Hello, dear reader. This post is a sequel to my previous post on Neurotoxin, Nerves, Neurons and Impulses #2 where I discussed the action potential, depolarisation, repolarisation, and the disease of the nerves. In today’s post, I will extensively give an insight into the communication between neurons i.e talking about the synapse.
When an action potential reaches the end of an axon, it is passed on to the next neuron, or on to an effector cell such as a muscle or gland. The axon of one neuron does not usually make direct contact with the cell body of the next; the two cells are separated by a gap called a synapse.
The cell that carries a signal towards a synapse is a presynaptic cell; the cell carrying the signal away from the synapse is a postsynaptic cell. Presynaptic cells are always neurons but postsynaptic cells can be either neurons or effector cells.
THE MAIN FEATURES OF A CHEMICAL SYNAPSE
The axon terminal of a presynaptic neuron is swollen, and is often called the synaptic bulb or synaptic knob. It meets the cell body of the next axon, leaving a gap or synaptic cleft of about 20 nm. This is small – you would have to split a hair 250 times to get it to fit sideways into this gap. Even so, synapses have a high electrical resistance, and this gap is too big to allow the action potential to simply jump from one neuron to the next.
How do synapses work?
So how does the action potential get across? It is relayed by chemicals that diffuse across the gap and initiate an action potential in the neuron at the other side. The synaptic bulb contains many mitochondria, which provide energy for the manufacture of chemicals called neurotransmitters.
Neurotransmitters are small molecules and they can diffuse easily across the synaptic cleft. Synaptic vesicles are temporary vacuoles (membrane-bound spheres) that store neurotransmitter chemicals, the most common being acetylcholine. Synapses that have acetylcholine as their transmitter are called cholinergic synapses.
Types of neurotransmitters
Hundreds of neurotransmitters have been identified and there are certainly more to find. There are four main groups:
- Acetylcholine (neurons that release acetylcholine are described as cholinergic).
- Amino acids such as gamma-aminobutyric acid (GABA), glycine and glutamate
- Monoamines such as noradrenaline, dopamine and serotonin (neurons that release noradrenaline are described as adrenergic ). Synapses that use noradrenaline affect heart rate, breathing rate and brain activity. This is similar to the effect of the hormone adrenaline, which prepares the body for emergencies.
- Neuropeptides (chains of amino acids) such as endorphins .
Acetylcholine also acts throughout the brain, modifying the activity of other neurotransmitters. Nerve pathways in which acetylcholine is a neurotransmitter seem to be involved in motivation and memory. A very fast-acting enzyme called acetylcholinesterase breaks down acetylcholine into acetic acid and choline. These substances are reabsorbed through the presynaptic membrane. ATP energy from mitochondria is used to resynthesise acetylcholine, which is then returned to the vesicles. The chemicals in some ‘nerve gases’ work by inhibiting acetylcholinesterase. Many drugs and poisons exert their effect because they interfere with the functioning of synapses. And, in some people, release of too much noradrenaline causes the heart to race. One way of treating this is to use drugs known as beta-blockers. These drugs have molecular shapes similar to noradrenaline. Nerve gases used in war contain organophosphates that block the enzyme acetylecholinesterase, disrupting transmission of nerve impulses at synapses. Many insecticides contain organophosphates, which is why they are so dangerous to people working in agriculture. If exposed to insecticides in large quantities, nerve and brain damage can result.
Transmission at a synapse – a detailed explanation
As you read the next section, follow the stages of chemical transmission at a synapse numbered in the figure below:
- An action potential arrives at the synaptic bulb.
- Calcium channels open in the presynaptic membrane . As the calcium ion concentration inside the bulb is lower than outside, calcium ions rush in.
- As the calcium concentration increases, synaptic vesicles move towards the membrane.
- The vesicles fuse with the membrane, releasing neurotransmitters in the synaptic cleft.
- The short journey across the synapse takes about a millisecond, longer than an electrical signal takes to travel the same distance. This time is therefore called the synaptic delay .
- At the postsynaptic cell, the neurotransmitter binds to receptors the postsynaptic cell surface membrane.
- Some neurotransmitters open sodium channels in the postsynaptic membrane, causing an inflow of sodium ions. This creates an excitatory postsynaptic potential (EPSP) in the membrane. This potential lasts for only a few milliseconds and can travel only a short distance, but it makes the membrane more receptive to other incoming signals.
- Once the neurotransmitter has acted on the postsynaptic membrane, It is immediately released. If the transmitter remained, it could continue to stimulate the neuron, even without new impulses coming from the presynaptic cell.
