When an axon ends, the action potential which it carries can no longer be transmitted by the same medium. Axons end in a structure known as a synapse, the synapse allows the action potential to be propagated by means of chemicals (as opposed to electrically charged ions). An axon which terminates on an individual muscle fibre is known as a neuromuscular junction.
The terminating end of the axon has a bulbous structure, known as the presynaptic bulb. Within this bulb there can be one of many types of chemicals known as neurotransmitters. These neurotransmitters are the chemicals which transmit the action potential across the synapse (the space between the presynaptic bulb and the post synaptic structure is known as the synaptic cleft).
The most commonly found chemical used as a neurotransmitter is acetylcholine; however others include adrenaline, serotonin and dopamine. These neurotransmitters are housed in the presynaptic bulb contained in vesicles.
The process of transmission is as follows:
- An action potential propagated to the presynaptic bulb (caused by an earlier stimulus)
- The action potential depolarises the plasma membrane, this opens voltage gated channels in the membrane that allow the influx of Ca2+
- The influx of Ca2+ results in some of the neurotransmitter containing vesicles to fuse with the presynaptic bulb membrane, resulting in the expulsion of the neurotransmitter into the synaptic cleft
- The neurotransmitter diffuses across the synaptic cleft and binds to neurotransmitter specific receptors on the postsynaptic bulb
- These receptors are ligand-gated ion channels and once the ligand (neurotransmitter) binds to the receptor, it opens allowing Na+ and K+ to diffuse through the channel
- The influx of Na+ and efflux of K+ ions generates an action potential in the postsynaptic bulb which is propagated further
- The neurotransmitter is released from the receptor causing it to close
- The neurotransmitter is recycled, initially being broken down by an enzyme in the synaptic cleft (e.g. acetycholinesterase breaks down acetylcholine into acetate and choline)
- Some of the neurotransmitter is taken up again by the presynaptic bulb (e.g. choline is pumped back into the presynaptic bulb by a choline carrier)
- Enzymes convert the molecule back into a neurotransmitter (e.g. choline converted into acetylcholine) and the neurotransmitter is repackaged in an empty vesicle
It is possible for the neurotransmitter to be inhibitory as well i.e. prevent the generation of an action potential, e.g. glutamate is the primary excitatory neurotransmitter of the brain whereas GABA is the brain’s primary inhibitory neurotransmitter.
Types of Post Synaptic Receptors
As mentioned in the typical transmission above, neurotransmitters bind to a post synaptic receptor to result in either the inhibition or generation of an action potential. However, there are other types of post synaptic receptors which do not bind the neurotransmitter directly. The main 3 types are given below:
- Ligand-Gated Ion Channels: (Fast – 0.1ms delay) also known as ionotropic receptors, these are the type of postsynaptic receptors spoken about earlier. They require the binding of a specific neurotransmitter, the binding of this neurotransmitter results in a conformational change causing the channel to open and allow the passage of ions. They are associated primarily with excitatory neurotransmitters such as acetylcholine and glutamate.
- Metabotropic Receptors: (Slow – 10ms delay) unlike ionotropic receptors, these receptors are not directly associated with an ion channel. Instead they indirectly link with ion channels by means of signal transduction mechanisms, often G-proteins. Neurotransmitters will bind to the metabotropic receptor, resulting in the activation of these secondary messenger signal transduction mechanisms. The result is the opening of an ion channel and from this point, the process continues as in an ionotropic receptor.
- Electrical Synapses: (Very Fast – <0.1ms delay) unlike either the ionotropic or metabotropic receptors, there is no association with an ion channel. Instead gap junction like channels pass directly through the presynaptic bulb and synaptic cleft heading directly into the postsynaptic bulb. This means the action potential can head straight through into the next axon without having to stop. This type of system is extremely fast and very uncommon. It is found in only a few specialised systems within the body.
The process of action potential propagation across synapses can vary. Most post synaptic terminals have a threshold which must be met in order for the action potential to be propagated. Therefore if a weak action potential arrives and is sub-threshold, the action potential ends there. It is not transmitted any further. There is an exception to this – summation.
A post synaptic structure such as a motor neurone may synapse with more than one presynaptic sensory neurone. If this is the case, then it is possible for summation to occur. Summation is when two sensory neurones fire simultaneous sub-threshold action potentials. Normally, as they are sub-threshold, they would not be propagated any further, but as there are two, the effect stacks in the process known as summation.
The above form of summation is known as spatial summation – the action potential of two neurones combine to allow threshold to be reached.
There is another form of summation however, temporal summation. Temporal summation is possible from just one sensory neurone. It works when a neurone is able to generate two action potentials in short succession. By the time the second action potential reaches the synapse, neurotransmitters from the previous action potential have not yet unbound from the postsynaptic receptors. This means the effects from both action potentials stack and threshold is reached.
Welcome to VetSciWe have a wide range of articles for you to access, including a number of veterinary, biological and medical science topics. If you can't find what you're looking for try the search bar! Subscribe to our newsletter
Search the Web
Tagsadhesin animal antibiotic antibody antigen avian bacteria behaviour bird blood bordetella bronchiseptica canine capsule cell diagnosis disease egg enzyme evolution female fish foraging gametes gene glucose hamilton immunity inflammation maynard smith mutation oxygen parasite parental investment prevention prostaglandin protection reproduction resistance secretion signal transduction sperm staphylococcus toxicity treatment tumour