Physiology: Chp 11 Part C PDF

Physiology: Chp 11 Part C Autonomic & Somatic Motor Control Juan J. Bustamante, Ph.D. Assistant Professor Pharmaceutical Science Phone (361) 221-0643 Email: [email protected] Office: Room 223 © 2016 Pearson...

Physiology: Chp 11 Part C Autonomic & Somatic Motor Control Juan J. Bustamante, Ph.D. Assistant Professor Pharmaceutical Science Phone (361) 221-0643 Email: [email protected] Office: Room 223 © 2016 Pearson Education, Inc. © 2016 Pearson Education, Inc.  Anaphylaxis Shock Hives dilate bronchoconstrict https://nursekey.com/wp-content/uploads/2016/07/image02017.jpeg © 2016 Pearson Education, Inc. https://businessmirror.com.ph/2018/08/09/anaphylactic-shock-a-life-threatening-reaction/ © 2016 Pearson Education, Inc. https://www.optometricmanagement.com/archive/2009/February/Supplements/Alcon/images/OM_Alcon_Suppl_February_A02_Fig02.jpg © 2016 Pearson Education, Inc. © 2016 Pearson Education, Inc. © 2016 Pearson Education, Inc.  Epipen: When given intramuscularly or subcutaneously it has a rapid onset and short duration of action. Epinephrine acts on both alpha and beta adrenergic receptors. Through its action on alpha adrenergic receptors, epinephrine lessens the vasodilation and increased vascular permeability that occurs during anaphylaxis, which can lead to loss of intravascular fluid volume and hypotension. © 2016 Pearson Education, Inc. https://www.accessdata.fda.gov/drugsatfda_docs/label/2012/019430s053lbl.pdfv  Autonomic Pathways Control Smooth and Cardiac Muscle and Glands The neuroeffector junction is the synapse between a postganglionic autonomic neuron and its target cells (effector). Note: The structure of an autonomic synapse differs from the model synapses © 2016 Pearson Education, Inc.  Autonomic Pathways Control Smooth and Cardiac Muscle and Glands Autonomic neuron targets: Smooth muscle Cardiac muscle Many exocrine glands Few endocrine glands Lymphoid tissues Some adipose tissue © 2016 Pearson Education, Inc. Figure 11.7a Autonomic synapses Varicosities are series of swollen areas at their distal ends containing neurotransmitters Neurotransmitters diffuse in synapse and bind to receptor Autonomic varicosities release neurotransmitter over the surface of target cells. Vesicle containing neurotransmitter Varicosity Axon of postganglionic Mitochondrion autonomic neuron Smooth muscle cells Varicosities Note: The primary autonomic neurotransmitters, acetylcholine and norepinephrine, can be synthesized in the axon varicosities © 2016 Pearson Education, Inc. Figure 11.7b Autonomic synapses Slide 1 Adrenergic receptors in postganglionic sympathetic target cells Norepinephrine (NE) release and removal at a sympathetic neuroeffector junction Action potential arrives at the varicosity. Depolarization opens voltage-gated Ca2+ channels. Axon varicosity Ca2+ entry triggers MAO exocytosis of synaptic vesicles. Tyrosine Axon NE binds to adrenergic receptor on target. NE Action potential Receptor activation ceases when Exocytosis NE diffuses away from the synapse. Voltage-gated Ca2+ channel Active transport Ca2+ NE is removed from the synapse. NE Diffuses away Blood G NE can be taken back into vessel synaptic vesicles for re-release. Response Adrenergic Target cell NE is metabolized by receptor monoamine oxidase (MAO). © 2016 Pearson Education, Inc. Figure 11.7b Autonomic synapses Slide 2 Norepinephrine (NE) release and removal at a sympathetic neuroeffector junction Action potential arrives at the varicosity. Tyrosine Axon NE Action potential Blood vessel Target cell © 2016 Pearson Education, Inc. © 2016 Pearson Education, Inc. Figure 11.7b Autonomic synapses Slide 3 Norepinephrine (NE) release and removal at a sympathetic neuroeffector junction Action potential arrives at the varicosity. Depolarization opens voltage-gated Ca2+ channels. Tyrosine Axon NE Action potential Voltage-gated Ca2+ channel Ca2+ Blood vessel Target cell © 2016 Pearson Education, Inc. Figure 11.7b Autonomic synapses Slide 4 Norepinephrine (NE) release and removal at a sympathetic neuroeffector junction Action potential arrives at the varicosity. Depolarization opens voltage-gated Ca2+ channels. Ca2+ entry triggers exocytosis of synaptic vesicles. Tyrosine Axon NE Action potential Exocytosis Voltage-gated Ca2+ channel Ca2+ NE Blood vessel Target cell More neurotransmitters © 2016 Pearson Education, Inc.  