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Chapter 7 Synaptic Transmission

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Title: Chapter 7 Synaptic Transmission


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Chapter 7Synaptic Transmission
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Synapse
  • A functional connection between a neuron
    (presynaptic) another cell (postsynaptic)
  • Chemical electrical synapses
  • Synaptic transmission in chemicals is via
    neurotransmitters (NT)
  • Electricals are rare in NS

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  • Signaling between cells was originally thought to
    have occurred only by electrical signaling.
  • In 1921, Otto Loewi published an experiment
    suggesting signaling by chemical transmission.

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Synaptic Transmission
  • APs travel down axon to depolarize bouton
  • Open VG Ca2 channels in bouton
  • Ca2 driven in by electrochemical gradient
  • Triggers exocytosis of vesicles release of NTs

Neurotransmitter Release
  • Rapid because vesicles are already docked at
    release sites on bouton before APs arrive
  • Docked vesicles are part of fusion complex
  • Ca2 triggers exocytosis of vesicles

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Synaptic Transmission continued
  • NT (ligand) diffuses across cleft
  • Binds to receptor proteins on postsynaptic
    membrane
  • Chemically-regulated ion channels open
  • Depolarizing channels cause EPSPs (excitatory
    postsynaptic potentials)
  • Hyperpolarizing channels cause IPSPs (inhibitory
    postsynaptic potentials)
  • These affect VG channels in postsynaptic cell

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Acetylcholine (ACh)
  • Most widely used NT
  • NT at all neuromuscular junctions
  • Used in brain
  • Used in ANS
  • Where can be excitatory or inhibitory
  • Depending on receptor subtype
  • Nicotinic or muscarinic

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Ligand operated channels
Ligand
Receptor
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Receptors Exhibit Two Types of Specificity
(1) Ligand Specificity-which ligand(s) are bound.
Similar to the specificity of an enzyme for its
substrate. (2) Effector Specificity-the response
to ligand binding
  • Same ligand binding to a receptor can have
    different effects in different cell types ? same
    ligand specificty, different effector specificity
  • Different ligands binding to different receptors
    on the same cell or different cells can have the
    same effect? different ligand specificity, same
    effector specificity

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G Protein-Operated Channels
  • Receptor is not part of the ion channel
  • Is a 1 subunit membrane polypeptide
  • Activates channel indirectly through G-proteins

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Muscarinic ACh Channel
  • Binding of 1 ACh activates G-protein cascade
  • Opens some K channels, causing hyperpolarization
  • Closes others, causing depolarization

Fig 7.25
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Acetylcholinesterase (AChE)
  • Inactivates ACh, terminating its action located
    in cleft

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Neuromuscular Junction (NMJ)
  • Cholinergic neurons use acetylcholine as NT
  • Large synapses on skeletal muscle are termed end
    plates or neuromuscular junctions
  • Produce large EPSPs called end-plate potentials
  • Open VG channels beneath end plate
  • Cause muscle contraction
  • Curare blocks ACh action at NMJ

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Monoamine NTs
  • Receptors activate G-protein cascade to affect
    ion channels

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Monoamine NTs
  • Include serotonin, norepinephrine, dopamine,
    epinephrine
  • Serotonin is derived from tryptophan
  • Norepi dopamine are derived from tyrosine
  • Called catecholamines

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Serotonin
  • Involved in regulation of mood, behavior,
    appetite, cerebral circulation
  • LSD is structurally similar
  • SSRIs (serotonin-specific reuptake inhibitors)
    include antidepressants
  • Prozac, Zolof, Paxil, Luvox
  • Block reuptake of serotonin, prolonging its action

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Dopamine
  • Involved in motor control emotional reward
  • Degeneration of dopamine motor system neurons
    causes Parkinson's disease
  • Reward system is involved in addiction
  • Schizophrenia treated by anti-dopamine drugs

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Norepinephrine (NE)
  • Used in PNS CNS
  • In PNS is a sympathetic NT
  • In CNS affects general level of arousal
  • Amphetamines stimulate NE pathways

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Amino Acids NTs
  • Glutamic acid aspartic acid are major CNS
    excitatory NTs
  • Glycine is an inhibitory NT
  • Opens Cl- channels which hyperpolarize
  • Strychnine blocks glycine receptors
  • GABA (gamma-aminobutyric acid) is most common NT
    in brain
  • Inhibitory, opens Cl- channels

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EPSPs
  • Graded in magnitude
  • Have no threshold
  • Cause depolarization
  • Summate
  • Have no refractory period

Fig 7.27
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Spatial Summation
  • Cable properties cause EPSPs to fade quickly over
    time distance
  • Spatial summation takes place when EPSPs from
    different synapses occur in postsynaptic cell at
    same time

Fig 7.31
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Temporal Summation
  • Temporal summation occurs because EPSPs that
    occur closely in time can sum before they fade

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Synaptic Plasticity
  • Repeated use of a synapse can increase or
    decrease its ease of transmission
  • synaptic facilitation or synaptic depression
  • High frequency stimulation often causes enhanced
    excitability
  • Called long-term potentiation
  • Believed to underlie learning

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Synaptic Inhibition
  • Postsynaptic inhibition
  • GABA glycine produce IPSPs
  • IPSPs dampen EPSPs
  • Making it harder to reach threshold
  • Presynaptic inhibition
  • Occurs when 1 neuron synapses onto axon or bouton
    of another neuron, inhibiting release of its NT

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