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In today's video we will be discussing synaptic transmission.
After watching this video,
you should be able to do the following three things: first,
identify and draw the main types of synapses found in the nervous system;
second, you should be able to describe the mechanism of
synaptic vesicle release; and finally,
you should be able to describe how neurotransmitters can cause a change in
postsynaptic membrane potential.
In the last video we talked about how an action potential is propagated down an axon.
In some cells, this action potential can propagate
to the next neuron through gap junctions. As shown here.
These gap junctions allow electrical connectivity between two cells.
so that current and ions can flow directly into the post synaptic cell.
More typically though, we think of neurons communicating through chemical
means
by the release of neurotransmitters from synaptic vesicles.
You can see in this electron micrograph, here's your presynaptic bouton here
and you can see the synaptic vesicles.
This presynaptic bouton is making two synapses.
onto two postsynaptic neuron as shown here.
synaptic vesicle releases neuron transmitter and it acts
on receptors on the postsynaptic side. A typical neuron makes about a thousand
synapses with other cells
and receives from anywhere from 10,000 to
over a hundred thousand synapses itself. So it's not
usually a one to one, one single neurons synapsing onto another single neuron.
There's a lot of integration that goes on in the cell. There are three main
types of synapses in the nervous system.
The axodendritic
synapse, shown here, for the axon from the presynaptic cell synapses
onto the postsynaptic dendrite. Second, you have an axosomatic
synapse. the axon from the presynaptic synapses onto the soma, cell body if
the person X
and finally you have an axle exxon synapse
with the Aksana the pre synaptic you're on
synapses onto the accent the postsynaptic in addition to the
different anatomical OT locations at the synapses
you also have some functional differences in general
most if you accidentally take steps is are excitatory
most view axis semantics in taxes are inhibitory
moco axo AKPsi nixon axes
a modulatory that means that they alter their mountaineer transmitter that's
released from their posts
Excel some the accident relates annexes
situps and a specialized structures on the dendrite called dendritic spines
these dendritic spines provide a postsynaptic micro-environment
for synaptic transmission to occur this may confirm it has been implicated in
naked plasticity as well as learning unlike the cell soma
or dendrites the AKPsi an increase in Africa time do not contain represents
so local protein synthesis cannot occur this means that the prisoner *** rutan
exxon land transport from the same many things are transported from the so much
the prisoner it put on
including the neurotransmitters that will be released to the snap kick that
schools
medic Andrea receptors
cytoskeletal elements as will set aside proteins this change what is a two way
street though
because some things must be transported from the prison after
who turned back to the same this includes things like proteins for
degradation
make Andrea as well as growth factors transport along the exxon
requires the use of motor proteins 30 main motor proteins involved
each of these can only travel in one direction down the microtubule
pennies in is a plus directed motor
protein and it takes its cargo from the soma
to the pre-snap time dining
goes the reverse direction it's a minus directed more protein
it goes from the pre-snap Bhutan back to the same
not think that schools are formed in the pre-snap a terminal
due time it's not the best schools are pinched after the monthly the secular
complex
these vesicles had two important proteins
soon after previn and not attack man
and they're loaded with no transmitter these vesicles then moved to the apt
active zone where the core complexes formed
which allows the best schools to dock in the active zone get ready for the signal
to release neurotransmitter
now there are three important proteins that you should know
it for miss core complex and I love the school docking
the first listen after Braden which is on the school itself
she talked about before anything to proteins are found on the active zone
membrane
that snap-25 and syntaxin
and again together this complex is called the core complex
deep polarization at the crease not take Bhutan causes the opening
a voltage-gated calcium channels calcium
can then flew into the cell and bind
anderson et attackman this capitalizes membrane fusion so this not successfully
fuses at the membrane
and then opens up to release neurotransmitter
the fact that calcium is necessary for pre-snap it best to release
commission by this extent you take a preset I think you're on
and place it in a zero calcium no exercise either calcium
you put a stimulating electrode into the pre-snap Excel
and recording lectured on the post Excel
if you then similar decrease in ethics L shown here so you can see that little
blip
that's your pre synaptic action tension
stimulation you have no calcium
you also require the personal Excel no EPSP
or no change in membrane voltage Sep even though
the prisoner XL has been depolarized since no kassin can flow through those
with educated calcium channels
you'll get no change in person at the membrane potential
if instead you pop a bit calcium with this electrode
right before you stimulate the prisoner Excel
