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Synaptic transmission. Chapter 6 pages 156 - 169. Information transmission. Action potentials (APs) initiated by depolarizing stimulus Two general sources of depolarizing stimulus in neurons Receptor potentials from sensory transduction Information transmission between neurons

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Synaptic transmission

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synaptic transmission

Synaptic transmission

Chapter 6

pages 156 - 169

information transmission
Information transmission
  • Action potentials (APs) initiated by depolarizing stimulus
  • Two general sources of depolarizing stimulus in neurons
    • Receptor potentials from sensory transduction
    • Information transmission between neurons
  • APs are intracellular events that encode information
    • Limited to individual cells by the cell membrane
information transmission1
Information transmission
  • Transmission of information usually requires multiple cells
    • Convergence - multiple cells with a single target
    • Divergence - single cell with multiple targets
  • Need mechanism to “inform” target cells of APs
  • Two types of mechanisms for transmitting information encoded by APs
    • Direct electrical coupling
    • Release of chemical messengers
electrical coupling
Electrical coupling
  • Cells are connected by ion channels that span two lipid bilayers
  • AP in one cell creates a voltage difference
  • Ions flow down voltage gradient and depolarize second cell
  • Advantages
    • Very rapid transmission of information
  • Disadvantages
    • Does not reflect all-or-none nature of APs (any depolarization is transmitted)
    • Effects on target cell limited to depolarization or hyperpolarization
electrical coupling1
Electrical coupling
  • Used to coordinate contraction in cardiac and smooth muscle
    • Coordinated contraction of heart to optimize blood flow
    • Coordinated contraction of smooth muscle lining digestive system and other organs
  • Recently found to have important role in some areas of the brain
    • Synchronizes oscillatory activity in small networks of interneurons
    • May be important for timing or gating of information transmission
chemical coupling
Chemical coupling
  • AP can lead to release of chemical messenger
    • Hormones
    • Neurotransmitters
  • Advantages
    • Ligand release coupled to APs
    • Can evoke a variety of responses in target cell
    • One way communication
  • Disadvantages
    • Slower than electrical coupling
  • Juxtaposition of chemical release and target receptors reduces transmission delay
  • By far most common method of information transmission in body
    • Neuron → neuron
    • Neuron → muscle
    • Neuron → gland or organ
which of the following is an advantage of electrical coupling
Which of the following is an advantage of electrical coupling?
  • Signal initiated only in response to APs
  • Faster than chemical coupling
  • Produces a variety of postsynaptic effects
  • Maintains one way communication
  • All of the above
synapse structure
Synapse structure
  • Presynaptic – transmitting information
  • Postsynaptic – receiving information
  • Synaptic terminal protrudes from axon of presynaptic cell
    • Usually small size (100 – 500 nm across)
  • Contains vesicles of neurotransmitter ligand
  • Postsynaptic density on postsynaptic cell dendrite contains neurotransmitter receptors
    • Ionotropic (change ions) receptors are ligand-gated ion channels
    • Metabotropic (change metabolism) receptors initiate intracellular signaling cascades
  • Presynaptic terminal and postsynaptic density separated by very small (10 – 20 nm) synaptic cleft
    • This minimizes transmission time from presynaptic → postsynaptic
presynaptic release of neurotransmitter
Presynaptic release of neurotransmitter
  • Neurotransmitter release initiated by AP propagating into presynaptic terminal
  • Large transient depolarization of presynaptic terminal opens voltage-gated Ca2+ channels
  • Increase in intracellular free Ca2+ initiates a cascade of events that result in exocytosis of vesicles containing neurotransmitter
    • Vesicle membranes contain specialized Ca2+ binding proteins
    • SNARE proteins facilitate docking of vesicles on inner surface of plasma membrane
    • Ca2+ binding protein synaptotagmin initiates fusion of vesicle and plasma membrane for exocytosis
presynaptic release of neurotransmitter1
Presynaptic release of neurotransmitter
  • Higher presynaptic [Ca2+]i increases rate of exocytosis until saturation
    • [Ca2+]i increases with number and rate of APs traveling toward presynaptic terminal
  • Neurotransmitter ligand diffuses across synaptic cleft and binds to postsynaptic receptors
  • Ligand binding is terminated by enzymatic breakdown within cleft or active reuptake of neurotransmitter molecules by neighboring cells
  • Many psychiatric and psychotropic drugs function to prevent neurotransmitter uptake or breakdown
    • Prolongs ligand - receptor binding by maintaining ligand concentration in synaptic cleft
how does a depolarization from a presynaptic ap lead to the release of neurotransmitter
How does a depolarization from a presynaptic AP lead to the release of neurotransmitter?
  • Ca2+ influx through voltage-gated Ca2+ channels
  • K+ influx through voltage-gated K+ channels
  • Na+ influx through voltage-gated Na+ channels
  • Vesicle docking proteins are voltage-gated
postsynaptic potentials
Postsynaptic potentials
  • Neurotransmitter binding can open ligand-gated ion channel on postsynaptic density
