Neurophysiology revision

Question 1

What are the functions of neurons?

Answer 1

They carry out cell processes, interconnect cells, transmit information and use electrical signals

Question 2

How do neurons work

Answer 2

Information arrives at the cell body via dendrites (and cell bodies) where it is assimilated and processed

Processed information is then digitised into action potentials which are transmitted along the axon

At the end of the axon th information is passed to the target (muscle or neuron) at boutons

Question 3

How do action potentials occur?

Answer 3

Action potentials are an all or nothing response, they can be more intense or spread out. They are graded by frequency more or less rapid (bullets from gun or vibration)

They occur mainly in axons and start at the cell body (axon hillock)

They are transmitted towards the end of the axon (synapse)

Question 4

What is the charge inside a neuron and how does this affect transmission of action potentials?

Answer 4

Inside a neuron has a negative potential of about -70mV which is called the resting membrane - maintained by ion pumps.

The resting potential means that we need enough positive sodium ions to come into the cell to reach threshold so we can trigger an action potential.

Question 5

Why is the refractory period important?

Answer 5

It ensures that only 1 impulse is generated at a time forcing it to travel in one direction

Question 6

What are the steps to trigger and action potential?

Answer 6

1). Na + channels open and Na + begins to enter the cell (rapid depolarisation)

2). K + channels open and K + begins to leave the cell

3). Na + channels come refractory and no more Na + enters the cell

4). K + continues to leave the cell causing a repolarisation and the membrane to return to resting level (hyperpolerisation occurs with overshoot)

5). K+ channels close and Na + channels reset

6). Extra K + outside diffuses away

Question 7

Describe how the voltage dependent sodium channels work?

Answer 7

At resting potential Na + channels are closed - the activation gate is closed

Depolarisation opens the activation gate and Na + flows into the cell along the electrochemical gradient

A delayed component of voltage dependent activation is blocking of th channel by th inactivation gate (after about 0.5ms - in built timer)

Depolarisation of the cell re-sets the two gats to their equilibrium positions

Question 8

How does the voltage dependent sodium channel affect the refractory period?

Answer 8

The voltage dependent sodium channel helps to set the refractory period of the action potential

During the absolute refractory period the cell cannot b stimulated to its threshold potential - all Na channels closed

During relative refractory period a strong stimulus than normal could induce an action potential - some Na + ready but more K_ channels are open than usual - cell still hyper polarised

Question 9

How can we increase the speed of conduction?

Answer 9

Increasing the diameter
increases the speed of conduction as there is decreased resistance

To increase speed for a diameter the axon is insulated in a fatty sheath called myelin

Question 10

What helps to build myelin?

Answer 10

Schwann cells in the PNS

Oligodendrocytes in the CNS

Question 11

How do local currents travel in myelinated axons

Answer 11

By salutatory (jumping) conduction

local currents can extend further as the normal current leakage is restricted with the addition of the myelin sheath (decreased capacitance)

This causes the nerve impulse to flow rapidly along the inside of the axon to the node where ionic depolarisation takes place. This requires fewer ions and is energy saving. and then fast conduction along side of the axon resumes

Action potentials only exit at the node of Ranvier

Question 12

How do unmyelinated nerves work?

Answer 12

Unmyelinated fibres, larger diameter = faster conduction

Question 13

Why do we have nerves myelinated ?

Answer 13

To keep the nervous system compact so small diameter myelinated fibres can conduct faster than large unmyelinated ones

Question 14

If conduction in a myelinated axon slowed down what would be the reason for this?

Answer 14

Demyelination

Question 15

What is the most basic way to describe a neuron?

Answer 15

They are elongated secretory cells - polarised (axon - apex; dendrites - base)

Question 16

What do secreted chemical signals into a narrow gap cause?

Answer 16

They influence another cell, whether another neuron or muscle to make in impulse

This occurs in the synapse

Question 17

How do neurons communicate?

Answer 17

The axon terminal of the presynaptic cell forms a swelling called a bouton. The bouton is next to the synaptic cleft where the postsynaptic cell will be on the other side of this cleft.

The bouton contains vesicles which transports molecules of neurotransmitters

Question 18

How are vesicles sat at the bouton and released?

Answer 18

Vesicles and the presynaptic membrane recognise each other.

v-Snare and t-Snare complex folds strongly to draw the vesicle membrane and pesynaptiic membrane close

The vesicle is then docked on the membrane (exocytosis cannot happen here as it is ‘clamped’ by complexin). This created a pool of docked vesicles at the synapse and helps synchronising release.

Action potentials triggers calcium influx at end bulb. Calcium induces synaptotagmin to displace complexin - which triggers exocytosis

Question 19

How can toxins affect SNARE mechanisms?

Answer 19

Toxins target regulators of synaptic SNARE mechanisms

E.g botulinum toxins - stop vesicle release - global paralysis caused

Tetanus toxins - stop vesicle release - glycine/GABA (tetany)

Question 20

How are neurotransmitters recycled?

Answer 20

They are released by exocytosis and diffuse to the post-synaptic membrane where they bind to receptors - then inactivated by diffusion, re-uptake or enzyme inactivation

Question 21

How can we class our receptors?

Answer 21

How they are activated;
- Ionotropic - directly gate ion flow
or
- metabotropic - indirectly gate ion flow or activate other pathways

Positive/negative effects;
- excitatory
or
- inhibitory (depending on the ions they let into/out of the cell)

Question 22

How does ionotropic receptors work?