now you can get any PSP remember in both the change
any person exciting if you wait and hope that calcium
into after the prison after Excel has been simulated
so by now the voltage-gated calcium channels are close
you still get no person acting membrane potential change
so if we measured calcium permeability or
company calcium channels are open as the increase in deep polarization the
pre-snap Excel
your increase the number of calcium channels that are open
hey this make sense they're voltage-gated CD polarize
the prison epic Bhutan because your action potentials come down
you can open those both educated calcium channels and that calcium it
as you increase the amount of calcium inside the cell
inside the prison at XM you also increase the amount of neurotransmitter
that's released
that means the more molecules casting you have
the more soon after tagging can be bound and more
syntactic that schools can be released
you should know understand how calcium causes the fusion often affect the
school's
onto the piece in epic returns membrane this allows for the release an urgent
if you can't fuse in synaptic vesicles without recycling them
your prison after went on to become huge
won an Emmy mechanisms that's cool recycling is clathrin mediated
endocytosis
is now I think that's cool flattens out
on the present a good time membrane and is then
could with clathrin endorse a toast
this and I think that's cool can then Hughes back to the multiverse secure
complex to the endosome
and be made into additional it that schools
this entire cycle can take out now a minute
another mechanism for vesicle recycling is a so-called Kissin right technique
when it's not the best of uses it opened just no
the neurotransmitter to come out it then refuses
in Buda back into this
many different substances can be used as neurotransmitters
but the most common classes in their transmitters are the amino acid
neurotransmitters
glutamate is the main excitatory neurotransmitter
gather is the main inhibitory neurotransmitter in the brain
walkway thing is the main inhibitory neurotransmitter in the spinal
the chemical means another common fastener transmitters
these include the main your transmitters for the autonomic nervous system
norrköping different and different as well as dopamine
which is involved in many things including mood reward
as well as movement
there are many different kept a neuro transmitters these peptides are usually
three to thirty me know acids
they include the hope you ate which met in Kaplan
is one example they also include the technique einon's
like substance P it later transmitters are
often poll released with other neurotransmitters likely to me
or gap
your transmitters bind to postsynaptic receptors
these receptors can either directly or indirectly alter the membrane potential
the post except the neurotransmitter
thanks to its receptor like a lock into a key
oftentimes you know transmitters connect to multiple receptors
and multiple receptors can be opened but not for their transmitters
all the binding efficiencies will vary
the first maintain a postsynaptic receptor are the ionotropic receptors
once found by the inner Chancellor like end these aortic shipping
receptors directly open ion channels lol I and stuff
either into or out of the CEP
the temperature pic receptors for the second main class at neurotransmitter
receptors
following binding in the neurotransmitter to metabotropic
receptor
a G-protein starts intracellular signaling cascade
these receptors are often called g-protein-coupled receptors
the intracellular signaling cascade can lead to number changes in the cell
they can directly open in: channels they can
change the password nation-state the ion channel
to alter the open probability that I am channel
and they can also alter receptor trafficking to the membrane
temperature big receptor responses take a longer time to develop
then ionotropic receptor responses since the energetic receptors directly open
and chips
the temperature pic receptors monster can be more long-lasting
and can be an amplified response since you're starting the signaling cascade
there are many steps where you can amplify the response
in future videos we will be talking more about these postsynaptic receptors
and their function and how they can be involved in things like synaptic
plasticity
now that we know 100 transmitters are at least and whether sated action is
going to talk about how you can turn off communication across finances
you want to nitpick communication to start when you want it
and stop quickly so that you can have sharp differences in thing
so the first way that you turn off the net the transmission
if you remove the caffeine signal if you do not have deplores asiana the pre
snap *** rutan you are have calcium influx into the cell
in binding to sit at the Technion and genetic that's cool release
second you can simply remove the neurotransmitter from the synaptic cleft
this is accomplished in a variety of ways somewhere transmitters can be
reacting into the cell
using special rhea take prompt
sumner transmitters are destroyed by an insight
for instance acetylcholine is a sure they feel equally necessary
in the synaptic cleft itself and finally
the neurotransmitter can just diffuse away from the synaptic
junction between the two cells
that concludes our video internet the transmission
hopefully now you can identify in Java main takes it in *** is found in the
nervous system
describe the mechanism synaptic vesicle release
and described under transmitters can cause a change in postsnapback membrane
potential