Neuron Neuron Synapses (EPSP vs. IPSP)
Summary
TLDRThis video script delves into the intricacies of synapses and neuron-to-neuron communication, highlighting the many-to-one relationship where one neuron receives input from several others. It explains how action potentials are transmitted via synaptic connections, primarily on cell bodies or dendritic membranes, and the role of neurotransmitters like acetylcholine and glutamate in generating excitatory postsynaptic potentials. The script also contrasts this with inhibitory postsynaptic potentials caused by neurotransmitters like GABA, affecting neuron excitability. Clinical implications of altered neuronal excitability, such as weakness or hyperreflexia, are also discussed, along with causes like ion imbalances, neuron loss, and the impact of toxins and drugs.
Takeaways
- đ§ Synaptic connections are primarily on the cell body or dendritic membranes.
- đ Neuron-to-neuron relationships are often many-to-one, with one neuron receiving input from several others.
- đ Action potentials at the synapse cause depolarization of the presynaptic membrane, leading to neurotransmitter release.
- đ Sodium influx is the main current responsible for depolarizing the postsynaptic membrane.
- đ Threshold potential at -10 millivolts is critical for initiating an action potential.
- đïž The axon hillock is the only region near dendrites with a high density of fast voltage-gated sodium channels.
- đ Synapses closer to the axon hillock have a greater influence on whether an action potential is generated.
- đ The sum of inputs from multiple presynaptic cells determines if a postsynaptic cell fires an action potential.
- đïž Excitatory postsynaptic potentials (EPSPs) bring the membrane potential closer to the threshold, increasing neuron excitability.
- đ Inhibitory postsynaptic potentials (IPSPs) hyperpolarize the neuron, decreasing its excitability and likelihood to fire an action potential.
- đ Clinical signs of decreased neuronal excitability include weakness, ataxia, hyperreflexia, paralysis, and sensory deficit.
Q & A
What are the common types of neuron-neuron relationships?
-The common type of neuron-neuron relationship is many-to-one, where one neuron takes input from several neurons, creating several synaptic regions.
Where are synaptic connections mainly located?
-Synaptic connections are mainly located on a cell body or in dendritic membranes.
What happens when an action potential reaches a dendritic synaptic point?
-The action potential depolarizes the presynaptic membrane, causing vesicles to release neurotransmitters like acetylcholine into the synaptic cleft.
How does the neurotransmitter acetylcholine affect the postsynaptic membrane?
-Acetylcholine binds with its receptor on the postsynaptic membrane, opening channels that increase sodium and potassium conductance, leading to sodium influx and depolarization of the postsynaptic membrane.
What is the threshold potential in a neuron?
-The threshold potential is at -10 millivolts, and when reached, it allows the current to travel along the dendritic and cell body membranes up to the axon hillock.
Why can't current flow at dendrites initiate an action potential?
-Current flow at dendrites cannot initiate an action potential because they lack fast voltage-gated sodium channels.
What is the role of the axon hillock in generating an action potential?
-The axon hillock has a high density of voltage-gated sodium channels, and when current flows up to it, it can take the membrane potential to the threshold potential, initiating an action potential.
How does the proximity of a synapse to the axon hillock affect its influence?
-The closer the synapse is to the axon hillock, the greater its influence in determining whether an action potential is generated.
What is an excitatory postsynaptic potential (EPSP)?
-An EPSP is a depolarization of the postsynaptic membrane, such as when glutamate is released and binds to its receptor, allowing sodium influx that makes the neuron more likely to fire an action potential.
What is an inhibitory postsynaptic potential (IPSP)?
-An IPSP is a hyperpolarization of the postsynaptic membrane, such as when GABA is released and binds to its receptor, opening chloride channels and moving the membrane potential away from the threshold, decreasing the neuron's excitability.
What clinical signs might indicate decreased neuronal excitability?
-Clinical signs of decreased neuronal excitability might include weakness, ataxia, hyperreflexia, paralysis, and sensory deficit.
What are some causes of decreased neuronal excitability?
-Causes of decreased neuronal excitability include ion disturbances, loss of neurons, demyelination, and toxins or drugs that affect the neuromuscular junction.
Outlines
đ§ Neuron-to-Neuron Communication
This paragraph discusses the synapses, which are the junctions between neurons. It explains the many-to-one relationship where one neuron receives input from several others. The importance of synaptic connections being primarily on the cell body or dendritic membranes is highlighted. The script then delves into the process of action potential transmission from one neuron to another, focusing on the release of neurotransmitters like acetylcholine and the subsequent depolarization of the postsynaptic membrane. It also touches on the threshold potential and the role of the axon hillock in initiating an action potential. The influence of the proximity of synapses to the axon hillock on the likelihood of action potential generation is also discussed.
