BIOL 460 1nd Edition Lecture 5Outline of Last Lecture I. Sympathetic division a. Sympathoadrenal systemII. Parasympathetic division III. Autonomic Function IV. NTMs in ANSa. Achi. Cholinergic neurons ii. Cholinergic receptors Outline of Current Lecture I. NTM in ANS continueda. Norepinephrinei. Adrenergic neurons ii. Adrenergic receptors1. Alpha 12. Alpha 23. Beta b. Nonadrenergic/noncholinergic fibersCurrent Lecture1. Norepinephrine a. Adrenergic neurons i. All adrenergic receptors are g-protein linked ii. Norepinephrine raises heart rate (EPSP), relaxes smooth muscle in bronchi (IPSP) iii. Most sympathetic post-ganglionic neurons are adrenergic iv. Exception are axons helping visceral effector in somatic parts of body (Ach)b. Adrenergic receptors i. Alpha1. Alpha 1 – vascular smooth muscle in skin and viscera, generate EPSPSs, causing vasoconstriction a. Figure 11.9→ pathway for alpha 1 receptors i. Bond to norepinephrine These notes represent a detailed interpretation of the professor’s lecture. GradeBuddy is best used as a supplement to your own notes, not as a substitute.ii. Phospholipase C/Ca2+ 2nd messenger system iii. G-protein turn on phospholipase C (enzyme)iv. Phospholipase C (in plasma membrane) takes phospholipid from PM and breaks phosphate off (ester bond) v. Produces 2 molecules that can be 2nd messengers1. Inositol triphosphate (IP3)- polar, hydrophilic2. Diacyl glycerol (DAG)-, hydrophobic, restricted to PM vi. IP3 moves through cytoplasm to ER, pump constantly pumps Ca2+ into ERvii. IP3 bonds to Ca2+ ligand gated channel on ER membraneviii. Channel opens, Ca2+ diffuses into cytoplasm and binds to calmodulin, gives Ca2+/Calmodulin complex which activates protein kinases, causing the physiological effect ix. Turning off 1. Ca2+ pumped back into ER2. Protein phosphatases reverse protein kinaseeffects 3. IP3 destroyed by an enzyme 4. G protein turns itself off 5. NTM destroyed2. Alpha 2- terminal boutons of sympathetic post-ganglionic neurons- negative feedback system used to monitor sympathetic division a. Use andenylate cyclase/cAMP pathway b. On terminal boutons of some sympathetic post-ganglionic neurons c. Norepinephrine released d. Binds to A1, B1, B2 on post-synaptic celle. Alpha 2 on terminal bouton f. Some norepinephrine bond to alpha 2 receptor, functions like beta receptors, andenylate cyclase/cAMP STP g. Result is to open K+ ligand gated channelh. K+ diffuses out, creating IPSPi. Interferes with opening of Ca2+ VGC on terminal bouton j. Decreases release of norepinephrine, keeping sympathetic nervous system in checkk. They have found an A2 agonist- captapres or clonidine- lowers blood pressure by decreasing sympathetic responseii. Beta1. Beta 1- on heart, generates EPSP (heart rate up, stronger contraction) 2. Beta 2- smooth muscle (SM) of bronchioles, relaxes (bronchodilation); nonvascular SM of viscera (IPSPS )3. B blockers designed to block B1 which lowers heart rate 4. B adrenergic receptor pathway a. Andenylate cyclase/cAMP 2nd messenger system b. Norepinephrine bindsc. G protein does its thingd. Turns on andenylate cyclase e. ATP→ (hydrolyze)→ cAMP and pyrophosphate f. Protein subunits are dimersi. Catalytic subunit→ bind to cause IPSPii. Inhibitory subunit→ greater affinity to catalytic subunit iii. In absence of cAMP inhibitory subunit will bind to catalytic subunit, preventing actiong. Turn off i. cAMP broken down by phosphodiesteraseii. protein kinases reversed by phosphatases 5. beta blockersa. original used for hypertensionb. propranolol i. blocks B1 and B2 ii. b antagonist (blocked B2- not good)c. atenolol i. B1 antagonistii. Decreased blood pressure, but no bronchoconstriction6. Asthma a. Inhaler used to contain epinephrine b. Caused bronchodilation and increased heart rate, blood pressure c. Also bonded to alpha 1 and alpha 2d. Now use terbutaline i. Selective b2 agonist ii. Causes bronchodilation iii. Side effect- constipation 2. Nonadrenergic/noncholinergic Fibersa. Fibers can release several NTMb. One is