nerves

Question 1

What are the 3 layers of meninges?

Answer 1

Dura, arachnoid and pia matter.

Question 2

What are the 3 main parts of the brain and what do they contain?

Answer 2

1) Forebrain (cerebrum and diencephalon), 2) midbrain (tectum and tegmentum), 3) hindbrain (cerebellum, pons and medulla)

Question 3

What are the 3 types of membrane potentials?

Answer 3

Resting membrane, graded and action. Resting membrane keeps cells ready to respond, graded potentials decide when action potentials should be fired and action potentials transmit signals over long distances to allow something to happen.

Question 4

Which ion moves out of the cell at rest?

Answer 4

K+ through leaky K+ channels. As it moves out it develops an electrical gradient.

Question 5

What is the equilibrium potential?

Answer 5

The membrane potential at which the electrical potential is exactly equal and opposite to the concentration gradient.

Question 6

Which equation can predict equilibrium potential?

Answer 6

Nernst for a single ion species.

Question 7

What is the threat of bananas?

Answer 7

They contain a lot of K+. If there is a lot of extracellular K+ then this reduces the concentration gradient and increases the RMP. The cell depolarises and releases an AP. Hyperkalaemia causes ventricular fibrillation.

Question 8

What is RMP in striated muscle and normal cells?

Answer 8

Striated muscle cells -90mV. Normal cells -70mV due to other leaky channels –> Na and Cl which are both at higher concentrations outside the cell.

Question 9

When is RMP lost?

Answer 9

When K+ moves out of the cell down its concentration gradient. If extracellular K+ rises the concentration gradient is decreased.

Question 10

When would a cell become hyperpolarised?

Answer 10

If K+ channels or Cl- channels are opened as this would make the cell more negative. Opening Ca2+ channels or Na+ channels makes the cell depolarise.

Question 11

What happens if the Na/K pump is poisoned?

Answer 11

Little immediate effect as cell will only depolarise a few mV. Major contributor is K+.

Question 12

When Na+ channels open, Na+ enters the cell because?

Answer 12

Electrical and concentration gradients push it in.

Question 13

What makes a cell depolarise?

Answer 13

External stimuli acting on specific sets of ion channels. Threshold is -55mV.

Question 14

What are EPSP’s and IPSP’s?

Answer 14

EPSP’s make a cell fire an AP. IPSP’s stop the cell reaching threshold.

Question 15

What are the 4 main properties of graded potentials?

Answer 15

Decremental (only useful over short distances), electrotonic, non-propagated and local. They can also summate and are depolarising/hyperpolarising.

Question 16

Give examples of graded potentials.

Answer 16

Generator potentials at sensory receptors. Post-synaptic potentials at synapses. End-plate potentials at NMJ. Pacemaker potentials at pacemaker tissues. These all determine whether an AP will be fired.

Question 17

Does the strength of the stimulus have an effect on the graded potential?

Answer 17

Yes. Strength is encoded in amplitude. More neurotransmitter, for example, will make a bigger potential.

Question 18

Give 2 examples of IPSP’s hyperpolarising a cell.

Answer 18

A neurotransmitter binds to the Cl- ion channel (ionatropic receptor). Cl- flows in and the cell becomes more negative. This is a fast IPSP. K+ is a metabotropic receptor. If more K+ channels are opened K+ flows out which makes the cell more negative. This is a slow IPSP.

Question 19

Give 2 examples of EPSP’s depolarising a cell.

Answer 19

A fast EPSP is to open channels permeable to Na+ and K+. More Na+ gets in than K+ gets out. A slow EPSP is to block leaky K+ channels.

Question 20

What is the difference between ligand-gated and voltage-gated ion channels?

Answer 20

Ligand-gated are when neurotransmitters bind to ion channels to open or close them. Voltage-gated are when the membrane potential depolarises and this opens ion channels like AP’s.

Question 21

What is the difference between temporal and spatial summation?

Answer 21

Summation is when graded potentials add on to each other. Temporal is when one EPSP occurs and a second occurs shortly after. Spatial is the same effect but for more than 1 neuron. Temporal and spatial summation always occur together. This is synaptic integration and it decides whether or not a cell will fire an AP.

Question 22

What happens when the cell reaches threshold (-55mV)?

Answer 22

There is a sudden massive depolarisation that shoots up to +30mV then rapid repolarisation beyond resting level. This is the action potential.

Question 23

What is the ionic basis of the AP?

Answer 23

When a cell reaches threshold, voltage-dependent Na+ channels open and Na+ floods as there is a massive increase in permeability. Then repolarisation occurs when K+ permeability rises and K+ channels slowly begin to open. This causes hyperpolarisation. Eventually they shut and RMP returns to normal.

Question 24

What is the refractory period?

Answer 24

The period immediately after an AP has been fired when no matter how much depolarisation occurs, another AP cannot be fired as ion channels need to rest.