đ Excitatory and Inhibitory Postsynaptic Potentials
The second paragraph focuses on the concepts of excitatory and inhibitory postsynaptic potentials (EPSP and IPSP). It describes how the release of excitatory neurotransmitters like glutamate leads to the opening of sodium and potassium channels, resulting in a depolarization known as EPSP. This process brings the membrane potential closer to the threshold, increasing the neuron's excitability. Conversely, the paragraph also explains how inhibitory neurotransmitters like GABA cause hyperpolarization, known as IPSP, which moves the membrane potential away from the threshold, decreasing the neuron's excitability. The clinical implications of these processes are also mentioned, including conditions that can lead to decreased or increased neuronal excitability.
đ Clinical Implications of Neuronal Excitability
The final paragraph explores the clinical signs associated with both decreased and increased neuronal excitability. It lists symptoms such as weakness, ataxia, hyperreflexia, paralysis, and sensory deficits that can result from decreased excitability. Causes for this decrease can include ion disturbances, loss of neurons, demyelination, and the effects of certain toxins and drugs. The paragraph also discusses the causes of increased neuronal excitability, such as ion disturbances, demyelination, and the influence of certain toxins. It concludes by mentioning disorders of the neuromuscular junction and the effects of drugs and toxins on neuronal excitability.
Mindmap
Keywords
đĄSynapses
đĄAction Potential
đĄPresynaptic Membrane
đĄPostsynaptic Membrane
đĄAxon Hillock
đĄThreshold Potential
đĄExcitatory Postsynaptic Potential (EPSP)
đĄInhibitory Postsynaptic Potential (IPSP)
đĄNeurotransmitters
đĄDendrites
đĄNeuromuscular Junction
Highlights
Synapses are crucial for neuron-to-neuron communication.
The common neuron relationship is many-to-one, where one neuron receives input from several others.
Synaptic connections are primarily found on cell bodies or dendritic membranes.
Action potential transmission involves depolarization of the presynaptic membrane and release of neurotransmitters.
Neurotransmitters like acetylcholine can bind to receptors, affecting sodium and potassium conductance.
Sodium influx due to neurotransmitter action can depolarize the postsynaptic membrane.
The threshold potential at -10 millivolts is critical for initiating an action potential.
Dendrites and neuronal bodies lack fast voltage-gated sodium channels, preventing action potential initiation.
The axon hillock is the only region with a high density of voltage-gated sodium channels near dendrites.
An action potential in the presynaptic cell is not enough to produce one in the postsynaptic cell; convergence of inputs is required.
The closer a synapse is to the axon hillock, the greater its influence on action potential generation.
Excitatory postsynaptic potential (EPSP) brings the membrane potential closer to the threshold, increasing neuron excitability.
Inhibitory postsynaptic potential (IPSP) hyperpolarizes the neuron, decreasing its excitability.
Glutamate and acetylcholine are examples of excitatory neurotransmitters, while GABA and glycine are inhibitory.
Decreased neuronal excitability can manifest as weakness, ataxia, hyperreflexia, paralysis, and sensory deficits.
Increased neuronal excitability might present as hyperreflexia, spasms, muscle fasciculation, tremors, paresthesias, and convulsions.
Ion disturbances, loss of neurons, demyelination, toxins, and drugs can affect neuronal excitability.
Neuromuscular junction disorders and certain drugs/toxins can specifically impact excitability at the neuromuscular junction.
