mechanisms of intercellular communication. internet resources phys/endocrine/index.html
TRANSCRIPT
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MECHANISMS OF INTERCELLULAR COMMUNICATION
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INTERNET RESOURCES
• http://www.vivo.colostate.edu/hbooks/pathphys/endocrine/index.html
• http://www.uri.edu/pharmacy/animation/huangAnim.htm
• http://www.infochembio.ethz.ch/links/en/biochem_hormone.html
• http://www.scientia.org/cadonline/Biology/endocrine/action.ASP
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TYPES OF INTERCELLULAR COMMUNICATION
• DIRECT COMMUNICATION• SYNAPTIC COMMUNICATION• AUTOCRINE COMMUNICATION• PARACRINE COMMUNICATION• ENDOCRINE COMMUNICATION
– http://www.wisc-online.com/objects/index_tj.asp?objid=AP13704
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DIRECT COMMUNICATION
• GAP JUNCTIONS
• CYTOPLASM TO CYTOPLASM
• IONS
• SMALL MOLECULES IN SOLUTION
• LIPID SOLUBLE MOLECULES
• LIMITED TO ADJACENT CELLS
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SYNAPTIC COMMUNICATION
• NEUROTRANSMITTERS
• SYNAPTIC CLEFTS
• LIMITED TO SPECIFIC AREAS
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LOCAL CHEMICAL MESSENGERS
• AUTOCRINE
• PARACRINE
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ENDOCRINE COMMUNICATION
• TARGET CELLS THROUGHOUT BODY
• HORMONES
• CARRIED IN CIRCULATORY SYSTEM
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DIFFERENCES BETWEEN NERVOUS AND ENDOCRINE SYSTEMS
NERVOUS ENDOCRINE• FREQUENCY-
MODULATED SIGNALS
• FASTER ACTING• SHORT DURATION• GENERALLY LESS
DISTRIBUTED
• AMPLITUDE-MODULATED SIGNALS
• LONGER ACTING• LONGER
DURATION• GENERALLY
MORE WIDELY DISTRIBUTED
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RELATIONSHIP BETWEEN ENDOCRINE AND NERVOUS
• CANNOT BE SEPARATED ANATOMICALLY OR FUNCTIONALLY
• NEURONS INNERVATE ENDOCRINE GLANDS
• SOME NEURONS SECRETE NEUROHORMONES INTO BLOOD
• SOME HORMONES AFFECT NERVOUS SYSTEM
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TYPES OF MESSENGERS
• AMINO ACID DERIVATIVES
• PEPTIDE HORMONES
• LIPID DERIVATIVES
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AMINO ACID DERIVATIVES
• SIMILAR TO AMINO ACIDS• BIOGENIC AMINES• CATECHOLAMINES
– EPINEPHRINE– NOREPINEPHRINE– DOPAMINE
• THYROID HORMONE• MELATONIN
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PEPTIDE HORMONES
• CHAINS OF AMINO ACIDS
• SHORT PEPTIDE CHAINS
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LIPID DERIVATIVES
• STERIOD HORMONES
• EICANOSOIDS
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STEROIDS
• LIPIDS SIMILAR TO CHOLESTEROL
• ANDROGENS
• PROGESTINS
• ESTROGENS
• CORTICOSTEROIDS
• CALCITROL
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EICOSANOIDS
• LIPID DERIVATIVES OF ARACHIDONIC ACID
• LEUKOTRIENES
• PROSTAGLANDINS
• THROMBOXANES
• PROSTACYCLINES
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HORMONE REGULATION
• HORMONE SECRETION INCREASES AND DECREASES
• USUALLY CONTROLLED BY NEGATIVE FEEDBACK
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MECHANISMS OF CONTROL
• ACTION OF SUBSTANCES OTHER THAN HORMONES
• NEURAL CONTROL OF ENDOCRINE GLAND
• ACTIVITY OF ONE ENDOCRINE GLAND CONTROLLED BY HORMONES FROM ANOTHER
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ACTION OF SUBSTANCES OTHER THAN HORMONES
• CONCENTRATION OF GLUCOSE IN BLOOD AFFECTS INSULIN AND GLUCAGON SECRETION
• CONCENTRATION OF CALCIUM IN BLOOD AFFECTS CALCITONIN AND PARATHYROID HORMONE SECRETION
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CONTROL OF INSULIN SECRETION BY BLOOD
