A synapse is the site of communication between the end of an axon and the beginning on a dendrite. It can also be between a neuron and a non-neuron cell such as a muscle cell. In the olden days people used to think that there were no gaps between neurons, and they just extended continuously throughout the body (silly eh?). Now we know better, much better. More for you to learn!
Let’s just get the overall picture first: a signal may be transmitted from one neurone to another via axons and dendrites. A sending neurone passes the signal to a receiving neurone which may pass it on to another receiving neurone, thus becoming itself a sending neurone…
Clearly, each nerve cell (=neurone) only has one axon but multiple dendrites. How does this regulate the way in which certain signals are deemed to pass the threshold required for them to be passed along as opposed to them ceasing there?
There are 2 ways: either multiple signals are sent via the same synapse in a short space of time, or single signals are sent via synapses at different locations. Therefore, the first is called temporal summation while the second is called spatial summation. Summation simply refers to the sum of signals sent to reach the threshold for transmission.
Another nugget to be gotten out of the way: the signal transmitted is always axon –> dendrite, unidirectional, because specific neurotransmitter receptors are only found on the dendrites!
Now let’s delve into the details…
The first is a pre-synaptic neurone, the second is a post-synaptic neurone. Before and after the synaptic gap itself, or the synaptic cleft. The action potential reaching the pre-synaptic neurone causes some calcium channels which respond to voltage to open. These are called voltage-gated ion channels. Essentially this step converts the electrical energy into chemical energy. Ca+ ions rush inside.
As a result, vesicles (membrane-bound spaces containing a specific compound) migrate towards the outer edge of the neurone membrane and fuse (exocytosis) so that their contents – neurotransmitters in our case (you know, the good stuff like serotonin, oxytocin, dopamine, etc.) – are released into the synaptic gap.
Specific neurotransmitter receptors found on the post-synaptic neurone bind the neurotransmitters causing Na+ channels to open. Na+ ions rush into the post-synaptic neurone. If they’re angry enough (we’re talking about a steep electrochemical gradient of course), an action potential will be initiated and carried forward. Chemical energy has once again been converted into electrical energy. Magic.
Not all synapses are excitatory and encourage a signal to be carried forward. Some are inhibitory and prevent an action potential being carried forward. A common signal molecule (neurotransmitter) for this is GABA. Upon binding to receptors on the membrane, it triggers an uptake of chlorine ions into the cell, or a release of sodium ions out of the cell; both of which shift the transmembrane potential downwards, making it more negative.
Unlike a synapse, a neuromuscular junction has a signal travelling from a motor neurone to a muscle cell’s motor end plate. Everything happens just the same, except that the specific neurotransmitter involved here is acetylcholine. Eventually there is not another action potential created, but rather a depolarisation of the motor end plate which results in muscle contraction as it spreads along muscle fibers.
What regulates this? It has to stop somehow right? Either the acetylcholine diffuses from the synaptic cleft, or it is broken down by an enzyme called acetycholinesterase into products including choline. This can be uptaken by the pre-synaptic neurone which then synthesises it back into acetylcholine. Recycling gone mad. Not funny though, these neurotrasmitters really can be involved with some nasty mental illness. Going back to the neuromuscular junction, problems with the acetycholine receptors are also the cause of certain muscle conditons.