Answer 22

1). Neurotransmitter binds to the outside of the channel

2). this causes a conformational change and the channel opens

3). ions flow across the membrane

Question 23

How does metabotropic receptors work?

Answer 23

1). Neurotransmitter binds to the outside of a g-protein linked receptor

2). this causes the G-protein to be activated

3). The G-protein subunits or intracellular messengers modulated ion channels

4). The subunits opens the channel

5). ions flow across the membrane

Question 24

How does neurotransmitters effect cells postsynaptically?

Answer 24

In their target cells (neurons and muscles) the neurotransmitter causes a change in the potential f the post synaptic membrane

This is NOT an action potential and has a special name

Post synaptic potential of which there are 2 types;
- Post synaptic excitatory potential (EPSP)
- Post synaptic inhibitory potential (IPSP)

Question 25

How do PSP’s work?

Answer 25

Post synaptic potentials are caused by the passage of ions through ion channels which have been opened following receptor/neurotransmitter interactions

Question 26

How does EPSP work?

Answer 26

A net flow of positive ions into the cell depolarises the membrane (bringing it closer to threshold) and thus termed EXCITATORY.
Single EPSP’s rarely result in an action potential

Question 27

How does IPSP work?

Answer 27

A net flow of negative ions into the cell hyperpolarises the membrane (bringing it further away threshold) and thus termed INHIBITORY.

Question 28

What happens to the amplitude of the signal from PSP’s with distance and time?

Answer 28

For both PSP’s the amplitude of the signal decreases with distance from the receptors and also with time

Question 29

How do EPSP’s and IPSP’s work together?

Answer 29

They can do summation and integration.

In spatial summation the action potentials arrive close together in space along different parts of the axon. You can keep adding until you generate an action potential

In temporal summation the action potentials arrive sloe together in time along the same axon, these are close enough together to summate.

This causes integration of information at the post synaptic membrane

Question 30

How are action potential communicated in sensory receptors?

Answer 30

A stimulus will activate the sensory receptor and trigger an action potential which will be sent to the sensory neurons which will then pass that information onto the CNS.

There is myelin on a lot of these to speed up flow into CNS

Question 31

How do sensory receptors tell the brain how long and the extend of the sensation they are feeling?

Answer 31

They code duration and magnitude of external signals as a greater potential - usually stronger external signals the higher the frequency of AP’s in the axon.

Question 32

What are the 2 different ways sensory receptors can adapt to stimulus?

Answer 32

Slowly adapting generator potential - They can respond to a constant stimulus

Rapidly adapting generator potential - just responds to a change in impulse then stops

Question 33

Hoe do stretch reflexes work?

Answer 33

They enable the muscle to oppose external forces that tend to elongate them

These are mediated by sense organs within the muscle known as muscle spindles

Question 34

Describe the spindle fibre mechanism?

Answer 34

The spindle has contractile Gamma motor neuron efferent from the spinal cord in the top and bottom portions of the spindle as well as elasticity. The motor neuron efferent regulates the degree of contraction

The middle portion is less elastic/contractile and is the sensory portion which sends sensory afferent to the spinal cord with info on the stretch . The Group 1A primary and Group 2 secondary sensory afferents are found here in this middle portion.

Question 35

How does reflexes work?

Answer 35

A stretch is detected in the muscle by the sensory afferent 1A (primary) and Group 2 (secondary) receptors. This information is set to a-motoneuron in the spinal cord which contracts the muscle and the synergist muscle to deal with the weight load. The inhibitory neuron in the spinal cord relaxes thee antagonist muscle to make movement of targeted muscle easier and prevent muscle rupture.

The brain sends control signals before all of this happens to present the responsiveness of the sensory receptors etc

Question 36

How do we measure nerve conduction?

Answer 36

We do not measure individual action potentials we measure the sum of all the action potentials in a nerve or the resulting stimulus detected in target cells e.g - skeletal muscle

Question 37

What are 2 nerve conduction studies?

Answer 37

CMAP - compound muscle action potential -
Stimulate into muscle then measure changes in muscle cells in target (records at muscle)

SNAP - Sensory nerve action potential - Can stimulate a nerve then measure reading at extremity (records along nerve)

Question 38

What happens in neuropathy?

Answer 38

There is slowed conduction velocity - less myelin (manifests as increased latency and also increased difference between latency for both sites - e.g Multiple Sclerosis

Question 39

Name some neuropathy conditions?

Answer 39

Multiple Sclerosis

Carpal tunnel syndrome (median nerve is compressed at wrist resulting in numbness or pain)

Question 40

Name some channelopathies

Answer 40

Channelopathies are diseases that develop because of defects in ion channels caused by either genetic or acquired factors

Inherited - calcium, chloride potassium, sodium, glycine, GABA, Ach

Autoimmune
- Myasthenia gravis
- Lambert-eaton myasthenia syndrome (associated with small cell lung Ca)
- Limbic encephalitis (memory loss; associated with underlying neoplasm)

Question 41

What goes wrong in Myasthenia Gravis?

Answer 41

Its an Auto-immune disease that causes;
• skeletal muscle weakness that increases during periods of activity and improves after
periods of rest

• eye and eyelid movement, facial expression, chewing, talking, and swallowing are especially susceptible

• paralysis of the respiratory muscles

Due to production of auto-antibodies;
- most commonly directed against the acetylcholine receptor (nicotinic)
- some impair the ability of acetylcholine to bind to receptors
- some lead to the destruction of receptors

Can treat with supplement of neurotransmitter e.g ACh