Question 25

How do local anaesthetics and toxins work?

Answer 25

Procaine and lidocaine block the voltage-gated ion channels so APs cannot be transmitted. Puffer fish tetrodotoxin and shellfish saxotoxin also have this effect.

Question 26

Give 7 properties of AP’s.

Answer 26

1) have a threshold, 2) are all or none, 3) they cannot encode stimulus intensity in their amplitude, only in frequency, 4) self-propagate, 5) mediated by voltage-gated channels, 6) have a refractory period, 7) travel slowly but improved by myelination.

Question 27

Why does depolarisation only move forward down an axon?

Answer 27

Na+ channels open in one part of the membrane, which in turn opens voltage-gated Na+ channels in the next part. This cannot move backward as these channels are in the refractory state.

Question 28

Which cells perform myelination in the PNS and CNS?

Answer 28

Schwann cells in the PNS and oligodendrocytes in the CNS. These form the myelin sheath around neurones.

Question 29

Where are Na+ channels in the membrane?

Answer 29

In gaps between myelin called the nodes of Ranvier.

Question 30

What is saltatory conduction?

Answer 30

Myelin increases the resistance of the membrane so that AP’s spread like a local current to the next segment and evoke a new AP there. It speeds up conduction down a neurone.

Question 31

What are the effects of de-myelination?

Answer 31

Local current decays faster and cannot depolarise the next node to threshold. Examples include MS (damage to myelin) and Guillaine-Barre syndrome (immune system attacks the PNS).

Question 32

What is the classification of nerve fibre types?

Answer 32

1) afferent (sensory) which detect changes in sensory stimuli, 2) interneurones which are in the spinal cord and decide what to do with the stimulus, 3) efferent (motor) carry effectors.

Question 33

Describe the different nerve fibres in the compound action potential.

Answer 33

Large ones are most sensitive to pressure. Smaller ones most sensitive to anaesthetics. A-alpha: efferent and for proprioception. A-beta: touch and pressure. A-gamma: motoneurones of muscle spindles. A-delta: afferent sensory. B: pre-ganglionic un-myelinated. C: heat and slow pain, un-myelinated.

Question 34

How does an AP evoke contraction in muscles?

Answer 34

Contraction is triggered by AP’s in sarcolemma (tubular sheath that envelops the fibres of skeletal muscle).

Question 35

Describe the events at the NMJ (11).

Answer 35

AP in a motor neuron. Opens voltage-gated Ca2+ channels in the pre-synaptic terminal. Triggers fusion of vesicles. ACh is released. ACh difuses across the synaptic cleft. Binds to ACh nicotinic receptors. Opens ligand-gated Na+/K+ channels. Evokes a graded (local) potential (end-plate potential). Adjacent membrane is always depolarised to threshold. This popens voltage-gated Na+ channels and evokes a new AP. ACh is removed by acetylcholinesterases.

Question 36

What does joro spider toxin do?

Answer 36

Blocks Ca2+ channels so stops transmitter release.

Question 37

What does botulinium toxin do?

Answer 37

Disrupts the release machinery so blocks transmitter release.

Question 38

What does curare do?

Answer 38

Blocks ACh receptors so prevents end-plate potential.

Question 39

What do anti-acetylcholinesterases do?

Answer 39

Block Ach breakdown so increase transmission at the NMJ.

Question 40

What is synaptotagmin?

Answer 40

A Ca sensor in the membrane of the pre-synaptic terminal that interacts with SNARE proteins.

Question 41

Which neurotransmitter is the only one inactivated by breakdown?

Answer 41

ACh. All others are inactivated by uptake.

Question 42

Give examples of neurotransmitters.

Answer 42

ACh, NA, Dopamine, Seratonin, Histamine, Glutamate (most important in CNS), GABA (most important inhibitory), etc.

Question 43

Contrast NMJ and CNS synapses.

Answer 43

NMJ has 1 big end-plate potential. CNS can have fast/slow IPSP/EPSP’s. In NMJ anatomical arrangement of synapses stays the same. In the CNS, synapses can be axo-somatic/dendritic/axonal. In the NMJ, connectivity is always motor neurone to muscle cell. In CNS, convergence/divergence. Convergence is when multiple neurones feed into just a few. Divergence is when few neurones feed into multiple.

Question 44

What is modulation?

Answer 44

When a neuron uses 1 or more neurotransmitters to regulate diverse populations of neurones. This is in contrast to classical synaptic transmission when 1 pre-synaptic neuron directly influences a single post-synaptic partner.

Question 45

Why is the CNS more complicated than the NMJ?

Answer 45

Range of neurotransmitters, range of post-synaptic potentials, small potentials (synaptic integration - how neurones add up before generating an AP), variations of anatomical arrangements and variations of connectivity of neurons.