Coding the strength of a stimulus Frequency of action potentials determines how many neurotransmitter is released © 2016 Pearson Education, Inc. Figure 11.7b Autonomic synapses Slide 5 What is different about the receptor number? Norepinephrine (NE) release and removal at a sympathetic neuroeffector junction Action potential arrives at the varicosity. Depolarization opens voltage-gated Ca2+ channels. Ca2+ entry triggers exocytosis of synaptic vesicles. Tyrosine Axon NE binds to adrenergic receptor on target. NE Action potential The more neurotransmitter means Exocytosis Voltage-gated Ca2+ channel a longer or stronger response Ca2+ NE The autonomic control of target by modulating the concentration of Blood vessel G neurotransmitter in the synapse Response Adrenergic Target cell receptor Neurotransmitters (NT) diffuse in synapse and bind to receptor Note: All adrenergic receptors are G-protein coupled receptors rather than ion channel – the response is slower to start and stop © 2016 Pearson Education, Inc. Figure 11.7b Autonomic synapses Slide 6 Norepinephrine (NE) release and removal at a sympathetic neuroeffector junction Action potential arrives at the varicosity. Depolarization opens voltage-gated Ca2+ channels. Ca2+ entry triggers exocytosis of synaptic vesicles. Tyrosine Axon NE binds to adrenergic receptor on target. NE Action potential Receptor activation ceases when Exocytosis NE diffuses away from the synapse. Voltage-gated Ca2+ channel NT removal Ca2+ NE Diffuses away Blood G vessel Response Adrenergic Target cell receptor © 2016 Pearson Education, Inc. Figure 11.7b Autonomic synapses Slide 7 Norepinephrine (NE) release and removal at a sympathetic neuroeffector junction Action potential arrives at the varicosity. Depolarization opens voltage-gated Ca2+ channels. Ca2+ entry triggers exocytosis of synaptic vesicles. Tyrosine Axon NE binds to adrenergic receptor on target. NE Action potential Receptor activation ceases when Exocytosis NE diffuses away from the synapse. Voltage-gated Ca2+ channel Active transport NT removal Ca2+ NE is removed from the synapse. NE Diffuses away Blood G vessel Response Adrenergic Target cell receptor © 2016 Pearson Education, Inc. Figure 11.7b Autonomic synapses Slide 8 Norepinephrine (NE) release and removal at a sympathetic neuroeffector junction Action potential arrives at the varicosity. Depolarization opens voltage-gated Ca2+ channels. Ca2+ entry triggers exocytosis of synaptic vesicles. Tyrosine Axon NE binds to adrenergic receptor on target. NE Action potential Receptor activation ceases when Exocytosis NE diffuses away from the synapse. Voltage-gated Ca2+ channel Active transport NT removal Ca2+ NE is removed from the synapse. NE Diffuses away Blood G NE can be taken back into vessel synaptic vesicles for re-release. Response Adrenergic Target cell receptor © 2016 Pearson Education, Inc. Figure 11.7b Autonomic synapses Slide 9 Norepinephrine (NE) release and removal at a sympathetic neuroeffector junction Action potential arrives at the varicosity. Depolarization opens voltage-gated Ca2+ channels. Axon varicosity Ca2+ entry triggers MAO exocytosis of synaptic vesicles. Tyrosine Axon NE binds to adrenergic receptor on target. NE Action potential Receptor activation ceases when Exocytosis NE diffuses away from the synapse. Voltage-gated Ca2+ channel Active transport Ca2+ NT removal NE is removed from the synapse. NE Diffuses away Blood G NE can be taken back into vessel synaptic vesicles for re-release. Response Adrenergic Target cell NE is metabolized by receptor monoamine oxidase (MAO). © 2016 Pearson Education, Inc.  Autonomic Receptors Have Multiple Subtypes Muscarinic receptors in postganglionic parasympathetic target cells – G protein–coupled – Second messenger pathways – At least five subtypes © 2016 Pearson Education, Inc. Figure 8.20 Synthesis and recycling of acetylcholine Slide 1 Ach is synthesized from choline and acetyl CoA in the varicosities Note: There are 2 types of cholinergic receptors 1. Muscarinic Mitochondrion 2. Nicotinic Acetyl CoA CoA Axon Acetylcholine (ACh) is made terminal Enzyme from choline and acetyl CoA. A Acetylcholine Ch A Synaptic Ch vesicle In the synaptic cleft, ACh is rapidly Ch broken down by the enzyme acetylcholinesterase. A Ch Choline is transported back into the axon terminal by cotransport Na+ Ch Choline Cholinergic with Na+. A receptor A Ch Recycled choline is used to make Acetate Acetylcholinesterase (AChE) Postsynaptic more ACh. cell © 2016 Pearson Education, Inc. © 2016 Pearson Education, Inc. © 2016 Pearson Education, Inc.  