A neuron transmits nerve impulses through itself but when its time to send a message
to another cell, most neurons will send chemicals to the next neuron across a very small gap
between them.
The junctions between neurons and the next cell are called synapses.
There are three major types of cells that neurons will form synapses with:sensory receptor
cells, other neurons, and effector cells.
A sensory cell could be part of the eye, ear, nose, skin or any other place where senses
are used.
This sensory cell is connected to the skin and will pick up pain sensations.
The pain message may be sent to another neuron that could be part of the spinal cord or brain.
These intermediate neurons are also called interneurons.
The message can then be sent to a cell that will have an effect on another cell so they
are called effector cells.
In this example the effector cell is going to signal a muscle cell which would move this
area of the skin away from the source of pain.
These three cell types together make a simple reflex arc, going from sensation, to the central
nervous system to an action.
The chemicals released into the synapse are called neurotransmitters.
Many neurons have a very small fluid filled gap between the pre-synaptic cell and the
post-synaptic cell.
This gap is called the synaptic cleft and it’s only about 20 nm wide.
It’s a really, really tiny gap.
Now that we know some of the basics, we can look at the steps of synaptic transmission
in more detail.
First, a nerve impulse in the pre-synaptic neuron reaches the end of the membrane.
This causes calcium ions to diffuse into the cell through channels in the membrane.
the influx of calcium causes vesicles with neurotransmitters in them to move and fuse
to the membrane.
The neurotransmitters are released into the synaptic cleft by exocytosis.
They diffuse across the synaptic cleft and bind to receptors on the post-synaptic membrane.
The binding of neurotransmitters trigger sodium ion channels to open and pass the threshold
potential.
The action potential is propagated along the post-synaptic neuron.
Then the neurotransmitters are broken down and removed from the synaptic cleft.
If there isn’t enough neurotransmitter binding to receptors, then there won’t be enough
sodium flowing into the cell to reach the threshold potential.
This means that there is an “all or nothing” response.
Either there is enough neurotransmitter to start the action potential and the impulse
is sent, or there is no impulse.
In this case, there was not enough neurotransmitter released to trigger an action potential, so
the neurotransmitters will be broken down and the sodium potassium pumps will restore
resting potential in the post-synaptic cell.
There are many different types of neurotransmitter, but we’ll look at one in more detail right
now: Acetylcholine.
This neurotransmitter is made of an acetyl group and choline which must be combined together
in the pre-synaptic cell before it’s packaged into a vesicle.
Then it can be released into the synaptic cleft.
After acetylcholine binds with a receptor it is rapidly broken down by acetylcholinesterase,
an enzyme that is present in the synaptic cleft.
The acetyl group and choline can then be reabsorbed by the pre-synaptic neuron and combined again
into acetylcholine for reuse.
One type of insecticide takes advantage of the acetylcholine receptors to paralyze and
kill insects.
Neonicotinoids are synthetic compounds that are similar to nicotine but bind permanently
to the acetylcholine receptors.
the acetylcholinesterase cannot break the neonicotinoids down and the neurons can no
longer receive messages or send action potentials.
This is what leads to paralysis and death in the insects.
The effects are very small in humans and mammals, but the neonicotinoids don’t discriminate
between types of insects.
Honeybees and other beneficial insects are inadvertently killed by neonicotinoids too.