Synapse and Neurotransmitters Flashcards

1
Q

What is a synapse?

A

Contact between a neuron and another neuron or its effector cell

 - Pre-synaptic neuron (axon)
 - Post-synaptic neuron (dendrite or cell body) OR a cell (ie. muscle)
 - Cells separated by the synaptic cleft
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2
Q

CHEMICAL Synapses (7)

A
  • Predominant type of synapse
  • Unidirectional
  • Uses neurotransmitters
  • Fast (ionotropic) or slow (metabotropic)
  • Signal can be amplified
  • Can be excitory or inhibitory
    • Short term effects
  • Metabolism of neuron can be changed altering the properties of the synapse
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3
Q

Neuroactive Peptides (4)

A
  • Made in cell body, transported to axon terminal
  • Found in brain and ENS
  • Chains of AAs
  • Metabotropic receptors
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4
Q

Small-molecule Neurotransmitters (4)

A
  • Made in axon terminals
  • Amino Acids
    • glutamate, glycine
  • Amines
    • Acetylcholine
    • norepinephrine
  • Metabotropic OR Ionotropic receptors
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5
Q

Key Criteria to be a Neurotransmitter (4)

A
  • Must be present in the pre-synaptic terminal
  • Released upon stimulation (depolarization and calcium)
  • Neurotransmitter in extracellular fluid must elicit same response as the synaptic event
  • Mechanism for removal must exist
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6
Q

Neurotransmitters may elicit a variety of post-synaptic responses

A

Dependent on receptor types (ionotropic vs. metabotropic), which is dependent on cell type

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7
Q

Neurotransmitters are active for a ____ time.

A

SHORT
Small-molecule NT:Enzymatic destruction
Re-uptake
-Independent from vesicular re-uptake
Neuroactive Peptides: Extracellular peptidase digestion

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8
Q

IONOTROPIC Chemical Synapses (4)

A

Directly alter membrane permeability to ions (open/close ion channels)

Signal transduction

Fast

Excitory and Inhibitory effects

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9
Q

METABOTROPIC Chemical Synapses (4)

A

Produce a metabolic change in the post-synaptic cell (usually with secondary messengers)

Modulation of neuronal function

Slow

Excitory, Inhibitory and other (cytoplasmic) effects

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10
Q

Basic overview to chemical synapses

A
  • Neurotransmitter released into synaptic cleft

- Binds receptor on post-synaptic effector (neuron or target cell) and alters post-synaptic cell function

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11
Q

How is the neurotransmitter released? (3)

A
  • Neurotransmitter is synthesized in pre-synaptic cell
  • Stored in vesicles at either the active site or interior of axon terminal
  • Each vesicle contains ~5,000 neurotransmitter molecules
    • Quantal packets
  • Release requires membrane depolarization and calcium influx
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12
Q

How is the neurotransmitter released? (Last 2)

A

-Depolarization of the axon terminal opens voltage gated calcium channels
-Action potential travelling down axon reaches the axon terminals and depolarizes the membrane
-Influx of Ca2+ when the channels open
-Un-depolarized neurons have very low
Ca2+ concentrations in the cytosol
-Ca2+ influx into the cytosol triggers exocytosis of vesicles
-Vesicles fuse to the plasma membrane
-Neurotransmitter released into synaptic cleft

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13
Q

Ligand-gated Channels (4)

A

-Synaptic transmission (fast, ionotropic)
-Permeability dependent on neurotransmitter
binding (voltage independent)
-Located on dendrites and cell body
-Generate potentials that are graded and spread
decrementally (length constant)

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14
Q

Voltage-gated Channels (4)

A
  • Action potential generation (Na+ and K+ channels on axon)
  • Neurotransmitter release (Ca2+ channels in axon terminal)
  • Permeability dependent on membrane potential (voltage dependent)
  • Generate potentials that are “all or nothing” and propagated
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15
Q

Synaptic Potentials (4)

A
  • Occur in ionotropic synapses (ones that involve a change in membrane permeability in the post-synaptic cell)
  • Graded change in post-synaptic neuron’s (or cell’s) resting membrane potential
  • PSP = post-synaptic potential
    • Not an action potential- only small changes in membrane potential… one alone is not enough to reach threshold
  • Inhibitory (IPSP) or excitory (EPSP)
    • Inhibitory: hyperpolarizes (makes more “–” than resting)
    • Excitory: depolarizes (makes less “-” than resting)
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16
Q

A single nerve stimulated in rapid succession- continues to release NT

A

Temporal Summation

17
Q

Several pre-synaptic neurons acting on the same post-synaptic neuron are stimulated simultaneously

A

Spacial Summation

18
Q

Summation of PSP (Post-synaptic potential)

A

Each individual synapse (the effect 1 action potential’s NT binding) depolarizes (or hyperpolarizes) the membrane only very slightly
-Not enough to generate an action potential in the post-synaptic cell

