Let’s delve into the basics of nervous transmission by looking at a motor neurone. Here is the structure of a myelinated motor neurone:
Labelled “insulating sheath”, the myelin sheath is responsible for protecting the electrical impulses that run across the neurone.
But first, what happens in a resting state where no impulses are being sent?
This is the resting potential where the membrane permeability differentiates between sodium (Na+) and potassium (K+) ions so that at any given time there are more Na+ ions outside than inside and more K+ ions inside than outside.
According to these electrochemical gradients, Na+ ions should move back inside to balance out their concentration (equilibrate) while K+ ions should move back outside the membrane until the concentrations are equal inside and out. This clearly isn’t the case, so what gives?
Found on the membrane there are Na+/K+ pumps which carry out active transport against the electrochemical gradient of these ions. The resting potential of the membrane is negative on the inside and positive on the outside – but how? Aren’t both sodium and potassium ions positively charged? This is achieved by the pump transferring 3 Na+ ions out while taking only 2 K+ ions in. This is where the difference comes from.
Now we know that in the absence of an action potential the resting potential of the neurone membrane is negative (about -70mV; millivolts). What precedes an action potential and how does it unfold?
A stimulus may depolarise the membrane by opening up Na+ channels for those ions to rush into the axon. An action potential will occur only if the depolarisation passes a certain threshold. For example, if it reaches -60mV up from -70mV it will not trigger an action potential with a threshold of >-45mV.
Therefore, the power of an action potential is not proportional to that of its stimulus. It either happens or it doesn’t. This is called the all-or-nothing principle.
This is how the voltage of the axon membrane changes during an action potential:
The rush of Na+ ions into the membrane during depolarisation causes the voltage to become positive. Note how only the depolarisation that has passed the threshold initiates an action potential.
Repolarisation occurs when Na+ channels begin to close and K+ channels open, resulting in a rush of K+ ions out of the axon. Before all the K+ channels close, hyperpolarisation occurs which briefly sees the voltage drop below the resting potential level.
This also represents the refractory period where either no stimulus however strong can initiate another action potential (absolute refractory period), or a stimulus slightly greater than usual would be required for an action potential to occur (relative refractory period).
Finally the resting potential is achieved.
The Myelin Sheath
This insulating sheath made up of Schwann cells is key in ensuring fast signal transmission. The signal is able to “jump” along the axon without losing its strength. Instead of the signal being gradually weakened by the resistance that an axon membrane exposed to the environment creates, this signal is shielded by the myelin sheath. The nodes of Ranvier in between the Schwann cells are the only points of axon membrane permeability to its environment.
Each pink cell is a Schwann cell. Due to the jump-like action, this conduction is termed saltatory conduction. Factors that affect conduction other than myelination and saltatory conduction (which allow speeds many times faster compared with no myelination) include temperature and axon diameter.
Since chemical movement (kinetic energy) relies on temperature, an optimal temperature maximises conduction. A temperature lower than this would slow it down. This is due to a slower opening of sodium channels for example, and also a slower inactivation resulting in a longer delay.
Axon diameter affects conduction in terms of resistance. The signal travelling along a thin axon encounters the resistance of the axon membrane, while for an axon with larger diameter, a smaller proportion of the signal is met with resistance in this way. The signal carried on the inner section of the axon has no resistance and can travel faster.
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.