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SYNAPSE
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What is a synapse?
A synapseis the junction between 2 neurones. There is a very narrow gap of about 20nm
between neurones called the synaptic cleft.
An action potential cannot cross the synapticcleft, so nerve impulses are carried by
chemicals called neurotransmitters.
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The synapse is where the nerve impulsepasses from one cell to the next
The electrical signal (the action potential)stops and a chemical signal takes over to
cross the gap between the cells The chemical messenger is called aneurotransmitter
The neurotransmitter crosses the gap bydiffusion, which creates a small delay
2008 Paul Billiet ODWS
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Neurotransmitter
Neurotransmitter is made by thepre-synaptic neuroneand is stored
in synaptic vesselsat the end of the
axon. The membrane of thepost-synaptic
neuronehas chemical-gated ionchannels called neuroreceptors.
These have specific binding sites
for neurotransmitters.
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Designer signals
The advantage of using neurotransmitteris that the nerve impulse can be givensome more specificity
Neurotransmitters can also control theoperation of the nervous system by
inhibition orexcitation Many drugs that try to cure problems in
the nervous system operate at synapses
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Neurotransmitters and hormones
In many ways neurotransmitters arehormonesworking over a very shortdistance (about 20 nm)
Some of them work both at synapsesand in the circulatory system
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A Synapse
Pre-synaptic neurone = neurone sending impulse
Post-synaptic neurone = neurone receiving impulse
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Cholinergic Synapses
Acetylcholine is acommon transmitter.
Synapses that haveacetylcholine transmitterare called cholinergicsynapses.
Some neurones formmore than 1 synapse. This is an electron
micrograph of synapsesbetween nerve fibres anda neurone cell body.
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1. Action potential arrives at
terminal button
Membrane receptor
for neurotransmitter
Ca2+
channel
Vesicle storing
neurotransmitter
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Dept of Biology, Saint Louis University
http://starklab.slu.edu/neuro/Cumulative.htmhttp://starklab.slu.edu/neuro/Cumulative.htm8/10/2019 sinapsis_Rizki Fauziah_3415110139.ppt
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Ca2+ Ca2+ Ca2+Ca2+
2.Depolarisationopens Ca2+channels
Ca2+enters terminal
button
3.Ca2+stimulates
vesicles to fuse
with membrane
4.Exocytosis of
neurotransmitter
It diffuses 20nm across
the synaptic cleft
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The passage across the synapse
An action potential travels down an axon to theterminal buttonsor synaptic knobs at the end The action potential depolarises the membrane of a
terminal button causing voltage-gated Ca2+channels
to open Ca2+ions flood into the terminal button This stimulates hundreds of synaptic vesicles, packed
with neurotransmitter, to fuse with the membrane ofthe terminal button
By exocytosis The Ca2+ions are then pumped out again
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6.Localised
depolarisation as
ions leak in or out
of membrane.
5.Neurotransmitter
receptor sites on the
postsynaptic membrane
are ion channels.They open when the
neurotransmitter binds
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The passage across the synapse
The neurotransmitter diffusesacross cleftto postsynaptic membrane The neurotransmitter molecules bind with
specific receptor siteson postsynapticmembrane
The receptor sites are part of a ligand-gated ion channel
These channels let Na+ions in or K+ions outcausing localised depolarisationof themembrane
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8.Neurotransmitter
destroyed by
enzymes in the cleft.
Stops signal being
perpetuated.
7.Action potential
generated which
travels down the
postsynaptic cell.
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A new action potential
If the localised depolarisations build up tothe nerve cell threshold, a full actionpotentialwill be produced
This will travel away, down the postsynapticneurone
The action of the neurotransmitters stops:(i) as they dilute by diffusionin the synapticcleft(ii) by hydrolysisthrough the action ofenzymesthere
Important:The signal must not beperpetuated indefinitely 2008 Paul Billiet ODWS
Figure 48 15
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Presynapticcell
Postsynaptic cell
Axon
Presynapticmembrane
Synaptic vesiclecontainingneurotransmitter
Postsynapticmembrane
Synaptic
cleft
Voltage-gatedCa2 channel
Ligand-gatedion channels
Ca2
Na
K
2
1
3
4
Figure 48.15
Figure 48 16
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Figure 48.16
Postsynapticneuron
Synapticterminalsof pre-synaptic
neurons
5
m
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Neuromuscular Junctions
Same stages ascholinergic synapses but in this case the
postsynaptic membraneis the muscle fibremembrane,(Sarcolemma).
Depolarisation of thesarcolemma leads tocontraction of musclefibre.
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The neuromuscular junction is asynapse
The motor end plateis the terminal button
of a motor neuronethat makes contact witha muscle cell
The motor end plate releases the
neurotransmitter acetylcholinethatultimately causes the muscle cell to contract
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Motor end plates
David B. Fankhauser, Ph.D., Professor of Biology and Chemistry, University of Cincinnati Clermont College
http://biology.clc.uc.edu/fankhauser/Labs/Anatomy_&_Physiology/A&P202/Nerve_Histology/Nervous_Tissue_Histology.htmhttp://biology.clc.uc.edu/fankhauser/Labs/Anatomy_&_Physiology/A&P202/Nerve_Histology/Nervous_Tissue_Histology.htmhttp://biology.clc.uc.edu/fankhauser/Labs/Anatomy_&_Physiology/A&P202/Nerve_Histology/Nervous_Tissue_Histology.htmhttp://biology.clc.uc.edu/fankhauser/Labs/Anatomy_&_Physiology/A&P202/Nerve_Histology/Nervous_Tissue_Histology.htm8/10/2019 sinapsis_Rizki Fauziah_3415110139.ppt
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Drugs
Drugs which have molecules ofsimilar shape to transmittersubstances can affect protein
receptors in postsynapticmembranes.
Drugs that stimulate a nervoussystem are called AGONISTS
Drugs that inhibit a nervous systemare called ANTAGONISTS.
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Various effects of drugs on
synapses:DRUG ACTION EFFECT
Mimic a neurotransmitter Switch on a synapse
Stimulate the release of a
neurotransmitter
Switch on a synapse
Open a neuroreceptor channel Switch on a synapse
Block a neuroreceptor channel Switch off a synapse
Inhibit the breakdown enzyme Switch on a synapse
Inhibit the Na+K+ATPase pump Stop action potentials
Block the Na+or K+channels Stop action potentials
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Effect of nicotine and atropine
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Thank
You