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Lecture 15

Lecture 15 & 16.docx

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Department
Biology
Course
BIOL 370
Professor
Dinu Nesan
Semester
Fall

Description
Lecture 15 Physiology of Signalling Animals have a variety of signaling mechanisms that allow for communication between cells - Neural, paracrine, hormonal Receptor-ligand interactions are critical for the specificity of target effects of these signals - Receptor expression, binding characteristics, inactivation methods Hormones control a variety of effects throughout the body, including the released of other hormones - The hypothalamus and the pituitary are key regulating organs - Major signalling mechanisms: o Paracrine/Autocrine signaling: Local cell-to-cell communication, involves variety of molecules “cytokines” for signal translocation o Nerve impulses: Long distance fast conduction, electrical signals can occur on order of ms o Endocrine signaling: Long distance signal through bloodstream, very slow - Major signalling mechanisms: o Direct cell signalling via Gap junctions o Autocrine & Paracrine Signaling via Chemical messengers o Endocrine signalling via Hormones travelling through bloodstream o Neural signalling via Electrical signals, can be directly received through gap junction or indirectly received by sending neurotransmitters - Peptide hormones (<50 AA) o Fast acting hormones, t1/2rom sec to hours o Hydrophilic in nature, cannot cross cell membrane & are soluble in aqueous solution “blood”  Synthesized on the ribosome of the Rough ER as preprohormone (1+ copies of peptide hormone & a signalling sequence for secretion)  Preprohormone enters Rough ER & the signal sequence is cleaved off  Prohormone  Prohormone are packaged into vesicles, travels to the Golgi apparatus, and are packaged into secretory vesicles containing proteolytic enzymes  Prohormones are cleaved into active hormones and are expelled into extracellular fluid via exocytosis, they travel unbound in blood o E.g. Glucagon, Insulin, ACTH, GH, Prolactin, Vasopressin, Gastrin etc. - Steroid hormones (common precursor is cholesterol) o Slow acting hormone o Hydrophobic in nature, can cross cell membrane so they are synthesized on demand, & are not soluble in blood so they are bound by carrier proteins (e.g. albumin)  Synthesized by steroidogenic cells that expresses different cleavage enzymes  Cleaved to form glucocorticoids, mineralocorticoids, & sex steroids o Insect steroid: Ecdysone “Prohormone”  20-hydroxy ecdysone “Hormone”  Expressed via trophic hormone input “prothracicotrophic hormone” @ insect brain  Stimulates the molting “shedding of exoskeleton” process & transition between larval stages into adulthood “larva  pupa  adult”  Activity in vertebrate systems is unclear - Amine derived hormones (common precursors are tyrosine, tryptophan, histidine) o Can act as neurotransmitters or hormones (peptide + steroid) o E.g. Catecholamines, dopamine, norepinephrine, epinephrine, serotonin, melatonin, thyroid hormones - Other signalling molecules: o Eicosanoids: Lipid messengers derived from membrane phospholipids  E.g. Prostaglandin (PGF) are involved in pain reception, synthesis is blocked by pain killers o Nitric oxide: Gaseous messengers that diffuses freely, potent vasodilator o Purines: Nucleic acid derivatives, including AMP, ATP, GMP - Ligand-Receptor Interactions o Only cells that expresses receptors can respond to a signalling molecule o Tissue specific responds: Intracellular effects caused by the same ligand varies depending on the tissue o Receptor affinity varies among different isoforms  Increase in [ligand]  increase in the % of bound receptors until saturation  With the same [ligand], cells with more receptors have more # of bound receptors & respond to messengers more strongly than cells with less receptors on surface  Cells with high affinity receptor will have higher % of ligand binding until saturation o The ligand-receptor binding must be turned off to cease the signal  Ligand degradation by extracellular enzymes or taken up by other cells  Receptor removed from the surface, degraded by own cell via endocytosis, or inactivated by intracellular phosphorylation  Ligand + Receptor are degraded by own cell via endocytosis  Intracellular signal protein can be inactivated - The endocrine system o Endocrine glands “ductless”: Release hormones into the circulatory system, usually long distance o Exocrine glands “ducts”: Signals are released into ducts connected to the external surface of the body, usually local-acting - The hypothalamus: Major regulating centre for homeostatic control o Integration site for numerous different body sensors “optical, olfactory, hormonal, & neural inputs” o Source for various hormones  Corticotropin RH, GHRH, Gonadotropin RH  Adenohypophysis  Oxytocin & Vasopressin  Neurohypophysis o Specialized vascular system “Microcirculation”  Hypothalamic-hypophyseal-portal system: Allows neurohormones to be carried from the hypothalamus to the Adenohypophysis without being diluted “small amount needed” - The pituitary: The master regulator of growth & development, not a part of the brain o Neural “neurohypophysis – outcropping of hypothalamus” & endocrine “adenohypophysis – pure endocrine gland” tissues  Anterior: Neurohormones of the hypothalamus are released into the HHPS & stimulates the anterior pituitary to release hormones into the blood  Posterior: Nerve endings at the posterior pituitary releases neurohormones into the blood o “Trophic hormones”: Adrenocorticotrophic H, Thyroid stimulating H o “Non-trophic hormones”: Prolactin, GH, Luteinizing H, Follicular stimulating H - Feedback Regulation: Regulation can occur at multiple levels o Negative Feedback: Most common pattern “end product inhibition” o Positive Feedback: Very rate, external factors are required to terminate the loop o Direct: Stimulus  Endocrine gland releases hormone  target organ response back by terminating the stimulus o First order: Stimulus  Sense organ  Sensory neuron to Integrating center & neuron out  target organ response back by terminating the stimulus o Second order: Stimulus  Sense organ  Sensory neuron to Integrating center & neuron out  Endocrine gland releases hormone  target organ response back by terminating the stimulus or the release of hormone @ endocrine gland o Third order: Stimulus  Sense organ  Sensory neuron to Integrating center & neuron out  Endocrine gland 1 releases hormone  targets endocrine gland 2 to release hormone  target organ
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