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Neural Conduction and Synaptic Transmission

Neural Conduction and Synaptic Transmission

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Neural Conduction and Synaptic Transmission

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  1. Neural Conduction and Synaptic Transmission

  2. Neural Conduction:Action Potential I. Stages of NeuronalDepolarization: • Neuron is at rest (-70mV) - this is a transient state due to concentration gradient, electrostatic pressure, & Na/K+ pump • Excitatory Neurotransmitter (e.g. Glutamate) binds to receptors - EPSP begins, moving charge to a less negative state (toward positive) due to Na+

  3. 3. EPSPs continue until the charge summates both spatially and temporally. When the charge reaches a –65mV at the axon hillock, the action potential begins Charge arriving at different times becomes additive or summates Charge across membrane becomes additive or summates Charge at the Axon Hillock triggers the AP

  4. Na+ channels at the start of the axon open. These are voltage gated channels that open due to the electrical charge along the membrane. • K+ channels open as the charge becomes more positive. • Na+ channels close when this ion is in. equilibrium across the membrane (+55mV). • K+ leaves in massive quantities reducing the charge of the cell. • K+ diffuses away and gradually the charge returns to the Resting Membrane Potential.

  5. Not in Book

  6. II. States of the Action Potential Relative Refractory Period Absolute Refractory Period All-or-None Principle Rising Phase Repolarization Hyperpolarization • AP in Nonmyelinated Neurons - ions are exchanged at channels along the length of the axon - slow process yet the axon length is small, so the effect is rapid.

  7. Not in Book

  8. AP in Myelinated Axons - ions exchanged at the Nodes of Ranvier - conduction is saltatory (jumps) - charge decreases slightly under the myelin - speed is rapid despite size of axon

  9. Not in Book

  10. Not in Book

  11. Synaptic Transmission Three stages leading to release of NT • Ca++ channels open in response to the the depolarization of the terminal membrane • Vesicles containing NTs mobilize and fuse with the membrane • NTs are released into the Synaptic Cleft (exocytosis) via fusion of vesicle with the terminal membrane

  12. Inactivation of the Neurotransmitter 1. Reuptake 2. Enzymes that degrade the NT (enzymatic degradation) NTs are sequestered back into vesicles, which have been formed through pinocytosis (i.e. pinching off of the cell membrane to form vesicles). ___________________________________ Note: although EPSPs leading to an Action Potential seem to get all the attention, our neurophysiology is always in a balance between EPSPs and IPSPs.

  13. What is the significance of the IPSP? IPSPs lead to a Hyperpolarized State (where have you heard this word before?) - inside of the neuron becomes more negative, reaching as low as –90mV - gradual influx of Cl- occurs due to the effects of a NT with an inhibitory effect. Behavior occurs when neurons are released from inhibition – that is, when the EPSPs override the IPSPs.

  14. Neurotransmitters 80 plus chemical substances that provide communication between cells. Some of these are actually NTs and others are neuromodulators (i.e. they augment the activity of the NT)

  15. Neurotransmitters have 7 actions • Synthesized • Stored • Enzymatically destroyed if not stored • Exocytosis • Termination of release via binding with autorecpetors • Binding of NT to receptors • NT is inactivated

  16. Study Session • A seizure disorder is the result of too much neuronal excitation in combination with too little neuronal inhibition. Explain what this means from neurophysiological and behavioral perspectives. • Under what conditions or disorders would you use an agonist or an antagonist drug?