Synaptic transmission
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Explainer Video
Summary
Synaptic transmission
In a nutshell
Synapses enable action potentials to be transmitted to other neurones and effector cells. Neurotransmitters are used to transfer action potentials from one cell to another. Different drugs can have varying effects on synapses and neurotransmitters.
Synapse
Definition
A synapse allows information transmitted through a neurone to pass onto another cell. A synapse can connect a neurone to a plethora of cells including another neurone, muscle cells and gland cells. Without synapses, instructions that come from the brain can not be translated into useful actions.
At the end of the neurone there is a synaptic knob accommodating many synaptic vesicles filled with neurotransmitters which are utilised to transport information across the synaptic cleft. The postsynaptic membrane is across the synaptic cleft and is the beginning of the next cell.
Neurotransmitters are chemicals which interact with specific receptors on the postsynaptic membrane. Specific receptors on the postsynaptic membrane enable specific reactions including innervation of action potentials, muscular contraction and hormone release.
Cholinergic synapse
Definition
Synapses can be defined by the neurotransmitter employed to travel across the synaptic cleft. Cholinergic synapses utilise the neurotransmitter acetylcholine (ACh).
| 1. | Initiation of synaptic transmission begins with an action potential reaching the end of a neurone. The action potentials stimulates voltage-gated calcium ion channels to open. move into the synaptic knob via diffusion down the electrochemical gradient. Influx of stimulates the exocytosis of ACh vesicles. Exocytosis is a process where the ACh vesicles move to and subsequently fuse to the presynaptic membrane releasing ACh into the synaptic cleft. |
| 2. | ACh moves across the synaptic cleft and interacts with specific receptors on the postsynaptic membrane. This interaction triggers the opening of sodium ion channels in the postsynaptic neurone leading to diffusion of into the postsynaptic neurone. This diffusion causes depolarisation of the postsynaptic neurone altering the membrane potential. If the diffusion of into the postsynaptic membrane causes a membrane potential of around then an action potential will be generated. |
Discrete synaptic transmission
| 1. | To keep action potentials discrete ACh needs to be removed from the postsynaptic cleft to stop depolarisation of the postsynaptic neurone. Acetylcholinesterase (AChe) is an enzyme which is utilised to digest ACh. The products of the digestion are re-absorbed into the presynaptic knob through endocytosis. The digested ACh now contained in vesicles in the synaptic knob is recombined to create ACh for the next cholinergic synaptic transmission. |
Neurotransmitters
To transmit the correct signal across a synapse different neurotransmitters can be excitatory and inhibitory. Some neurotransmitters can be both excitatory and inhibitory depending on which area of the body they are operating in.
Excitatory | One excitatory neurotransmitter is ACh at cholinergic synapses in the central nervous system, where the neurotransmitter generates an action potential at the postsynaptic neurone. |
Inhibitory | ACh neurotransmitters are inhibitory at cholinergic synapses in the heart. Following ACh being released into the postsynaptic cleft it interacts with receptors which initiate the opening of potassium ion channels in the postsynaptic membrane. Potassium ion influx causes the opposite of depolarisation termed hyperpolarisation. This process can be utilised when heart rate needs to be reduced. |
Neuromuscular junction
Definition
A neuromuscular junction (NMJ) is a synapse which connects a motor neurone and a muscle cell. The process of synaptic transmission is similar to cholinergic synaptic transmission, however, there are some key differences which are important for you to remember.
Neuromuscular synapse transmission
Differences | Description |
| Receptors | The receptors on the postsynaptic membrane in neuromuscular transmission are termed nicotinic cholinergic receptors. The ACh interacts with these receptors after being released by exocytosis from the presynaptic knob. However, exocytosis is caused by the stimulation of an action potential, exactly the same process as cholinergic synaptic transmission. |
| Postsynaptic clefts | The postsynaptic membrane, termed the motor end plate, contains clefts which hold concentrated pockets of AChE. This digests ACh and the products are absorbed into the synaptic knob. The clefts allow faster digestion of ACh so messages can be transmitted more frequently across the neuromuscular synapse. |
| Number of receptors | There are more nicotinic cholinergic receptors on the motor end plate when compared to other synapses. |
| ACh | At the neuromuscular junction, ACh is always excitatory. Therefore following stimulation of the synaptic knob, a response in the muscle cell is always generated. |
Effects of drugs on synaptic transmission
There are different classes of drugs that affect synaptic transmission in different ways.
Agonists
Agonists have a similar shape to neurotransmitters and activate receptors at the postsynaptic membrane.
Example
Nicotine mimics ACh and interacts with nicotinic cholinergic receptors, this means more receptors are stimulated. A larger postsynaptic response is generated because more sodium ion channels are opened.
Antagonists
Antagonists have the ability to block postsynaptic receptors and reduce the amount of receptors that can be activated by neurotransmitters.
Example
Curare blocks nicotinic cholinergic receptors preventing interaction with ACh which stops postsynaptic action potentials from being generated. Curare can cause paralysis because it is such an effective antagonist.
Enzyme inhibitors
These compounds interact with the enzyme responsible for digesting the neurotransmitter after a postsynaptic action potential is generated.
Example
Nerve gases interact with AChE and prevents it from breaking down ACh. This means ACh cannot be reabsorbed through endocytosis and ACh binding to receptors is prolonged. Longer exposure to ACh means the motor end plate is constantly being depolarised and firing continuous action potentials. This results in a loss of muscle control.
Neurotransmitter stimulation and inhibition
Some compounds can stimulate the release of neurotransmitters and other compounds can inhibit the release of neurotransmitters.
Examples
- Amphetamines stimulate the release of ACh leading to more interactions with postsynaptic receptors increasing stimulation.
- Alcohol inhibits the release of ACh leading to less interactions with postsynaptic receptors decreasing stimulation.
FAQs - Frequently Asked Questions
At what synapses is acetylcholine inhibitory?
ACh neurotransmitters are inhibitory at cholinergic synapses in the heart.
How does ACh exit the synaptic knob?
ACh exits the synaptic knob by exocytosis. Exocytosis is a process where the ACh vesicles move to and subsequently fuse to the presynaptic membrane releasing ACh into the synaptic cleft.
What neurotransmitter is used at cholinergic synapses?
Cholinergic synapses utilise the neurotransmitter acetylcholine (ACh).