Neuron Neuron Synapses (EPSP vs. IPSP)

Summary

This 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

• 🧠 Synaptic connections are primarily on the cell body or dendritic membranes.
• 🔗 Neuron-to-neuron relationships are often many-to-one, with one neuron receiving input from several others.
• 💉 Action potentials at the synapse cause depolarization of the presynaptic membrane, leading to neurotransmitter release.
• 🚀 Sodium influx is the main current responsible for depolarizing the postsynaptic membrane.
• 🔑 Threshold potential at -10 millivolts is critical for initiating an action potential.
• 🏞️ The axon hillock is the only region near dendrites with a high density of fast voltage-gated sodium channels.
• 🌐 Synapses closer to the axon hillock have a greater influence on whether an action potential is generated.
• 📈 The sum of inputs from multiple presynaptic cells determines if a postsynaptic cell fires an action potential.
• 🏋️ Excitatory postsynaptic potentials (EPSPs) bring the membrane potential closer to the threshold, increasing neuron excitability.
• 🏃 Inhibitory postsynaptic potentials (IPSPs) hyperpolarize the neuron, decreasing its excitability and likelihood to fire an action potential.
• 🚑 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

00:00

🧠 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.

05:01

🔋 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.

10:04

🚑 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.

Keywords

💡Synapses

Synapses are the junctions through which neurons transmit signals to each other. They are crucial for neural communication and are the primary focus of the video. The script discusses how synaptic connections mainly occur on cell bodies or dendritic membranes and how they facilitate the transmission of action potentials.

💡Action Potential

An action potential is an electrical signal that travels along a neuron's membrane. The video explains how an action potential at a synapse can depolarize the presynaptic membrane, leading to the release of neurotransmitters. It is a fundamental concept in understanding how neurons communicate.

💡Presynaptic Membrane

The presynaptic membrane is the part of a neuron that releases neurotransmitters into the synaptic cleft. The video describes how depolarization of this membrane triggers the release of neurotransmitters like acetylcholine, which then bind to receptors on the postsynaptic membrane.

💡Postsynaptic Membrane

The postsynaptic membrane is the part of a neuron that receives neurotransmitters. The video explains how neurotransmitters like acetylcholine bind to receptors on this membrane, leading to changes in ion conductance and potential generation of an action potential.

💡Axon Hillock

The axon hillock is the region of a neuron where the cell body meets the axon. The video emphasizes its importance as the only region with a high density of fast voltage-gated sodium channels, which are necessary for the initiation of an action potential.

💡Threshold Potential

The threshold potential is the membrane potential at which an action potential is triggered. The video describes how reaching this potential level at the axon hillock leads to the opening of voltage-gated sodium channels and the initiation of an action potential.

💡Excitatory Postsynaptic Potential (EPSP)

EPSP is a membrane potential that brings the neuron closer to its threshold potential, increasing the likelihood of an action potential. The video uses the example of glutamate releasing and binding to receptors to create an EPSP, which depolarizes the membrane.

💡Inhibitory Postsynaptic Potential (IPSP)

IPSP is a membrane potential that moves the neuron further from its threshold potential, decreasing the likelihood of an action potential. The video explains how the release of inhibitory neurotransmitters like GABA leads to the opening of chloride channels and hyperpolarization, creating an IPSP.

💡Neurotransmitters

Neurotransmitters are chemicals that transmit signals across a synapse. The video discusses both excitatory neurotransmitters like glutamate and acetylcholine, which facilitate the generation of EPSPs, and inhibitory neurotransmitters like GABA, which lead to IPSPs.

💡Dendrites

Dendrites are the branched extensions of a neuron that receive most of the input from other neurons. The video mentions that current flow in the dendrites cannot initiate an action potential, which contrasts with the role of the axon hillock.

💡Neuromuscular Junction

The neuromuscular junction is the connection between a motor neuron and a muscle fiber. The video compares EPSPs to the endplate potential found at this junction, highlighting the role of excitatory neurotransmitters in signal transmission.

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