
Alesa Taylor
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Chapters 11 and 9.1
Human Physiology
James Stewart
Class Notes
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This 5 page Class Notes was uploaded by Alesa Taylor on Tuesday March 1, 2016. The Class Notes belongs to 3014 at Mississippi State University taught by James Stewart in Spring 2016. Since its upload, it has received 183 views.


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Date Created: 03/01/16
Week 7 Chapter 11  Hormones are chemical messengers, they are responsible for long-term, on-going functions in the body such as: growth and development, metabolism, regulation of internal environment (homeostasis), and reproduction o The root of the word is “hormân” which is Greek and means “to excite”  There are 3 basic ways that hormones act on target cells: 1. By controlling rates of enzymatic reactions 2. By controlling transport of ions or molecules across cell membranes 3. By controlling gene expression and synthesis of proteins  What makes a chemical a hormone? 1. Secreted by a discrete and identifiable cell or group of cells derived from epithelial cell lineage 2. Secreted into the blood 3. Transported to a distant target and bind to target receptor 4. Exert their effect at very low concentrations  The process of releasing hormones follows a basic pattern of a reflex: stimulus> sensor> signal input> signal integration> signal output> response  The endocrine cell is the sensor, it is the simplest reflex control pathway and a first order feedback loop; the cell directly senses stimulus and responds by secreting hormones, the cell acts as both sensor and integrating center, the output signal is released by a hormone, negative feedback turns off the reflex  Neurohormones- chemical signals released into the blood by a neuron o Divided into 3 major groups: 1. Catecholamines- tyrosine derived neurohormones (dopamine, epinephrine, norepinephrine) 2. Hypothalamic neurohormones secreted from the posterior pituitary 3. Hypothalamic neurohormones that control hormone release from the anterior pituitary  The anterior pituitary- it is a true endocrine gland, the hormones secreted are adenohypophyseal, it is a second order feedback loop system  Posterior pituitary- it is a false endocrine gland, it is an extension of neural tissue in the brain, the hormones that it secretes are made in the hypothalamus and are neurohypophyseal secretions, it is a third order feedback loop system  Vasopressin (antidiuretic hormone (ADH))- it is released from the posterior pituitary in response to low blood volume, it acts on the collecting ducts in the kidney nephrons to retain water in the body, it makes blood vessels constrict, decreased release or decreased sensitivity to this hormone leads to diabetes insipidus, hypernatremia (increased sodium concentration in the blood), polyuria (excess urine production), and polydipsia (thirst); too high levels of this hormone can lead to hyponatremia (hypo- or hypervolemia)  Oxytocin- it is released from the posterior pituitary, it plays an important role in the neuroanatomy of social trust and intimacy/ sexual reproduction; during childbirth it is released in large amounts causing distension of the cervix and the uterus; after childbirth, it facilitates maternal bonding, lactation, and milk ejection; it results from a positive feedback mechanism; the name is derived from oxytocic, which means “quick birth”  Anterior pituitary neurohormones- secretes 6 neurohormones (trophic hormones- controls the secretion of other hormones): 1. Prolactin (PRL): milk production 2. Thyrotropin (TSH): thyroid stimulating hormone 3: Adrenocorticotropin (ACTH): adrenal cortex hormone synthesis and secretion 4. Growth hormone (GH): somatotrophin- affects cellular metabolism 5. Follicle- stimulating hormone (FSH): gonadotrophin  Cholesterol derived hormones- ex. Estrogen, progesterone, testosterone, thyroid hormones: thyroxin, retinoids (vitamin A), cortisol, and vitamin D o Not soluble in plasma, must bind to a carrier protein, either a globulin or albumin, protects the hormone from degradation which extends its life, blocks entry into cells, can become unbound to enter cell and bind to the receptors o Cytosolic- hormone binding causes receptor conformational change (non-genomic) o Nuclear- hormone binding causes receptor conformational change (genomic) Chapter 9.1 2/25/16  Every physiological process depends