Topic 6: Human physiology : 6.5 Neurons and Synapses

Neuron

Saltatory conduction

Nerve fibres conduct electrical impulses along the length of their axons. Some of these axons such as interneurons are unmyelinated, and therefore the impulse travels much slower
The greater the diameter, the greater the speed of the nerve impulse
Some axons are surrounded by a mixture of protein and phospholipids called myelin that collectively form a myelin sheath
Many layers of myelin are deposited around the axon by special cells called Schwann cells
The myelin sheath insulates the axon and greatly increases the speed of the nerve impulse
In between the myelin are gaps called the nodes of Ranvier
In myelinated neurons, the impulse can jump from one node to the next. This is called saltatory conduction
This allows myelinated neurons to conduct impulses up to 100x faster than unmyelinated axons

Resting potential

The time period when a neuron that is not conducting a nerve impulse, but is ready to conduct one, is called the resting potential.
This membrane potential is due to an imbalance of positive and negative charges across the membrane
Sodium-potassium pumps pump \(Na^+\) out of the axon and \(K^+\) into the axon
Three \(Na^+\) are pumped out of the neuron and two \(K^+\) are pumped into the neuron
This creates a concentration gradient of \(Na^+\) (outside to in) and of \(K^+\) (inside to out)
The membrane is also much more permeable to \(K^+\) as \(Na^+\), so \(K^+\) diffuses back out of the neuron through leak channels
This means the Na+ concentration is much greater outside the neuron
There are also negatively charged ions permanently located in the cytoplasm of the neuron
These conditions create a resting membrane potential of -70 mV inside the neuron

Depolarisation

The arrival of an action potential caused by a stimulus causes a depolarization of the membrane as \(Na^+\) channels begin to open.
If the membrane potential reaches a threshold level of -55mV. Many more voltage-gated \(Na^+\) channels open and \(Na^+\) rapidly diffuses into the neuron
The inside of the neuron becomes more positively charged than the outside of the neuron (depolarization)
The voltage can rush up to +40mV

Repolarisation

\(K^+\) channels open and \(K^+\) ions diffuse out of the neuron making the inside negative again (repolarization)
After the action potential, there is a refractory period where the impulse cannot go back in the same direction. This ensures a one-way nerve impulse

Properties of action potential

As a depolarization occurs in one part of the neuron, the positive charge triggers the \(Na^+\) channels to open in the nearby regions causing an action potential to occur.
This action potential will cause a depolarization in the next region.
The propagation of action potentials will continue along the axon of the neuron.
Nerve impulses move in one direction along the neuron from one end of the neuron to the other end
A refractory period occurs after depolarization which prevent the electrical impulse from traveling backwards along the axon

Oscilloscope traces of action potential

Synapse

Synapses are junctions or structures between the pre-synaptic and post-synaptic membrane of two cells in the nervous system
The junction can be between a neuron and an effector such as a muscle or a gland
It can be between two different neurons.
A junction also exists between the sense receptor cells and the sensory neurons
Neurotransmitters are chemicals diffuse across a synapse from pre-synaptic membrane to post-synaptic membrane to send a signal to the next cell
As the nerve impulse reaches the axon terminal of the pre-synaptic neuron, the positive charge from the depolarization causes voltage-gated channels
permeable to \(Ca^{2+}\) to open.
\(Ca^{2+}\) flows into the pre-synaptic neuron increasing the amount of \(Ca^{2+}\) in the pre-synaptic neuron.
This \(Ca^{2+}\) causes vesicles containing neurotransmitters to bind to the membrane and release their neurotransmitters into the synaptic cleft (space between pre and post synaptic neuron).
These neurotransmitters diffuse across the synaptic cleft and bind to receptor sites on the membrane of the post synaptic neuron.
The binding of these neurotransmitters open ion channels allowing ions such as \(Na^+\) to diffuse into the post synaptic neuron.
This influx of positive charge possibly leads to an action potential and a depolarization in the post synaptic neuron.
The neurotransmitter is reabsorbed by the pre-synaptic neuron or broken down in the synapse by enzymes

The threshold potential is the critical level to which a membrane potential must be reach in order to initiate an action potential
Neurons fire or a nerve impulse is generated by an “all or nothing”
When a stimulus occurs, some \(Na^+\) channels open causing the membrane potential to become more positive
If enough \(Na^+\) diffuses into the neuron and action potential is generated
At a synapse, binding of a neurotransmitter at the post-synaptic membrane causes \(Na^+\) to diffuse into the neuron (if excitatory)
This can cause a depolarization of the neuron if enough neurotransmitters are released

Acetylcholine

Acetylcholine is a neurotransmitter
It is largely used at the neuromuscular junction, meaning it is released by motor neurons and binds to receptors on muscles
It is also used in the autonomic nervous system
Acetylcholine is created in the pre-synaptic terminal by combining a water soluble nutrient called choline with an acetyl group
Acetylcholine is secreted by the pre-synaptic membrane of a neuron
The neurotransmitter diffuses across the synapse and binds to a receptor on the post synaptic membrane (causing an action potential if a threshold is reached)
Once it has released from the receptor, an enzyme called acetylcholinesterase breaks down into choline and acetate
Choline is reabsorbed back into the pre-synaptic neuron where it is combined with another acetyl group to form another acetylcholine neurotransmitter

Pesticides using neonicotinoids

Neonicotinoids bind to acetylcholine receptors in cholinergic synapses in the CNS of insects
Acetylcholinesterase does not break down neonicotinoids therefore binding is irreversible
Acetylcholine now can’t bind and neural transmission is stopped
The insects go through paralysis and then death
A benefit to this pesticide is that it is very effective in killing pests and it is not highly toxic to humans and mammals
The problem is that it also effects beneficial insects such as honey bees. There is conflicting evidence if this is the case or not
Many places such as the EU and Ontario, Canada has banned neonicotinoid pesticides

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