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The Sodium-Potassium Pump

The Sodium-Potassium Pump. Consists of molecules in the neuronal membrane Exchanges NA+ ions for K+ ions across the membrane Requires energy for active transport of ions across the membrane. Membrane Permeability Determines Membrane Voltage. Membrane Voltage Determines Membrane Permeability.

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The Sodium-Potassium Pump

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  1. The Sodium-Potassium Pump • Consists of molecules in the neuronal membrane • Exchanges NA+ ions for K+ ions across the membrane • Requires energy for active transport of ions across the membrane

  2. Membrane Permeability Determines Membrane Voltage

  3. Membrane Voltage Determines Membrane Permeability

  4. Stimulator ++ + + + +++ Depolarize the Neuron

  5. Question: Why does a voltage change across the membrane change membrane permeability? Answer: There are voltage-gated ion channels embedded in the membrane. a. Proteins in the membrane b. 100,000 ions/sec can pass through c. Squid axon: 100-600 NA+ channels in 1.0 square micron of membrane d. Selectivity filter and gate

  6. Sodium Channel Blockers • Tetrodotoxin - Pufferfish ovaries • Scorpion Toxin • Batrachotoxin - South African frog

  7. Potassium Channel Blocker Tetraethyl Ammonium (TEA) Calcium Channel Blocker Cobalt

  8. Question: How do we know that a voltage change across the membrane opens ion channels? Answer: The Patch-Clamp Technique

  9. Llinas, 1992 • Visualized calcium entry into terminal bouton • Giant Squid axon • Inject bouton of axon with jelly fish protein • protein emits light when it binds with Ca++ • Experiment • a. Stimulate the axon to cause action potential • b. Detected rapidly flicking spots of light in • bouton at transmitter release sites

  10. Transmitter-gated Voltage-gated Channels Channels Transmitter binding to Na+ Channel opens receptor Opens NA+ channel Additional Na+ inflow Na+ inflow Depolarization reaches Threshold Depolarization Action Potential

  11. Two Different Systems of Neurochemical Transmission Small molecule neurotransmitters • Synthesized in terminal bouton • Short-lived effect on receptor Large molecule neurotransmitters • Peptides (chains of amino acids) • Synthesized in cell body • Transported in vesicles to bouton

  12. G-protein linked receptor G- protein has a subunit (alpha subunit) induces second messenger synthesis Bind to ion channelinfluence enter nucleus neuron metabolic activity gene expression Open or close channel Protein synthesis

  13. Transmitter - receptor Binding Two General Receptor Types 1. Ion-channel linked receptor - Ionotropic 2. G-protein linked receptor - Metabotropic

  14. Neurotransmitters Acetylcholine (ACh) Monoamines Epinephrine - adrenaline Norepinephrine - noradrenaline Dopamine Serotonin Amino acids Peptides Gases

  15. Acetylcholine(ACh) - Soma locations 1. Spinal motor neurons Skeletal muscles 2. Septum Hippocampus 3. Nucleus Basalis Cortex 4. Vagus nerve Smooth muscles (internal motor neurons organs-e.g., heart) 5. Interneurons

  16. Biosynthesis of Acetylcholine Acetyl coenzyme A (acetyl CoA) Coenzyme A (CoA) Acetate ion Acetylcholine Choline Choline Acetyltransferase (CAT) enzyme

  17. Two Types of ACh Receptors 1. Muscarinic Receptor smooth muscles (e.g., heart) brain neurons G protein-linked or metabotropic receptor muscarine = agonist atropine = antagonist

  18. 2.Nicotinic receptor skeletal muscles brain neurons ionotropic receptor nicotine = agonist curare = antagonist

  19. Antagonists of ACh Transmission 1.Clostridium Botulinum - bacteria in poorly canned food - produces botulin neurotoxin - inhibits ACh release 2. Black Widow Spider Venom - venom = protein - binds with bouton membrane - forms a pore - CA++ enters the pore - depletes neurotransmitter

  20. 3. Cobra Venom - venom = protein - binds to nicotinic receptor - prevents ACh binding to receptor 4. Organophosphates - irreversible acetylcholinesterase (AChE) inhibitors - nerve gas - prevent breakdown of ACh - promotes receptor desensitization ion channels close despite high ACh levels

  21. Myasthenia Gravis • Autoimmune disease • antibodies against nicotinic ACh receptor • receptor number reduced • clinical symptoms - muscle weakness (eyelids, limbs, respiration) • treatment - physostigmine = AChE inhibitor

  22. Dopamine Norepinephrine Epinephrine Monoamines Tyrosine L-Dopa Dopamine Norepinephrine Epinephrine ----------- ----------- Released from varicosities

  23. Dopamine Soma locations Substantia Nigra Ventral Tegmental Area (VTA) Receptors 5 subtypes (D1 - D5)

  24. Norepinephrine Soma locations Locus coeruleus Receptors Beta (B1. B2, B3) Alpha (A1, A2) Epinephrine Soma locations Medulla

  25. Serotonin (5-HT) Tryptophan 5-hydroxytrytophan (5- HTP) 5-hydroxytryptamine (5- HT) (Serotonin)

  26. Serotonin Soma locations Raphe nuclei Receptors 15 subtypes

  27. Amino Acids 1. Glutamic acid (glutamate) - main excitatory neurotransmitter Soma locations - Everywhere Receptors 10 subtypes

  28. Amino Acids - continued 2.Gamma-aminobutyric acid(GABA) - main inhibitory neurotransmitter Soma locations - everywhere Receptors two types GABA A - Chloride channel Benzodiazepines -Valium Librium GABA B

  29. Neuropeptides Enkephalins Vasopressin Oxytocin Substance P Cholecystokinen Neurotensin Somatostatin Neuropeptide Y Vasoactive intestinal peptide Angiotensin Corticotropin-releasing factor Beta-endorphin

  30. Soluble Gases Nitric oxide Carbon monoxide - Do not bind to receptors - diffuse into neurons - activate second messengers

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