on movement, movements such as: changes in cell shape, cell motility, intracellular transport, and muscle dependent locomotion  Intramuscular elements such as the cytoskeletal element and the motor protein element govern movement  The diversity of the body’s movements is possible because of the arrangement of its elements  There are 3 general ways that cells can use cytoskeleton elements to move o 1. Most common: roadway- motor proteins act like trucks carrying cargo (vesicles) over the complex cytoskeletal network, cells mediate traffic by controlling where roads go, who rides on the roads, and what type of cargo is being carried o 2. Active reorganization of the cytoskeletal networks. Cytoskeletal fibers act like bulldozers pushing cellular contents forward (amoeboid movement), regulated by controlling rate and direction of growth of cytoskeletal fibers o 3. Motor proteins pull on cytoskeletal rope. Cells organize the cytoskeleton in a way that translates tugging action into movement, cells regulate this movement by controlling the activity of the motor proteins  There are 3 classes of cytoskeletal filaments which are based on the filaments diameter and the types of protein that they contain 1. Actin filaments (microfilaments) 2. Intermediate filaments 3. Microtubules  Microtubules- hollow tubes about 25 nm in diameters, whose subunits are composed of the protein tubulin; it has alpha-tubulin and beta-tubulin dimers and is the most rigid of the filaments; they are easily arranged, most cells gather the ends of microtubules near the nucleus of the cells at the microtubule organizing center (MTOC), they radiate outward like spokes on a wheel where the ouward ends are anchored to PM integrated proteins, the motor proteins can move either toward the central MTOC or to the edge of the cell o Functions: cell division- they radiates from the centrosome for chromosome separation, motility- cilia cores, and protein trafficking o in nature animals use this network to control the movements of subcellular components such as vesicles and organelles, it also mediates the rapid changes in skin color for cryptic colorations, such as when a chameleon changes color  Microtubule formation rules: Composed of long strings of alpha and beta tubulin isoforms o Steps of growth: 1.Alpha and beta combine to form tubulin (dimer) 2. Polarity occurs on each dimer; alpha tubulin bound GTP and beta tubular bound GDP bound 3. Added end to end; line of magnets where the negative alpha (GTP) end attracts the positive beta (GDP) end 4. Chain (protofilaments) grows until it reaches a critical length 5. Protofilaments will then line up side by side to form a sheet that eventually rolls into a tube to form the microtubule  Once microtubule is formed, it can continue to grow by incorporating more dimers, or it may shrink by shedding them  Factors influencing microtubule dynamics o 1. Local concentration of tubulin: At high concentration, it will add more dimers and grow; At low concentrations, it will lose dimers and shrink; At critical concentration, growth and shrinkage are in balance and there is no net change in length. o 2. Microtubules maintain their constant length by balancing growth and shrinkage, while hydrolyzing GTP which is necessary cost to maintain dynamic instability, enhances the ability of the cell to regulate microtubule growth in space and time, systems in motion are much easier to alter than static systems  Microtubule- associated proteins (MAPS)- Normal cell function depends on the regulation of both assembly and disassembly of microtubules; preventing them from dissociating impairs many cellular processes, including cell division. Microtubule dynamics are also regulated by microtubule-associated proteins (MAPs), these proteins bind to the surface of microtubules stabilizing or destabilizing the structures  MAPs bind to (+) end; prevent transition from growth to shrinkage o Stable-tubule only polypeptides (STOPs) used to make long, stable microtubules o Abundant in nerves where microtubules are important for the development of long axons and dendrites  MAPs can act as protein cross-linkers, they join microtubules into bundles and link them to other cellular structures, such as membrane receptors  MAPs (katanin=sword) severs microtubules  MAPs activity is regulated by protein kinases and phosphatases  Changes in MAPs phosphorylation: o Alter its sub cellular location o Change its ability to bind a