Topic 9.2 The Mammalian Nervous System Flashcards

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1
Q

The nervous system

A
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2
Q

The peripheral nervous system

A

The PNS is made up of:
1) Sensory neurones- carry impulses from receptors towards the CNS
2) Motor neurones

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3
Q

Motor Nervous System

A

This can be subdivided into:
1) Voluntary nervous system: carries nerve impulses to the bodies and is voluntary and conscious.
2) Autonomic nervous system- carries nerve impulses to glands, smooth muscle or cardiac muscle; it is involuntary.

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4
Q

Para/sympathetic: Structural comparison

A

Similarities:
In both the sympathetic and parasympathetic NS, fibres leave the CNS in a ganglion (a collection of nerve fibres).
Difference:
-Sympathetic: the ganglia are close to the CNS
-Parasympathetic: the ganglia are close to the effector organ

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5
Q

Para/sympatheitc: Functional comparison

A

Sympathetic:
-Produces noradrenaline at the synapses
-Often involved in fight or flight responses
-Activated in times of stress or when active
Parasympathetic:
-Slower, more inhibitory effect on organ system
-Acetylcholine neurotransmitter produced
-Maintains normal functioning of the body (rest and digest)

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6
Q

Resting potential

A

Resting potential is when the inside of the axon is negatively charged compared to the outside of the axon.
-We describe the axon as being polarised.
-Resting potential is around -70mV.

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7
Q

Sodium potassium pumps (requirements)

A

-Requires energy (ATP)
-3 Na+ ions moved out of the membrane for every 2k+ ions in.
—> ATPase in pump uses ATP to move cations.

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8
Q

Resting potential- How it happens

A

1) Na ions actively transported out of the axon by Na-K pump.
2) K ions are actively transported into the axon by Na-K pump.
—> The active transport of Na ions is greater than that of K ions (3 Na move out for every 2 K ions that move in).

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9
Q

The action potential

A

-Stimulus is received by a receptor or nerve ending.
-Its energy causes a temporary reversal of the charge on the axon membrane.
-As a result, the negative charge of -70mV inside the membrane becomes a positive charge of around +40mv.
-Membrane depolarised.

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10
Q

Action potential simplified (8)

A

1) Na+ voltage gated channels open
2) Na+ diffuse rapidly into axon
3) Potential difference reversed
4) Na+ voltage gates close
5) K+ voltage gated chanells open
6) K+ diffuse out of axon
7) Inside axon returns to negative
8) Resting potential restored

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11
Q

Absolute refractory period (ARF)

A

-Sodium channels are completely blocked.
-Resting potential hasnt been resolved.
-Lasts a millisecond or less.
-Second stimulus will not trigger a second action potential.

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12
Q

Relative refractory period

A

-Potassium channels are able to depolarise the membrane and potassium ions diffuse out of axon.
-Normal resting potential cannot be restored until these K channels are closed.
-Lasts several milliseconds.
-During this time, a greater than normal stimulus is required to initiate an action potential.

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13
Q

Purpose of refractory period

A

1) Ensures that action potential are propagated in one direction only
2) Produces discrete impulses- action potentials are separated from each other
3) Limits the number of action potentials

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14
Q

How is an action potential propagated along an unmyelinated neuron?

A

1) Stimulus leads to influx of Na+ ions. First section of membrane depolarises.
2) Local electrical currents cause a sodium voltage-gated channels further along membrane to open. Meanwhile, the section behind begins to open.
3) Sequential wave of depolarisation.

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15
Q

Mylelinated nerves

A

Schwann cell membrane wraps around cell many times to form mylein sheith.
-Gaps called Nodes of Ranvier.
-Speeds up transmittion and protects from damage.

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16
Q

Repolarisation

A

-Voltage-gated potassium channels open so K ions move out the axon by facilitated diffusion down the concentration gradient.
-Cell is repolarised and becomes more negative.

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17
Q

Hyperpolarisation

A

-More potassium flows out.
-The inside is more negative than the outside so more negative than the resting potential.

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18
Q

After hyperpolarisation

A

-Gates on K+ channels now close and Na-K pumps Na to be out and K in.
-70 mV is reestablished.

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19
Q

Explain why myelinated axons conduct impulses faster than unmyelinated axons

A

Saltatory conduction: impulse ‘jumps’ from one node of Ranvier to another. Depolarisation cannot occur where myelin sheath acts as an electrical insulator.
So impulse does not travel along whole axon length.

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20
Q

Saltatory conduction

A

-Myelin is impermeable to Na+/K+
-Polarisation/depolarisation only at Nodes of Ranvier
-This elongates the local current and the action potential ‘jumps’ between Nodes of Ranvier

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21
Q

Transmission in unmyelinated axons

A

-A current (change in potential difference) occurs in a part of the neuron.
-This is detected in the adjacent part of the membrane.
-When it detects the current, it causes voltage gated channels to open and an action potential will occur when the threshold is reached.
-The nerve impulse is transmitted as a self-propagating wave of depolarisation.