GLUCOSE LEVELS • ELEVATED BLOOD LEVELS OF GLUCOSE
STIMULATE INSULIN SECRETION
• INSULIN ACTS ON TARGET TISSUES TO INCREASE UPTAKE AND USE OF GLUCOSE
• DECLINING BLOOD LEVELS OF GLUCOSE LEAD TO A DECREASE IN INSULIN PRODUCTION
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CONTROL OF ADRENAL MEDULLARY SECRETIONS BY
NEURAL MECHANISMS • STRESS ACTIVATES SYMPATHETIC
DIVISION OF THE ANS
• SYMPATHETIC NEURONS STIMULATE RELEASE OF EPINEPHRINE AND NOREPINEPHRINE FROM ADRENAL MEDULLA
• WHEN STRESS IS REMOVED EPINEPHRINE AND NOREPINEPHRINE LEVELS DECLINE
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HORMONES CAN STIMULATE OR INHIBIT SECRETON OF OTHER
HORMONES
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CONTROL OF THYROID STIMULATING HORMONE BY
THYROID RELEASING HORMONE• TRH IS RELEASED BY NEURONS IN HYPOTHALAMUS
• STIMULATES RELEASE OF TSH FROM ANTERIOR PITUITARY
• TSH STIMULATES SECRETION OF THRYOID HORMONE FROM THYROID
• CONTROLLED BY NEGATIVE FEEDBACK
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HORMONES MAY BE CONTROLLED BY ONE OR
MORE OF THESE MECHANISMS
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POSITIVE FEEDBACK MECHANISMS ARE USED
NEGATIVE FEEDBACK MECHANISMS LIMIT
PROCESSES
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MENSTRUAL CYCLE BEFORE OVULATION
• POSITIVE FEED BACK
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MENSTRUAL CYCLE AFTER OVULATION
• NEGATIVE FEED BACK MECHANISMS
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TRANSPORTATION OF HORMONES
• FREE STATE
• BOUND TO PLASMA PROTEINS
• THYROID BINDING GLOBULIN
• TRANSTHYRETIN
• ALBUMIN
• TRANSCORTIN
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HORMONES TRANSPORTED IN BOUND FORM
• EQUILIBRIUM EXISTS BETWEEN FREE AND BOUND FORM
• PREVENTS LARGE INCREASES OR DECREASES IN HORMONE LEVELS
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EXAMPLES
• THRYOID HORMONES ARE CARRIED BY THYROID BINDING GLOBULIN AND ALBUMIN
• PROGESTERONE IS CARRIED BY TRANSCORTIN AND ALBUMIN
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DISTRIBUTION OF HORMONES• WIDELY DISTRIBUTED
• DIFFUSE INTO INTERSTITIAL FLUIDS
• RATES OF DIFFUSION VARY
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METABOLISM AND ELIMINATION OF HORMONES
• LIMITS TO LENGTH OF TIME HORMONES ARE ACTIVE
• ALLOWS MORE PRECISE REGULATION
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HALF LIFE
• TIME IT TAKES FOR HALF A DOSE OF A SUBSTANCE TO BE ELIMINATED FROM CIRCULATORY SYSTEM
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SHORT HALF LIFE HORMONES
• HORMONES WITH SHORT HALF LIVES INCREASE AND DECREASE RAPIDLY IN PLASMA
• WATER SOLUBLE HORMONES
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LONG LIFE HORMONES
• HORMONES WITH LONG HALF LIVES HAVE RELATIVE STABLE LEVELS IN PLASMA
• STEROID HORMONES
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FACTORS THAT INFLUENCE THE HALF LIFE OF HORMONES
• ELIMINATION– EXCRETION– METABOLISM– CONJUGATION– ACTIVE TRANSPORT
• CONSERVATION– PROTECTION FROM EXCRETION – PROTECTION FROM METABOLISM– PROTECTION BECAUSE OF HORMONE STRUCTURE
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HORMONAL INTERACTIONS WITH TARGET CELLS
• HORMONES BIND TO TARGET CELL RECEPTORS
• ALTER RATE OF CELLULAR ACTIVITIESACTIVATE OR INACTIVATE
ENZYMESINCREASE OR DECREASE RATE OF
SYNTHESIS OF MOLECULES IN CELLSCAUSES CHANGES CELL MEMBRANE
PERMEABILITY
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HORMONE RECEPTORS
• PROTEIN OR GLYCOPROTEIN
• EACH RECEPTOR HIGHLY SPECIFIC FOR ITS HORMONE
• A HORMONE MAY HAVE DIFFERENT RECEPTORS