19
Q

Axodendritic

A

Synapse with dendrite = farther from hillock = less influence

20
Q

Axosomatic

A

Synapse with the cell body = closer to hillock = more influence

21
Q

Proximity of synapse to axon hillock (hillcock)

A
  • Spread of PSP from the dendrites or cell body to the site of the action potential is passive
  • The further from the axon hillock, the more the PSP is degraded
22
Q

Neuronal Integration:

Whether or not an action potential is generated in the axon is dependent on…

A

-Spatial and temporal summation
Overall effects of all of the pre-synaptic neurons acting on a post-synaptic neuron (or cell)
Some may depolarize, others may hyperpolarize
-Proximity of synapse to axon hillock (hillcock)

23
Q

Post-synaptic membrane permeability (3 Scenarios)

A
  • Neuromuscular junction (EPSP)
  • Excitory (Type 1) synapse (EPSP) in the CNS
  • Inhibitory (Type 2) synapse (IPSP) in the CNS
24
Q

Key features of a fast ionotropic receptor (4)

A
  • Channel opening is all or nothing
  • Channel opening depends on neurotransmitter concentration
    - More NT = more opening
  • Current flowing through channels contributes to neuron’s PSP
    • Currents through all channels can be summated
  • Can add to each other (if both IPSP or EPSP) or cancel each other out
25
Q

Sum of all ion currents flowing through channels at once

-Source of the EPSP/IPSP

A

Synaptic current

26
Q

Acetylcholine = neurotransmitter

A
  • Binds to a ligand-gated Na+/K+ membrane channel
  • Increases membrane permeability to BOTH Na+ and K+
  • Na+ flows in more rapidly than K+ flows out—WHY??
    Membrane depolarizes
27
Q

Neuromuscular EPSP

A

Synapse between a neuron and a skeletal muscle fiber (somatic nervous system)

28
Q

Relay synapse (3)

A
  • Each motor neuron action potential causes a large EPSP in the muscle
    • Lots of neurotransmitter released from pre-synaptic neuron
    • Generates a muscle action potential (muscle depolarized and contracts)
29
Q

Type 1 synapse (ionotropic) = Fast EPSP

A
  • Similar mechanism to neuromuscular EPSP
  • Smaller in magnitude, but results in membrane depolarization due to opening of the ligand gated Na+/K+ channels
  • Neurotransmitters:
    • ie: Glutamate (in CNS)
  • Smaller EPSP than neuromuscular
    • Only 1-2 vesicles released per synaptic transmission = less NT released = lesser effect on post-synaptic cell membrane potential
    • 1 EPSP does not depolarize the post-synaptic membrane enough to generate an action potential
    • NEED SUMMATION
30
Q

Type 2 synapse (ionotropic)= Slow IPSP

A
  • Inhibitory- hyperpolarizes membrane
  • Makes it harder for the neuron to reach the threshold membrane potential and generate an action potential
  • Neurotransmitters:
    • ie. GABA and glycine (in CNS)
  • Involves opening of ligand-gated chloride channels
    • Cl- floods in, making the inside of the cell more negative than resting membrane potential = HYPERPOLARIZES
      - Makes it harder to reach threshold and generate an action potential
31
Q

Key mechanisms of slow metabotropic receptors

A
  • G Protein-coupled receptors (GPCR)
    • Receptors are NOT ion channels as in ionotropic receptors
  • GPCR can move through the fluid membrane and interact with other proteins- trigger effects within the neuron
    • When neurotransmitter is bound, can initiate signaling cascades (usually with cAMP)
      - Phosphorylate membrane proteins (including ion channels- indirect effect on membrane permeability)
      - Phosphorylate cytoplasmic proteins- alter neuron function
      - Phosphorylate nuclear proteins- alter neuron function
32
Q

Other Metabotropic Regulatior Mechanisms

A
  • Secondary messenger does not have to be cAMP to cause phosphorylation
    • cGMP
    • via Phospholipase C: DAG, IP3 and Ca2+
  • Some GPCR can act without a secondary messenger
  • Interact directly with ion channels
  • Can be depolarizing (EPSP) or hyperpolarizing (IPSP), but these effects are slower than ionotropic channels
  • Also possible to have no effects on membrane permeability but to alter neuronal function or properties without contributing to the PSP
33
Q

Neurotransmitter release relies on TWO THINGS

A
  1. ) Axon terminal depolarizes –> Action Potential (AP) reaches terminal
  2. ) Ca2+ enters axon terminal (ESSENTIAL)
34
Q

Post-synaptic (MORE/LESS) likely to generate action potential

A

LESS

35
Q

Integration

A

Post synaptic neuron takes all incoming PSP information and “decides” whether or not it will have an action potential