MECHANISMS OF INTERCELLULAR COMMUNICATION

1. MECHANISMS OF INTERCELLULAR COMMUNICATION

2. 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

3. 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

4. DIRECT COMMUNICATION • GAP JUNCTIONS • CYTOPLASM TO CYTOPLASM • IONS • SMALL MOLECULES IN SOLUTION • LIPID SOLUBLE MOLECULES • LIMITED TO ADJACENT CELLS

5. SYNAPTIC COMMUNICATION • NEUROTRANSMITTERS • SYNAPTIC CLEFTS • LIMITED TO SPECIFIC AREAS

6. LOCAL CHEMICAL MESSENGERS • AUTOCRINE • PARACRINE

7. ENDOCRINE COMMUNICATION • TARGET CELLS THROUGHOUT BODY • HORMONES • CARRIED IN CIRCULATORY SYSTEM

8. FREQUENCY-MODULATED SIGNALS FASTER ACTING SHORT DURATION GENERALLY LESS DISTRIBUTED AMPLITUDE-MODULATED SIGNALS LONGER ACTING LONGER DURATION GENERALLY MORE WIDELY DISTRIBUTED DIFFERENCES BETWEEN NERVOUS AND ENDOCRINE SYSTEMSNERVOUS ENDOCRINE

9. 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

10. TYPES OF MESSENGERS • AMINO ACID DERIVATIVES • PEPTIDE HORMONES • LIPID DERIVATIVES

11. AMINO ACID DERIVATIVES • SIMILAR TO AMINO ACIDS • BIOGENIC AMINES • CATECHOLAMINES • EPINEPHRINE • NOREPINEPHRINE • DOPAMINE • THYROID HORMONE • MELATONIN

12. PEPTIDE HORMONES • CHAINS OF AMINO ACIDS • SHORT PEPTIDE CHAINS

13. LIPID DERIVATIVES • STERIOD HORMONES • EICANOSOIDS

14. STEROIDS • LIPIDS SIMILAR TO CHOLESTEROL • ANDROGENS • PROGESTINS • ESTROGENS • CORTICOSTEROIDS • CALCITROL

15. EICOSANOIDS • LIPID DERIVATIVES OF ARACHIDONIC ACID • LEUKOTRIENES • PROSTAGLANDINS • THROMBOXANES • PROSTACYCLINES

16. HORMONE REGULATION • HORMONE SECRETION INCREASES AND DECREASES • USUALLY CONTROLLED BY NEGATIVE FEEDBACK

17. MECHANISMS OF CONTROL • ACTION OF SUBSTANCES OTHER THAN HORMONES • NEURAL CONTROL OF ENDOCRINE GLAND • ACTIVITY OF ONE ENDOCRINE GLAND CONTROLLED BY HORMONES FROM ANOTHER

18. 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

19. 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

20. 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

21. HORMONES CAN STIMULATE OR INHIBIT SECRETON OF OTHER HORMONES

22. 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

23. HORMONES MAY BE CONTROLLED BY ONE OR MORE OF THESE MECHANISMS

24. POSITIVE FEEDBACK MECHANISMS ARE USED NEGATIVE FEEDBACK MECHANISMS LIMIT PROCESSES

25. MENSTRUAL CYCLE BEFORE OVULATION • POSITIVE FEED BACK

26. MENSTRUAL CYCLE AFTER OVULATION • NEGATIVE FEED BACK MECHANISMS

27. TRANSPORTATION OF HORMONES • FREE STATE • BOUND TO PLASMA PROTEINS • THYROID BINDING GLOBULIN • TRANSTHYRETIN • ALBUMIN • TRANSCORTIN

28. HORMONES TRANSPORTED IN BOUND FORM • EQUILIBRIUM EXISTS BETWEEN FREE AND BOUND FORM • PREVENTS LARGE INCREASES OR DECREASES IN HORMONE LEVELS

29. EXAMPLES • THRYOID HORMONES ARE CARRIED BY THYROID BINDING GLOBULIN AND ALBUMIN • PROGESTERONE IS CARRIED BY TRANSCORTIN AND ALBUMIN

30. DISTRIBUTION OF HORMONES • WIDELY DISTRIBUTED • DIFFUSE INTO INTERSTITIAL FLUIDS • RATES OF DIFFUSION VARY

31. METABOLISM AND ELIMINATION OF HORMONES • LIMITS TO LENGTH OF TIME HORMONES ARE ACTIVE • ALLOWS MORE PRECISE REGULATION

32. HALF LIFE • TIME IT TAKES FOR HALF A DOSE OF A SUBSTANCE TO BE ELIMINATED FROM CIRCULATORY SYSTEM

33. SHORT HALF LIFE HORMONES • HORMONES WITH SHORT HALF LIVES INCREASE AND DECREASE RAPIDLY IN PLASMA • WATER SOLUBLE HORMONES

34. LONG LIFE HORMONES • HORMONES WITH LONG HALF LIVES HAVE RELATIVE STABLE LEVELS IN PLASMA • STEROID HORMONES

35. 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

36. HORMONAL INTERACTIONS WITH TARGET CELLS • HORMONES BIND TO TARGET CELL RECEPTORS • ALTER RATE OF CELLULAR ACTIVITIES ACTIVATE OR INACTIVATE ENZYMES INCREASE OR DECREASE RATE OF SYNTHESIS OF MOLECULES IN CELLS CAUSES CHANGES CELL MEMBRANE PERMEABILITY

37. 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

38. RECEPTORS AND DOWNREGULATION • NUMBER OF RECEPTORS DECREASE AFTER EXPOSURE TO CERTAIN HORMONES • RESPOND TO SHORT TERM INCREASES IN HORMONE CONCENTRATIONS

39. MECHANISMS OF DOWN REGULATION • RECEPTOR SYNTHESIS DECREASES • COMBINATION OF HORMONES AND RECEPTORS INCREASE RATE OF RECEPTOR MOLECULE DEGRADATION

40. 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

41. TYPES OF RECEPTORS • MEMBRANE BOUND • INTRACELLLULAR

42. MEMBRANE BOUND RECEPTORS • WATER SOLUBLE HORMONES • REVERSIBLE BINDING • EQUILIBRIUM EXISTS

43. 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

44. 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

45. 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

46. 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

47. OXYTOCIN VASOPRESSIN LUTEINIZING HORMONE FOLLICLE STIMULATING HORMONE PROLACTIN ATRIAL NATRIURETIC HORMONE THYROID STIMULATING HORMONE PARATHYROID HORMONE GLUCAGON EPINEPHRINE ADRENOCORTICOTROPIC HORMONE HORMONES THAT ACTIVATE G PROTEINS

48. EFFECTS OF HORMONE BINDING • REGULATION OF MEMBRANE CHANNELS • INCREASING OR DECREASING INTRACELLULAR MEDIATORS c GMP & c AMP

49. 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

50. 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