• TARGET CELLS HAVE RECEPTORS-NONTARGET CELLS DO NOT
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RECEPTORS AND DOWNREGULATION
• NUMBER OF RECEPTORS DECREASE AFTER EXPOSURE TO CERTAIN HORMONES
• RESPOND TO SHORT TERM INCREASES IN HORMONE CONCENTRATIONS
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MECHANISMS OF DOWN REGULATION
• RECEPTOR SYNTHESIS DECREASES
• COMBINATION OF HORMONES AND RECEPTORS INCREASE RATE OF RECEPTOR MOLECULE DEGRADATION
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RECEPTORS AND UP REGULATION
• SOME TISSUES EXHIBITG PERIODIC INCREASES IN SENSITIVITY TO CERTAIN HORMONES
• THE EXPOSURE OF A TISSUE TO ONE HORMONE INCREASES ITS SENSITIVITY TO ANOTHER
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TYPES OF RECEPTORS
• MEMBRANE BOUND
• INTRACELLLULAR
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MEMBRANE BOUND RECEPTORS
• WATER SOLUBLE HORMONES
• REVERSIBLE BINDING
• EQUILIBRIUM EXISTS
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CHARACTERISTICS OF HOMONE RECEPTORS OF
THE CELL MEMBRANE
• GENERALLY LARGE MOLECULES
• ALMOST ALWAYS HIGHLY SPECIFIC FOR SINGLE HORMONE
• INACTIVE WHEN HORMONE IS NOT BOUND TO IT
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EFFECT OF HORMONAL BINDING TO RECEPTORS
• SELDOM DIRECTLY AFFECT INTRACELLULAR MACHINERY
• BINDING USUALLY ACTIVATES CELLULAR PROCESSES
• SOMETIMES BINDING INACTIVATES CELLULAR PROCESSES
• DIRECT OR INDIRECT EFFECTS
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DIRECT EFFECTS• CONFORMATIONAL CHANGE OF RECEPTOR
MOLECULE CHANGES MEMBRANE PERMEABILITY • ESPECIALLY SODIUM, CHLORIDE AND CALCIUM
IONS• ACETYLCHOLINE—a neurotransmitter• SEROTONIN---a hormone and neurotransmitter• GLYCINE—a neurotransmitter• GABA---a neurotransmitter• GROWTH HORMONE---a hormone
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INDIRECT EFFECTS
• HORMONES THAT ACTIVATE G PROTEINS AND ALTER MEBRANE CHANNELS OR ACTIVATE INTRACELLULAR MEDIATORS
• HORMONES THAT ALTER ACTIVITY OF INTRACELLULAR ENZYMES TO CATALYZE SYNTHESIS OR PHOSPHORYLATION
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HORMONES THAT ACTIVATE G PROTEINS
• OXYTOCIN• VASOPRESSIN• LUTEINIZING HORMONE• FOLLICLE STIMULATING
HORMONE• PROLACTIN• ATRIAL NATRIURETIC
HORMONE
• THYROID STIMULATING HORMONE
• PARATHYROID HORMONE
• GLUCAGON• EPINEPHRINE• ADRENOCORTICOTROPI
C HORMONE
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EFFECTS OF HORMONE BINDING
• REGULATION OF MEMBRANE CHANNELS
• INCREASING OR DECREASING INTRACELLULAR MEDIATORS
c GMP & c AMP
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HOW G PROTEINS REGULATE THE SYNTHESIS OF
INTRACELLULAR MEDIATORS
• G PROTEIN ALTERS ACTIVITY OF ENYZMES AT INNER SURFACE OF CELL MEMBRANE
ADENYL CYCLASE & GUANYL CYCLASE
• INCREASES OR DECREASES c AMP OR c GMP LEVELS IN CELL
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Cyclic AMP AS AN INTRACELLULAR MEDIATOR
• PROTEIN AND POLYPEPTIDE HORMONESCTH, TSH, LH, FSH, ADH, PTH, GLUCAGON, CATECHOLAMINES, SECRETIN AND HYPOTHALAMIC RELEASING HORMONES
• ACT BY cyclic ADENOSINE MONOPHOSPHATE MECHANISM
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ADENOSINE MONOPHOSPHATE SECOND MESSENGER SYSTEM
• HORMONE IS FIRST MESSENGER
• BINDS TO RECEPTOR ON OUTER SURFACE OF CELL MEMBRANE
• RECEPTOR ASSOCIATED A G PROTEIN
• SOME EXCITATORY-SOME INHIBITORY
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FUNCTION OF ADENYLATE CYCLASE
• CONVERTS ATP TO cyclic AMP
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ACTIVITY OF cyclic AMP
• ACTIVATES OTHER ENZYMES
• USUALLY IN AN ENZYME CASCADE