microtubule o Alter its functional properties  Many signaling pathways target maps to alter microtubule structure: o Hormones that regulate cell division; ensures that cellular components are equally divided between daughter cells o Cytokines induce changes in microtubule structure by regulating MAPs structure and activity  The 2 major motor proteins associated with microtubules: Kinesin and dynein  Are unrelated, but they work in similar ways: both undergo conformational changes, where they stretch out to grab a tubulin dimer, then bend to pull themselves along the microtubule  Structural changes in the motor protein are ATP hydrolysis dependent  Rate of movement determined by: ATPase domain of the proteins and regulatory proteins that associate with the motor proteins  Motor proteins recognize microtubule polarity; (-) ends arranged at MTOC and (+) ends at outer edges of cell, Each motor protein moves in a characteristic direction, Microtubule polarity allow for directional movement of cargo  Kinesin Structure: long neck, Fan-like tail- attaches to cargo, globular head has ATPase activity; attaches to the microtubule o Kinesin Function: Moves cargo in (+) direction; to outer edges of cell  Dynein Structure: Globular head, Neck, Tail o Dynein Function: Larger than kinesin and moves about 5x faster. Moves in (-) direction; to MTOC, Does not attach directly to cargo; large multiprotein accessory complexes link dynein to cargo, Provides layer of regulation of microtubule movement o 2 Classes of dyneins: Cytoplasmic- intracellular movement; Axonemal- driving force cilia and flagella movements  Intermediate filaments: Composed of twisted strands of several different proteins: Keratin, Desmin, Lamin o Functions: Cell shape, Anchoring nucleus, Tensile strength against mechanical stresses  Actin filaments: Composed of monomers of the protein Make up a major portion of cytoskeleton of all cells o G-actin (Globular actin) - assembles into a polymer of two twisting chains - F-actin (Filamentous actin) o Functions: Cell shape, Mobility, Cell division, Muscle cell contraction  Microfilaments: Spontaneously assemble and disassemble without the investment of energy  Polymerizes when its concentration is above a threshold, Growth occurs at both (+) and (-) ends, 6 to 10x faster at the plus end, If growth at (+) end exactly balances shrinkage at (-) end, the total length of the microfilament is constant call treadmilling  Accessory proteins can modulate the rate of microfilament growth  Capping proteins- bind and stabilize (-) end, preventing it from disassembling; increases the length of microfilaments more added than lost  Polymerization of filaments can cause movement which is important in 2 kinds of amoeboid movement in animals: o Filapodia – thin rodlike extensions of cells formed by actin fibers; microvilli o Lamellipodia – in animals cells, resemble pseudopodia found in prokaryotes, but they are thinner and more sheet-like  Myosin- Different arrangements of actin and myosin enable cells to transport vesicles and organelles, change shape, motility; large gene family (~17 different classes with different structural properties) most common are I, II, and V o II- muscle myosin, found in non-muscle cells o I and V- intracellular traffic; typically dimerized  Myosin Structure: Head- ATPase activity, which provides energy for movement; Tail- binds cargo (vesicles, organelles, PM); may also allow dimers to be formed (II and V); Neck- regulates activity of the myosin head directly, and also mediates the effects of proteins that associate with the neck, Myosin light chains  Myosin II- Essential and regulatory light chain, regulated by reversible phosphorylation o When phosphorylation by myosin light chain kinase (MLCK), they are structurally altered which alters the activity of the head  Sliding filament model- proposed by Hugh Huxley ~60 years ago describes the movement of myosin on an actin filament o Myosin head bound to actin called crossbridge o ATP binds causing myosin head to detach from actin o Myosin neck extends, moving myosin head forward o Myosin phosphorylates ATP to ADP releasing P energy o Actin is pulled forward called power stroke o ADP is released; crossbridge is reformed; myosin is able to bind to a new molecule of ATP  If no ATP is available (such as in a dead animal) myosin remains firmly attached to actin, creates condition of rigor


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