  • Resulting ionic flux can be depolarizing or hyperpolarizing depending on ionic species that permeates open channels
  • EPSP – excitatory postsynaptic potential
    • Depolarization due to opening of Na+ or Ca2+ permeant ligand-gated ion channels
    • Termed “excitatory” since Vm of postsynaptic cell is pushed closer to AP threshold
postsynaptic potentials1
Postsynaptic potentials
  • IPSP – inhibitory postsynaptic potential
    • Hyperpolarization due to opening of K+ or Cl- permeant ligand-gated ion channels
    • Termed “inhibitory” since Vm of postsynaptic cell is pushed farther from AP threshold
  • PSPs – general term for both EPSPs and IPSPs
  • Characteristic time course due to diffusion, binding and unbinding of neurotransmitter ligand
  • Desensitization - closing of ligand-gated ion channel while ligand is still bound to receptor
    • Similar to inactivation of voltage-gated Na+ channel during depolarization
    • Requires removal of ligand before channel can open again
a neurotransmitter activates a ligand gated k channel this should produce
A neurotransmitter activates a ligand-gated K+ channel. This should produce:
  • An EPSP
  • An IPSP
  • Both
  • Neither
synaptic integration
Synaptic integration
  • In most neurons, a single EPSP will not drive postsynaptic Vm past AP threshold
  • Postsynaptic APs are typically evoked by simultaneous synaptic inputs from convergent sources
  • Temporal summation – rapid EPSPs from same presynaptic terminal
    • Example: repetitive activation of terminal labeled “A”
  • Spatial summation – simultaneous EPSPs from different presynaptic terminals
    • Example: simultaneous activation of terminals labeled “A” and “B”
  • IPSPs will serve to negate EPSPs or drive Vm below AP threshold
synaptic strength
Synaptic strength
  • Unlike APs, PSPs are graded and can vary in amplitude and time course
  • Presynaptic factors affecting PSP amplitude and time course
    • Rate of neurotransmitter synthesis
    • Amount of neurotransmitter per vesicle
    • Amount of Ca2+ entry per presynaptic AP
    • Number of vesicles
    • Up or down regulation of neurotransmitter release via intracellular signaling molecules
  • Synaptic cleft factors affecting PSP amplitude and time course
    • Cleft geometry and neurotransmitter diffusion
    • Uptake or breakdown of neurotransmitters
  • Postsynaptic factors affecting PSP amplitude and time course
    • Spatial or temporal summation of PSPs
    • Number of neurotransmitter receptors
    • Up or down regulation of neurotransmitter receptors via intracellular messengers
synaptic strength1
Synaptic strength
  • Many drugs called neuromodulators act to modulate neurotransmitter release
  • Other neuromodulators prevent activation of neurotransmitter receptor by ligand
  • Many presynaptic terminals have axo-axonic synapses to modulate neurotransmitter release
  • Many presynaptic terminals have autoreceptors that bind to transmitters released from same terminal
    • Serves as negative feedback to prevent excess release of neurotransmitter
  • Many diseases affect synaptic transmission
    • Tetanus – bacterial toxin that destroys proteins involved in inhibitory neurotransmitter release
  • Most toxins from venomous species are potent antagonists of voltage- and ligand-gated ion channels
    • Paralyze or kill prey by preventing APs or synaptic transmission
a drug increases an epsp produced by a pre synaptic input this drug could be acting by
A drug increases an EPSP produced by a pre-synaptic input. This drug could be acting by:
  • Increased reuptake of the neurotransmitter
  • Increased Ca2+ influx through voltage-gated Ca2+ channel
  • Presynaptic autoreceptor that decreases vesicle docking
  • Postsynaptic GPCR that decreases response of ligand-gated ion channel
  • -ergic refers to the type of neurotransmitter a neuron releases
  • Acetylcholine (ACh) and cholinergic neurotransmission
    • Primary excitatory neurotransmitter in PNS
    • Used by somatic and preganglionic autonomic neurons
    • Degraded by enzyme acetylcholinesterase
    • Nerve gas Sarin inhibits acetylcholinesterase
  • Catecholamines – derivatives of tyrosine
    • Includes dopamine and epinephrine
    • Broken down by monoamine oxidase (MAO)
    • MAO inhibitors used to treat psychiatric disorders
    • Dopamine linked to Parkinson’s disease
    • Epinephrine (adrenaline) and norepinephrine (noradrenaline) regulate heart rate and blood pressure
  • Other biogenic amines
    • Called biogenic amines due to synthesis from amino acid precursors
    • Serotonin or 5-hydroxytryptophan (5-HT) associated with alertness, appetite, emotional state
    • Prozac blocks 5-HT uptake, LSD blocks 5-HT receptors
    • Histamine associated with immune and injury responses
    • Antihistamines to prevent cold symptoms and inflammation
  • Amino acids
    • Major source of excitatory and inhibitory neurotransmitters in brain
    • Glutamate receptors (GluRs) are majority of excitatory ligand-gated ion channels in brain
    • Glycine and GABA (g-amino butyric acid) are majority of inhibitory ligand-gated ion channels in brain
    • Many drugs including barbiturates and benzodiazepines (Valium) act at GABA receptors
  • Neuropeptides – small polypeptides
    • Mainly involved in pain sensation and analgesia
    • Opiate receptors target of morphine and codeine
  • Other neurotransmitters
    • ATP can act as neuromodulator
    • Diffusable gases nitric oxide and carbon monoxide act at intracellular receptors
    • Not classical neurotransmitter because they don’t require vesicles to be released
    • Release is of nitric oxide and carbon monoxide is driven by presynaptic production