Transcripts
[Music]
and this video will talk about synapses
between neurons there are several types
of relationships between the input to a
synapse and output but the common types
of neuron neuron relationship is many to
one meaning one neuron takes input from
several neurons creating several
synaptic regions it is very important to
know that synaptic connections are
mainly on a cell body or in a dendritic
membranes the places where we see ligand
gated channels we will see how an action
potential transmits from one neuron to
another first let me zoom here a single
dendritic synaptic point the action
potential comes and depolarizes the
presynaptic membrane the vesicles
release their content into the synaptic
cleft suppose it releases acetylcholine
this neurotransmitter binds with its
receptor and opens channels increasing
sodium and potassium conductance because
the net force on sodium is greater than
net force on potassium the main current
flowing is sodium influx sodium influx
depolarize the postsynaptic membrane
let's suppose from negative 72 zero
millivolt to value approximately halfway
between the equilibrium potentials for
sodium and potassium it is very
important to know that at negative 10
millivolts we have the threshold
potential when we reach the threshold
potential the current travels along the
dendritic and cell body membranes up to
the axon hillock it is important to know
that at dendrites as well as at neuronal
body the current flow cannot initiate an
action potential because here we do not
have
fast voltage-gated sodium channels the
only region near to the dendrites where
we do have a high density of
voltage-gated sodium channels is an axon
hillock let me zoom here the membrane of
the axon hillock when a current flows up
to the axon hillock it takes the
membrane potential from its resting
state up to the threshold potential as a
consequence the voltage-gated sodium
channels open up and we get a sodium
influx and this sodium influx initiates
an action potential this action
potential further transmits forward
along the axon another important point
is that the closer the synapse is to the
axon hillock the greater its influence
in determining whether an action
potential is generated in other words
out of these two synapses the second one
has greater chains to generate an action
potential because it is closer to the
axon hillock another important point
understand is that in these synapses an
action potential in a presynaptic cell
is insufficient to produce an action
potential in a postsynaptic cell instead
many presynaptic cells converge on the
postsynaptic cell these inputs are made
and the sum of the inputs determines
whether the postsynaptic cell will fire
an action potential in this part of the
video we will talk about the differences
between the excitatory postsynaptic
potential and inhibitory postsynaptic
potential first let's talk about
excitatory postsynaptic potential when a
presynaptic membrane depolarizes let's
suppose
it releases glutamate and excitatory
neurotransmitter glutamate attaches to
its receptor in a postsynaptic membrane
and opens non selectively permeable
channels for sodium and potassium
because of the net force sodium influx
dominates over potassium efflux the
sodium influx let suppose make the
membrane potential less negative perhaps
to negative 60 millivolts these 10
millivolts of depolarization is called
excitatory postsynaptic potential
excitatory postsynaptic potential brings
the membrane potential close to the
threshold potential which is at negative
10 millivolts this excitatory
postsynaptic potential increases the
excitability of the postsynaptic neuron
making the neuron more likely to fire an
action potential it is important to note
that excited to repost synaptic
potential is a similar to the endplate
potential found at the neuromuscular
junction and also some mates to reach
the threshold and generate an action
potential in addition to glutamate
excitatory neurotransmitters include
acetylcholine and aspartate second let's
talk about inhibitory postsynaptic
potential when a presynaptic membrane
depolarizes suppose it releases an
inhibitory neurotransmitter gaba in a
synaptic cleft
gabber attaches to its receptor in a
postsynaptic membrane and opens chloride
ion channels a type of ligand gated
channel because the membrane potential
in the postsynaptic membrane is Nega
70 millivolts and a chloride equilibrium
potential is negative 90 millivolts we
get a net force on chloride directed
inward
please note chloride is negatively
charged ion this chloride influx
hyperpolarizes the postsynaptic cell
toward its equilibrium potential suppose
from negative 70 to negative 85
millivolts this 15 millivolts of hyper
polarization is referred to as
inhibitory postsynaptic potential
inhibitory postsynaptic potential takes
the membrane potential away from
threshold this it decreases the
excitability of the postsynaptic neuron
making the neuron further from firing
and action potential
in addition of gaba inhibitory
neurotransmitters include glycine now
let's recap and sum up what we have
looked at in this section and add some
points which are important for clinical
purposes first let's talk about
decreased neuronal excitability
connection and increased neuronal
excitability or conduction clinical
signs of decreased neuronal excitability
and conduction could include weakness
ataxia hyperreflexia paralysis and
sensory deficit the causes of decreased
neuronal excitability include ion
disturbances that include hypokalemia
chronic hyperkalemia and hypercalcemia a
second possible cause of decreased
neuronal excitability and conduction
includes
loss of neurons demyelination as in case
of guillain-barre a amyotrophic lateral
scoliosis and normal physical aging the
third cause of decreased neuronal
excitability and conduction includes
toxins and drugs like local anesthetics
like cane drugs and toxins like
tetrodotoxin and saxitoxin the
neuromuscular Junction disorders drugs
and toxins also decrease the
excitability in neuromuscular Junction
because of decreased excitability in
neuromuscular Junction include
depolarizing muscular nicotinic receptor
blockers nondepolarizing muscular
nicotinic receptor blockers the diseases
like lambert-eaton syndrome
myasthenia gravis and botulinum toxin
next let's talk about increasing
neuronal excitability or conduction
clinical signs of increasing neuronal
excitability and conduction could
include hyperreflexia spasms muscle
fasciculation cad knee tremors
paresthesias and convulsions the causes
of increased neuronal excitability and
conduction include ion disturbances in a
case of acute hyperkalemia and
hypocalcemia we have already explained
the mechanisms loss of neurons
demyelination in a case of multiple
sclerosis third toxins like Sigma toxin
and batrachotoxin
the neuromuscular junction disorders
drugs and toxins also increase the
excitability in neuromuscular Junction
because of increased excitability in
neuromuscular Junction include
acetylcholine esterase
inhibitors and lateral toxin
you
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