Neural Conduction and Synaptic Transmission

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Neural Conduction and Synaptic Transmission
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Neural ConductionAction Potential

• I. Stages of Neuronal Depolarization
• 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

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

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Not in Book
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• 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.

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Not in Book
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• 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

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Not in Book
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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

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• 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.

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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.

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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)

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• 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

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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?