The somatic motor division Mostly voluntary © 2016 Pearson Education, Inc.  Figure 11.9-2 Efferent Divisions of the Nervous System Somatic pathways are always excitatory, unlike autonomic pathways, which may be either excitatory or inhibitory. Single neuron CNS origin: Cell body located either in the ventral horn of the spinal or in the brain. Myelinated Terminus Branches SOMATIC MOTOR PATHWAY ACh Nicotinic receptor CNS Target: skeletal muscle always excitatory - no antagonistic innervation to relax skeletal muscles-instead relaxation occurs when the somatic motor neurons are inhibited in the CNS © 2016 Pearson Education, Inc. Figure 11.10a Somatic Motor Neurons and the Neuromuscular Junction © 2016 Pearson Education, Inc. Figure 11.10c Somatic Motor Neurons and the Neuromuscular Junction Neuromuscular junction Synaptic vesicle (ACh) Presynaptic membrane Synaptic cleft Nicotinic ACh receptors Postsynaptic membrane of skeletal muscle fiber Is modified into a motor end plate. © 2016 Pearson Education, Inc. Figure 11.10d Somatic Motor Neurons and the Neuromuscular Junction An action potential arrives at the axon terminal, causing voltage-gated Ca2+ channels to open. Calcium entry causes synaptic vesicles to fuse with the presynaptic membrane and release ACh into the synaptic cleft. Presynaptic membrane Synaptic vesicle (ACh) Synaptic cleft Ca2+ Ca2+ ACh Acetyl + choline Postsynaptic Voltage-gated membrane is Ca2+ channel modified into a motor end plate. AChE Nicotinic Skeletal muscle receptor fiber Acetylcholine (ACh) is metabolized by acetylcholinesterase (AChE). © 2016 Pearson Education, Inc. Figure 12.11 Timing of E-C coupling Action potentials in the axon terminal (top graph) Motor Neuron Action Potential and in the muscle fiber (middle graph) are followed by a muscle twitch (bottom graph). +30 Muscle fiber Neuron membrane Action potential potential from CNS in mV −70 Time Motor Recording end plate electrodes Axon Muscle Fiber Action Potential terminal +20 Muscle fiber Muscle action membrane potential potential in mV −80 2 msec Time NAVIGATOR Neuro- muscular Development of Tension during One Muscle Twitch junction (NMJ) Latent Contraction Relaxation E-C period phase phase coupling Tension FIGURE QUESTIONS Movement of what ion(s) in what direction(s) creates Muscle (a) the neuronal action potential? 10–100 msec twitch (b) the muscle action potential? Time © 2016 Pearson Education, Inc. Figure 11.10e Somatic Motor Neurons and the Neuromuscular Junction The nicotinic cholinergic receptor binds two ACh molecules, opening a nonspecific monovalent cation channel. The open channel allows Na+ and K+ to pass. Net Na+ influx depolarizes the muscle fiber. action potential that causes muscle contraction of the skeletal muscle K+ Na+ ACh K+ Na+ Closed channel Open channel © 2016 Pearson Education, Inc. Interesting facts: The nAChR channels of the skeletal muscle are similar by not identical to the nicotinic Ach receptors found on the neurons. This difference is illustrated by the fact that the snake toxin α- bungarotoxin binds to nicotinic skeletal muscle receptors but not to those of the autonomic ganglia. © 2016 Pearson Education, Inc.  Myasthenia gravis Myasthenia gravis characterized by loss of ACh receptors Without communication between the motor neuron and the muscle the skeletal muscles for movement and posture weaken as do skeletal muscle for breathing. Neostigmine is used to treat myasthenia gravis. What is he MOA of an acetylcholinesterase inhibitor neostigmine? © 2016 Pearson Education, Inc. Figure 8.20 Synthesis and recycling of acetylcholine Slide 1 Ach is synthesized from choline and acetyl CoA in the varicosities Note: There are 2 types of cholinergic receptors 1. Muscarinic Mitochondrion 2. Nicotinic Acetyl CoA CoA Axon Acetylcholine (ACh) is made terminal Enzyme from choline and acetyl CoA. A Acetylcholine Ch A Synaptic Ch vesicle In the synaptic cleft, ACh is rapidly Ch broken down by the enzyme acetylcholinesterase. A Ch Choline is transported back into the axon terminal by cotransport Na+ Ch Choline Cholinergic with Na+. A receptor A Ch Recycled choline is used to make Acetate Acetylcholinesterase (AChE) Postsynaptic more ACh. cell © 2016 Pearson Education, Inc.  bind © 2016 Pearson Education, Inc.