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22
Q

Propagation in myelinated axons

A

-The myelin sheath acts as electrical insulator.
-Therefore, a local flow of current can only be set up between adjacent Nodes of Ranvier (as there is no myelin sheath at this nodes and the neuron is exposed to extracellular fluid).
-There are also more sodium ion channels at these nodes.
-When depolarisation occurs at one node, it will ‘leap’ to the next. This is called Saltory conduction.
-Therefore nerve impulses can be transmitted very quickly and efficiently (as relatively few ions cross the membrane, minimising the need for active transport).

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23
Q

Factors affecting nerve impulses: Myelinated

A

-Only vertebrates have a myelin sheath surrounding neurons
-Saltatory conduction increase the speed of propagation
-Unmyelinated- 1s/m
-Myelinated- 100m/s

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24
Q

Factors affecting nerve impulses: Axon diameter

A

-Fibres vary fro 0.5-1000 micrometers
-A wider axon can transmit nerve impulses faster than those with small diameters
-However, the advantage of myelinated is that there is no need for giant axons
-Therefore a highly complex nervous system with high conduction speeds wouldn’t take up much space.

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25
Q

Factors affecting nerve impulses: Temperature

A

-The higher the temperature, the faster the conduction speed (within limits).
-This is because the rate of diffusion of ions increases with temperature, ∴ propagation of an impulse increases with temperature.
-Temperature also affects the enzymes involved in active transport which is required to maintain resting potential.
-At very high temperatures, enzymes will denature, resulting in disrupted nerve conduction.

26
Q

Events at a synapse

A

1) Action potential depolarises the presynaptic neuron.
2) Calcium channels open and calcium diffuses in.
3) Synaptic vesicles move to and fuse with the pre-synaptic membrane.
4) The neurotransmitter is released into the synaptic cleft.
5) Neurotransmitter moves across cleft by diffusion.
6) Neurotransmitter binds to specific protein receptors on the sodium channel on the post synaptic membrane.
7) Sodium channels open and sodium diffuses in.
8) This causes a change in the potential difference of the membrane and an excitatory post-synaptic potential (EPSP) to be set up.
Then what?
If there are sufficient number of these EPSPs, the positive charge in the post-synaptic cell exceeds the threshold level and an action potential will occur.

27
Q

Inhibitory post-synaptic potential (IPSP)

A

-Different ion channels open in the membrane, allowing inward movement of negative ions.
-This makes the post-synaptic cell more negative than normal resting potential.
-This means an action potential is less likely to occur.

28
Q

Breakdown in synapse

A

-Neurotransmitter are broken down by hydrolytic enzymes.
-They then move back across the cleft, back into the synaptic knob, and are recycled.

29
Q

Acetlycholine

A

-Acetylcholine is the neurotransmitter which is found at the majority of synapses in humans.
-After it attached to the receptors on the sodium channels, it is broken down by an enzyme called acetylcholinesterase.
-It hydrolyses acetlycholine into separate acetate and choline.
-The acetyl and choline diffuse back into the cleft into the presynaptic neuron.
-This allows the neurotransmitter to be recycled.

30
Q

The two main types of synapse

A

1) Cholinergic
2) Adrenergic

31
Q

Adrenergic synapse

A

-Often found in the sympathetic nervous system
-Uses noradrenaline (and adrenaline) as neurotransmitter

32
Q

Cholinergic synapse

A

-Mostly found in parasympathetic nervous system
-Only neurotransmitter is acetylcholine

33
Q

How drugs work at the synapse: Nicotine

A

-It mimics the effect of acetylcholine
-It triggers an action potential in posy-synaptic neuron, but the receptors remain unresponsive for some time.
-Also triggers the release of dopamine, which can be associated with pleasure sensations
-At low doses, nicotine has stimulating effects. But at high doses, it can be lethal.

34
Q

How drugs work at the synapse: Lidocaine

A

-Used as local anaesthetic as dentists.
-Lidocaine blocks the voltage-gated Na channels, so preventing an action potential in sensory neurons.
-Also used to prevent some heart arrhythmias. Because it blocks the Na channels, it raises the depolarisation threshold and so prevents early extra potentials in the pacemaker.

35
Q

How drugs work at the synapse: Cobra venom

A

-Substance made by cobra which is toxic and often fatal.
-It binds reversibly to acetylcholine receptors and so prevents the transmission of impulses across synapses.
-In low doses, can be used to relax trachea muscles in asthma patients to save lives.
-In high doses, can stop breathing all together, and cause death.
-Means that muscles are not stimulated to contract ad so the person will become paralysed.

36
Q

Cillary muscles

A

Pull the lens for focusing.

37
Q

Cornea

A

Lets light into the eye and begins focusing.

38
Q

Iris

A

Controls the amount of light entering the eye.

39
Q

Lens

A

Focuses light onto the retina.

40
Q

Optic nerve

A

Sends signals to the brain.

41
Q

Pupil

A

Lets light through to the lens.