- At cholinergic synapses, the enzyme acetylcholinesterase splits acetylcholine into choline and ethanoic acid. These components then diffuse back into the presynaptic membrane, where they are resynthesised to acetylcholine using the ATP from the mitochondria.
- At an excitatory synapse, an action potential is set up in the postsynaptic cell.
Does the arrival of an impulse at a synapse mean that an action potential is always generated on the postsynaptic neuron? The answer is no, because it would lead to chaos; all neurons would automatically pass on the signal to others. The significance of synapses is that they allow us to select particular pathways. Thus, at any one time, many more synapses need inhibiting than need stimulating. For this reason there are inhibitory synapses. Impulses arriving at these synapses make it more difficult for an action potential to be generated.
The neurotransmitters made by inhibitory synapses open potassium and chloride channels rather than sodium channels, and the resulting ion movement causes an IPSP – inhibitory postsynaptic potential – in which the membranes are hyperpolarised (to about -90mV) rather than depolarised. Usually, whether or not an impulse is generated in a particular nerve depends on the balance of inhibition and excitation that neurons receive at one moment. Receptor binding can also lead to the formation a second messenger (a transmitter substance) such as cyclic AMP (cAMP). This also changes the ionic permeability of the membrane, but it has a longer-lasting metabolic effect on the ion channels. Such long-term changes to brain neurons are thought to underlie memory.
SYNAPSES IN ACTION: FACILITATION AND SUMMATION
Synapses have a vital role in information processing . Transmission of information across synapses is graded. They can amplify or damp down the information they receive. In many cases, they will not transmit it at all. Facilitation is a result of spatial summation. It is not a result of temporal summation, which is simply the accumulation of EPSPs arriving before the preceding EPSP has died down.
A neuron can be fed information by both excitatory synapses that produce EPSPs and inhibitory synapses that produce IPSPs. Whether or not the cell develops an action potential is determined by the sum of all the excitatory and inhibitory synapses at any particular moment. Put simply, impulses arriving at some synapses will ‘excite’ the cell, while others will calm it down’. Whether or not a neuron generates an action potential depends on the balance of the two types.
Imagine a synapse discharging its transmitter on to a postsynaptic neuron. This will set up an EPSP, but if it is not big enough to reach the threshold, no action potential is generated. However, if other synapses discharge their transmitter at the same time, or shortly after, the EPSPs will add up, or summate , until an action potential is generated.
Generally, there are two types of summation:
- Temporal summation (i.e related in time) – summation of two or more impulses that arrive rapidly one after the other down the same neuron.
- Spatial summation – summation of two or more impulses arriving down different neurons at the same time (spatial = related in space). One neuron can receive information from many others – this is synaptic convergence. It follows that the arrival of one excitatory impulse will leave the neuron more responsive to another one. This is known as facilitation , and results from the summation of two or more synapses discharging their transmitter substance at the same time.
As a simple example of this idea, imagine the touch receptors from one area of skin feeding into one sensory neuron. An action impulse down just one receptor is almost certainly an insignificant stimulus, and can be ignored. It will not create an EPSP large enough to generate an action potential in the sensory nerve. However, if several touch receptors are stimulated at the same time, they will summate and produce a sensory impulse.
WHY HAVE SYNAPSES?
Synapses are important because they allow the transfer of information in nerve networks to be controlled. Synapses:
- allow information to pass from one neuron to another.
- help ensure that a nerve impulse travels in one direction only,
- allow the next neuron to be excited or inhibited,
- can amplify a signal (make it stronger),
- protect nerve networks by not firing when over-stimulated; when this happens the synapse is said to be fatigued; over-stimulation might damage muscle or gland tissue,
- can filter out low-level stimuli, for example, you fail to notice the sound a clock ticking because synapses are ‘filtering out’ the signal of sound,
- aid information-processing by the action of summation (adding together the effect of all impulses received),
- are modifiable and can form a physical basis for memory.
Overall, the significance of synapses cannot be over-emphasized.
They allow us to select particular neural pathways. The process or learning is largely one of educating the synapses. People can play the violin or plano, or play tennis, because their synapses allow their brains to co-ordinate their senses and muscles in the right way. Your memories, too, have a basis in synapses choosing specific pathways. If you are asked, ‘What’s the capital of France?’ your synapses will (I hope) select a pathway of neurons in your brain which will lead you to the answer ‘Paris’.
I will pause here for now. But, in my next post, I will explain a special sort of synapse called the neuromuscular junction. I will also discuss the relationship between drugs and synapses.
Thanks for reading