• JUST A FEW cyclic AMP MOLECULES CAN HAVE POWERFUL EFFECT
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PROTEIN KINASES• ACTIVATED BY cyclic AMP• USE PHOSPHATES AND ENERGY FROM
ATP TO PHOSPHORYLATE ANOTHER ENZYME
• ACTIVATE OR INACTIVATE ENZYME• OFTEN ACTIVATION OF ENZYME IS THE
RATE LIMITING REACTION IN METABOLIC PATHWAY
• COMMON IN CELLS
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EXCITATORY G PROTEINS
• ACTIVATES ADENYLATE CYCLASE
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ACTION OF c AMP AND c GMP• ACTIVATING cyclic AMP or cyclic GMP
ACTIVATES PROTEIN KINASE/PHOSPHOKINASE
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GLUCAGON EFFECTS ON LIVER CELLS
• ELEVATE cyclic AMP LEVELS
• ACTIVATE ENZYME SYSTEM
• PROMOTES BREAKDOWN OF GLYCOGEN INTO GLUCOSE
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cyclic GUANOSINE MONOPHOSPHATESECOND MESSENGER SYSTEM• SOME CELLS USE INSTEAD OF cyclic
AMP
• ATRIAL NATRIURETIC HORMONE
• NITRIC OXIDE
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INTRACELLULAR MEDIATOR MOLECULES WILL HAVE DIFFERENT
EFFECTS IN THE VARIOUS CELLS THAT USE THEM
•
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G PROTEINS AND PHOSPOINOSITOL
• PHOSPHOLIPASE C
• ACTS ON PHOSPHOINOSITOL TO FORM DIACYLGLYCEROL & INOSITOL TRIPHOSPHATE
• INOSITOL TRIPHOSPHATE CAUSES RELEASE OF CALCIUM
• DIACYLGLYCEROL AND CALCIUM IONS ALTER ACTIVITY OF PROTEIN KINASES
ALTER CALCIUM PERMEABILITYALTER SYNTHESIS IN CELL
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EFFECTS ON SMOOTH MUSCLE• IN RESPONSE TO EPINEPHRINE• INOSITOL TRIPHOSPHATE STIMULATES CALCIUM
RELEASE FROM ENDPLASMIC RETICULUM AND/OR CELL MEMBRANE
• CALCIUM BINDS WITH CALMODULIN• CALMODULIN BIND TO ENZYME THAT
PHOSPHORYLATES MYOSIN MOLECULES TO STIMULATE CONTRACTION
• DIACYLGLYCEROL REGULATES ENZYMES THAT REGULATE SYNTHESIS OF PROSTAGLANDINS
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HORMONE RECEPTORS THAT DIRECTLY SYNTHESIZE AN
INTRACELLULAR MEDIATOR• ATRIAL NATRIURETIC HORMONE
BINDS WITH RECEPTOR• GUANYLYL CYCLASE ACTIVATED• PRODUCES cyclic GMP FROM GTP• cyclic GMP CAUSES INCREASED
EXCRETION OF SODIUM IONS• INCREASED WATER VOLUME IN
URINE
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HORMONES THAT BIND TO RECEPTORS THAT
PHOSPHORYLATE INTRACELLULAR HORMONES• MEMBRANE BOUND RECEPTORS
• RECEPTOR ACTS AS PHOPHORYLASE ENCYME
• ATCHES PHOPHATE FROM ATPs TO RECPTOR AND INTRACELLULAR PROTEINS
• INSULIN
• GROWTH HORMONE,
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CASCADE EFFECT
• FEW MEDIATOR MOLECULES ACTIVATE SEVERAL ENZYMES
• ACTIVATED ENZYMES ACTIVATE SEVERAL OTHER ENZYMES
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INTRACELLULAR HORMONE
RECEPTORS • PROTEIN MOLECULES INSIDE CELL• SOME FLOAT IN CYTOPLASM• OTHERS IN NUCLEUS• HORMONES BIND TO INTRACELLULAR RECEPTORS CALLED
HORMONE RECEPTIVE ELEMENTS• SEX STEROID• MINERALOCORTICOIDS• GLUCOCORTICOIDS• THYROID HORMONE• VITAMIN D
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STEROID HORMONES
• DIFFUSE ACROSS CELL MEMBRANE
• BINDS TO DINA SEMENTS CALLED HORMONE RESPONSIVE ELEMENTS
• TRIGGERS ACTIVATION OR INACTIVATION OF SPECIFC GENES
• ALTERS TRANSCRIPTION RATE
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ALDOSTERONE• AFFECTS RENAL TUBULAR CELLS
• COMBINES WITH SPECIFIC RECEPTOR PROTEIN
• COMPLEX MOVES INTO NUCLEUS
• COMPLEX ACTIVATES SPECIFIC GENES
• m RNA IS FORMED AND DIFFUSES INTO CYTOPLASM
• TRANSLATION PRODUCES NEW PROTEINS
• PROTEINS PROMOTE SODIUM REABSORPTION INTO TUBULES AND SECRETION OF POTASSIUM INTO TUBULES
• TAKES FROM 45 MIN TO SEVERAL HOURS