Nerve Transmission

Transmission of Action Potential (AP)
1. Neuron to Neuron
  1. Excitatory → causes new AP to keep moving
  2. Inhibitory → causes AP to stop moving
2. Neuron to Muscle
  1. Excitatory only

Nursing Points

General

Transmission of AP from neuron to neuron
1. Types of synapses
  1. Electrical synapse
    1. Mostly in brain
    2. Connected by gap junctions @ synapse
    3. Very quick
  2. Chemical synapse
    1. Requires movement of chemicals across space
      1. Neurotransmitters
    2. Structure of chemical synapse
      1. Synaptic knob/end foot
        
        Contains synaptic vesicles → contain neurotransmitters
      2. Synaptic cleft
      3. Postsynaptic membrane with receptors
2. Excitatory and inhibitory synapses
  1. Excitation @ Synapse
    1. AP reaches synaptic knob
    2. Calcium enters synaptic knob
      1. Stimulates exocytosis
        
        Vesicles release neurotransmitters (NT) into synaptic cleft
    3. NT diffuses across cleft to combine with receptors on postsynaptic membrane
      1. Causes local depolarization
      2. Membrane potential more positive
    4. Local depolarization summates until threshold reached
      1. Action Potential starts in postsynaptic neuron
      2. AP moves down axon
    5. NT are either absorbed or destroyed by enzymes
    6. Examples of excitatory NT’s
      1. Acetylcholine
      2. Norepinephrine
      3. Dopamine
  2. Inhibition @ Synapse
    1. Sequence
    2. Same start as excitation → AP reaches end foot → calcium → vesicles release NT → NT diffuse across membrane
    3. Inhibitory NT causes hyperpolarization in postsynaptic neuron due to either:
      1. Loss of Potassium (+)
      2. Gain Chloride (-)
    4. Membrane potential becomes more negative, therefore can’t initiate an AP
    5. Examples of inhibitory NT’s
      1. Serotonin
      2. GABA
Transmission of AP from neuron to muscle (neuromuscular junction)
1. Excitation only – no inhibitory
2. Same start as excitation → AP reaches end foot → calcium → vesicles release NT → NT diffuse across membrane
  1. Action depends on the NT released and the muscle(s) involved
3. Effects of exogenous chemicals on neuromuscular junction
  1. Atropine
    1. Inhibits Acetylcholine (Ach)
  2. Physostigmine and neostigmine
    1. Inhibit Acetylcholinesterase (Achase) activity
      1. The enzyme that deactivates Ach
      2. Net increase in Ach activity
    2. Clinical Application → Myasthenia Gravis
      1. Too much AChase activity in proportion to ACh activity
      2. Give physostigmine to inhibit Achase
      3. Refer to Myasthenia Gravis lesson in Neuro (Med-Surg) course

References
Betts, J.G., et al. (2017). Anatomy and physiology. Houston, TX: OpenStax, Rice University. Retrieved from https://openstax.org/details/books/anatomy-and-physiology?Book%20details

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Transcript

In this lesson we’re going to look at nerve impulse transmission.

So this impulse transmission could be from neuron to neuron or from neuron to muscle. With neuron to neuron transmission, we can either have excitatory or inhibitory signals. Excitatory means that it keeps that action potential going – it continues to send the signals or creates an action of some kind. Inhibitory is exactly the opposite – it means that when the signal gets there, it actually STOPS the action potential. So it inhibits sending the signal any further. When we see neuron to muscle, we only see excitatory – because it’s causing an action in that muscle.

There are also two types of synapses – remember a synapse is the just the connection between the neuron and whatever it is going to – either another neuron or a muscle. So you could have an Electrical Synapse or a Chemical synapse. Electrical synapse occurs when you have two axons that are right against each other and have what are called gap junctions. The signal literally just jumps right across from one axon to another. On the other hand, a chemical synapse utilizes neurotransmitters. These are chemical messengers that are housed in these vesicles in the axon terminal. And when a signal arrives here, it stimulates the vesicles to release those chemicals across the synapse. They bind with a receptor to produce whatever action they’re supposed to produce.

So remember there are two possible general actions – excitation or inhibition. A few examples of excitatory neurotransmitters are norepinephrine, dopamine, and acetylcholine. Each of these has their own specific type of receptor as well. So – here’s what excitation looks like at the synapse. The action potential arrives at the end foot and causes calcium to rush in – that stimulates the vesicles to release the neurotransmitters across the synapse. They arrive on the other side of the synaptic cleft and connect with their receptors. With excitatory neurotransmitters, this connection with the receptor will actually stimulate a NEW action potential to be started on the other side. If this is a neuron – it will send that action potential down the length of that neuron and on its way. If it’s a muscle, this action potential will stimulate a muscle contraction. Make sure you check out the muscle contraction lesson, too, to see what happens there!

Now, with inhibitory neurotransmitters – the whole process is the same right up until it hits the receptor. Action potential arrives, calcium causes the release of the neurotransmitter from the vesicles, the neurotransmitter goes across and binds with the receptor. BUT – then instead of causing depolarization and a new action potential – it actually causes HYPERpolarization and STOPS the Action Potential from propagating. So, it inhibits the signal from continuing. Two common inhibitory neurotransmitters are serotonin and GABA. Again – this is only in neurons, not in the neuromuscular junction.

One quick thing to know is that other exogenous chemicals can have an effect on this process at the neuromuscular junction. That just means that our nerves and muscles can be doing everything right, but if these chemicals are present at that synapse – it changes what goes on. The first one is Atropine – it actually inhibits acetylcholine. So acetylcholine gets released, but then can’t actually do its job. The other is neostigmine or physostigmine – these are drugs used in a condition called myasthenia gravis that will actually inhibit acetylcholinesterase. Acetylcholinesterase is an enzyme that deactivates acetylcholine once it’s no longer needed. That would be a normal process. But when physostigmine is present the enzyme can’t do its job. So that means that the acetylcholine can keep stimulating and keep working for longer. Check out the lesson on myasthenia gravis to understand why that can actually be a good thing.

So let’s review nerve transmission. Remember, it could be an electrical synapse using gap junctions or it could be a chemical synapse using neurotransmitters. That could cause either an excitatory signal to keep the action potential going or an inhibitory signal to stop the action potential altogether. And just remember there are many many specific neurotransmitters that each have their own receptors and actions at the synapse.

That’s it for the A&P of nerve transmission. Make sure you check out all the resources and associated lessons attached to this lesson. Now, go out and be your best self today. And, as always, happy nursing!

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