42
Q

Retina

A

Light-sensitive layer- sends signals to the optic nerve.

43
Q

Suspensory ligaments

A

Holds lens in place.

44
Q

Rods and cones: Transduction in the eye

A

-Converts light into a pattern of nerves impulses.
-Transduction takes place in the retina by a layer of photosensitive cells at the back of the eye.
-Rods and cones are attached to nerves.

45
Q

Rod cells

A

-Spread evenly across the retina (except at fovea where there are none).
-More numerous than cone cells.
-Provide images in black and white (greyscale).
-Because they can’t distinguish between different wavelengths of light.
-Used to detect light at very low intensity.
-A certain threshold must be detected before a generator can occur.
-Certain threshold must be detected before a generator potential can occur.
-Cannot distingush between close together things as only one impulse is generated.
-Connected to bipolar neurone - sensory neuron - optic nerve

46
Q

Rod cells- low light

A

-In order to create a generator potential, a pigment called rhodopsin must be broken down.
-Low light intensity has enough energy to break this down hence why rods work in low light.

47
Q

Cone cells

A

-Found lightly packed at the fovea
-There are 3 different types of cone cells each responding to different wavelengths of light
-Cone cells are often connected to own separate bipolar neurones.
-Cone cells only respond to high light intensity as summation can not occur.
-It also means that the brain can distinguish between separate sources of light.
-Cone cells contain iodopsin which requires a higher intensity of light to break it down.
-Cone cells contain different types of iodopsin (this is why they respond to different wavelengths of light).

48
Q

The retina: Fovea

A

-The fovea is formed from opsin and retinal.
-It receives the greatest intensity of light.
-Therefore, cone cells (but not rod cells) are found here.
-More rod cells are found at the edges of the fovea (lower light energy).

49
Q

How does rhodopsin work?

A

-Rhodopsin is formed from opsin and retinal.
-Retinal exists as 2 different isomers: cis-retinal and trans-retinal.
-In the dark all retinal is in the cis form.
-When a photon of light hits the rhodopsin, it converts from cis to trans form.
-This changes the shape of the retinal and puts strain on the bonding between opsin and retinal, breaking up the molecule.
-This is known as ‘bleaching’.

50
Q

Bleaching

A

-Rod cells are usually quite permeable to sodium ions.
-When rhodopsin is bleached, this causes the Na ion channels to close making it less permeable to sodium.
-However, the sodium pump continues to wok and so sodium ions are removed from the cell.
-This makes the inside of the rod cell more negative than normal.
-This hyperpolarisation is known as the ‘generator potential’.

51
Q

Control of heart rate: controlled 2 ways

A

1) Nervous control
-using baroreceptors
-using chemoreceptors
2) Hormonal control

52
Q

How to heart works

A

-The muscle found in the heart is myogenic:
-muscular tissue which initiates its own contractions.
-The Sinoatrial Node (SAN) acts a pacemaker for the heart:
-this generates an action potential which is transferred through the atria walls causing them to contract.
-The impulse pauses to the Atrioventricular Node (AVN) then down the Purkinje (or purkyne) fibres which cause ventricles to control.

53
Q

Changing heart rate

A

The cardiovascular centre in the medulla oblongata can affect heart rate:
-Stretch receptors in muscles detect movement of the limbs. An impulse is sent to CV centre and heart rate will increase.
-Chemoreceptors in the carotid artery, aorta and brain will detect a decrease in the pH of the blood caused by an increased production of CO2. An impulse is sent to the CV………..

54
Q

The brain

A
55
Q

The sensory neuron

A
56
Q

The motor neuron

A
57
Q

The relay neuron

A
58
Q

The sympathetic and parasympathetic reactions

A
59
Q

Neuron diagram

A
60
Q

Adrenaline

A

-Cardiac muscles. has receptors for adrenaline (and nor-adrenaline)
-Adrenaline increases the permeability of the cells to Ca^2+ ions
-This causes a more rapid depolarisation of the cell membrane
-This means an action potential is reached more quickly, causing heart rate to speed up

61
Q

Control of heart rate using pressure receptors

A

-Baroreceptors are found in the carotid arteries in the neck and on the aorta
-When exercise starts:
1) Blood vessels dilate in response to adrenaline released, causing blood pressure to fall a little
2) This reduces the stretch on the baroreceptors
3) In turn, the cardiac control centre sends signals along the sympathetic nerve to stimulate heart rate and increase blood pressure by vasoconstriction.

62
Q

Control of heart rate by chemoreceptors

A

-Chemoreceptors are found in the wall of the carotid arteries (blood vessels that serve the brain).
-They are sensitive to levels of carbon dioxide in the blood which causes changes in the pH.
1) When the blood has a higher carbon dioxide concentration than normal, the pH is lowered (more acidic).
2) Chemoreceptors detect this and increase the frequency of impulses to medulla oblongata.
3) This increases frequency of impulses via the sympathetic nervous system to the SAN- so HR increases.
4) Increased blood flow means more CO2 is removed from the lungs.