Facilitated Diffusion
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Facilitated Diffusion is a type of passive transport that allows specific molecules or ions to move across the cell membrane with the assistance of membrane proteins. Like simple diffusion, it occurs along the concentration gradient (from high to low concentration) and does not require energy (ATP). However, facilitated diffusion differs from simple diffusion because it relies on specific proteins to help substances that cannot directly pass through the lipid bilayer due to their size, polarity, or charge.
Types of Transport Proteins:
Types of Transport Proteins:
Carrier Proteins: These proteins bind to the specific molecule on one side of the membrane, undergo a conformational change, and then release the molecule on the other side. Carrier proteins are essential for transporting larger molecules such as glucose and amino acids. An example is the glucose transporter (GLUT), which moves glucose into cells.
Channel Proteins: These proteins form water-filled channels or pores through the membrane that allow specific ions or water molecules to pass through. The channels can be either always open or gated, opening in response to a stimulus (e.g., electrical or chemical signals). For example:
Aquaporins facilitate the rapid transport of water and Ion channels allow the passage of ions like sodium (Na+), potassium (K+), calcium (Ca2+), and chloride (Cl-). because Charged ions like sodium (Na+), potassium (K+), and chloride (Cl-) cannot cross the hydrophobic membrane without the help of ion channels. For instance, the sodium-potassium channel allows the regulated movement of these ions across the membrane.
Carrier Proteins
Illustration by Bio-Code Explorer
Steps in Facilitated Diffusion
Steps in Facilitated Diffusion
Example: Glucose Transporter (GLUT):
Example: Glucose Transporter (GLUT):
Glucose Transport: Glucose, a polar molecule, cannot diffuse directly through the hydrophobic core of the lipid bilayer. Instead, it moves into cells via a carrier protein called the glucose transporter (GLUT).
Binding: The specific molecule or ion binds to the transport protein on the side where its concentration is higher.
Conformational Change: The binding causes a change in the shape of the transport protein, allowing the molecule to move through the membrane.
Release: The molecule is released on the side where its concentration is lower, completing the diffusion process.
Channel Proteins
Illustration by Bio-Code Explorer
Ligand-gated channels, also known as ionotropic receptors, are a type of membrane protein that opens or closes in response to the binding of a chemical messenger, or ligand, such as a neurotransmitter.
These channels play a critical role in synaptic transmission, allowing ions to flow across the cell membrane when activated, which can lead to changes in the membrane potential and the initiation of cellular responses.
Mechanism of Action:
Mechanism of Action:
Resting State: In the absence of the neurotransmitter acetylcholine (ACh), the nicotinic acetylcholine receptor (a ligand-gated ion channel) is closed. Sodium (Na⁺) and potassium (K⁺) ions cannot pass through the channel. The cell membrane is at its resting potential, typically around -70 mV, where the inside of the cell is more negatively charged than the outside.
Ligand Binding: When acetylcholine (ACh) is released from the presynaptic neuron and binds to the receptor site on the nAChR in the postsynaptic membrane, it causes a conformational change in the receptor. This change opens the channel, allowing ions to flow through.
Ion Flow: Once the channel opens, Na⁺ ions flow into the cell (due to a higher concentration of sodium outside the cell and the electrochemical gradient).
K⁺ ions may also flow out, but the inward movement of Na⁺ dominates because the concentration gradient and electrochemical gradient strongly favor Na⁺ entry.
This influx of Na⁺ depolarizes the cell membrane, bringing the membrane potential closer to threshold (around -55 mV), potentially triggering an action potential if the depolarization is sufficient.
Channel Closure: Once the acetylcholine unbinds (or is degraded by the enzyme acetylcholinesterase in the synaptic cleft), the receptor undergoes another conformational change, closing the channel. Ion flow stops, and the membrane potential begins to return to its resting state, aided by other mechanisms such as the sodium-potassium pump (Na⁺/K⁺ pump), which actively restores the original ion concentrations by pumping Na⁺ out and K⁺ back into the cell.
Summary of Ion Movements:
Summary of Ion Movements:
Sodium (Na⁺): Flows into the neuron when the channel opens, causing depolarization.
Potassium (K⁺): May flow out of the neuron, but its effect is usually smaller than that of sodium.
In this example, the nicotinic acetylcholine receptor allows both Na⁺ and K⁺ to pass, but the influx of Na⁺ ions is primarily responsible for the depolarization, which is crucial for generating an action potential in neurons or muscle contraction in muscle cells.
Mechanism of Action:
Mechanism of Action:
Resting State:
In the absence of the neurotransmitter acetylcholine (ACh), the nicotinic acetylcholine receptor (a ligand-gated ion channel) is closed. Sodium (Na⁺) and potassium (K⁺) ions cannot pass through the channel.
The cell membrane is at its resting potential, typically around -70 mV, where the inside of the cell is more negatively charged than the outside.
Ligand Binding:
When acetylcholine (ACh) is released from the presynaptic neuron and binds to the receptor site on the nAChR in the postsynaptic membrane, it causes a conformational change in the receptor.
This change opens the channel, allowing ions to flow through.
Ion Flow:
Once the channel opens, Na⁺ ions flow into the cell (due to a higher concentration of sodium outside the cell and the electrochemical gradient).
K⁺ ions may also flow out, but the inward movement of Na⁺ dominates because the concentration gradient and electrochemical gradient strongly favor Na⁺ entry.
This influx of Na⁺ depolarizes the cell membrane, bringing the membrane potential closer to threshold (around -55 mV), potentially triggering an action potential if the depolarization is sufficient.
Channel Closure:
Once the acetylcholine unbinds (or is degraded by the enzyme acetylcholinesterase in the synaptic cleft), the receptor undergoes another conformational change, closing the channel.
Ion flow stops, and the membrane potential begins to return to its resting state, aided by other mechanisms such as the sodium-potassium pump (Na⁺/K⁺ pump), which actively restores the original ion concentrations by pumping Na⁺ out and K⁺ back into the cell.
Summary of Ion Movements:
Summary of Ion Movements:
Sodium (Na⁺): Flows into the neuron when the channel opens, causing depolarization.
Potassium (K⁺): May flow out of the neuron, but its effect is usually smaller than that of sodium.
In this example, the nicotinic acetylcholine receptor allows both Na⁺ and K⁺ to pass, but the influx of Na⁺ ions is primarily responsible for the depolarization, which is crucial for generating an action potential in neurons or muscle contraction in muscle cells.
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