Neural Function in Disease Flashcards

(70 cards)

1
Q

law of dynamic polarisation

A

there is a preferred cell-to-cell direction in which currents move

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

soma

A

cell body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Dendrite

A

collects signals from other neurons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Node of Ranvier

A

exposed axon that allows ions to diffuse in and out of the neuron

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

myelin sheath

A

insulation that speeds up transmission

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Astrocytes

A

fills spaces between neurons in brain and most numerous cell in organ, mop up chemical messengers that accidently diffuse into intercellular space to stop signal going to wrong cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

how can ions move across a membrane

A

through pumps (active) or channels (passive)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

where are K+ and negatively charged proteins concentrated?

A

cytoplasm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

where are Na+, Cl- and Ca2+ concentrated?

A

the ECF (extracellular fluid)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

at rest, state of potassium and sodium channels?

A
  • At rest, leak potassium channels are open (not voltage dependant) and respond to pH, oxygen potential and mechanical stretch
  • At rest, sodium channels are closed
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

resting potential of cell

A

-65mv due to large negative proteins that can’t diffuse out of cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

action potentials

A

short pulses of electricity fired when a neurone is stimulated, they are propagated along its length carrying information

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

process of generating an action potential

A

Sodium channels and voltage gated potassium channels are closed
Sodium channels open (depolarisation)
Sodium channel inactivate and voltage gated potassium channels open (repolarisation)
Voltage-gates potassium channels gradually close (hyperpolarisation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what does a sequence of APs show?

A

long stimulus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

After-hyperpolarisation

A

when the K+ tries to reach its own equilibrium potential of -80mV after repolarisation, so membrane potential undershoots before K+ VGICs can close

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Depolarisation

A

change in polarity in the membrane potential of a cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

mechanism of voltage gated ion channels

A
  1. Na+ VGIC are closed at rest to maintain the resting potential
  2. A stimulus depolarising the membrane to -40mV distorts the protein to open it specifically to Na+ ions
  3. This rapidly causes much faster depolarisation for 1ms
  4. The channel inactivates by covering the pore and then closes when the protein returns to its resting configuration after repolarisation of the membrane, the physical pore power is removed
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

why K+ VGIC are much slower to reopen after depolarisation ?

A

entry of K+ resets the membrane potential to resting, during the refractory period after an AP the cell cannon generate another AP so that depolarisations are discrete.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

propagation in unmyelinated neurones

A

In unmyelinated neurones, depolarisation at one point of the membrane (production of an AP) sets up local circuits, so depolarisation continues as a wave down the length of the neurone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

salutatory conduction in myelinated neurones

A

Between myelin, there are gaps called Nodes of Ranvier where there is a high density of ion channels. APs are initiated in an axon hillock (part of cell body of a neurone that connects to the axon) and jump from one node to the next

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

factors that increase conduction velocity

A

Myelin, increased axon diameter and higher temperatures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Mechanoreceptors

A

unmyelinated fibres in the skin sensitive to stretch/bend/pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Mechanosensitive ion channels

A

gates opened by stretching of membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

dermatome

A

the area of skin with innervation supplied by one nerve

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
stimulus detected by free nerve endings
Pain, temperature, crude touch
26
stimulus detected by pacinian corpuscles
Deep pressure, vibrations
27
synapses
gaps between neurones
28
neurotransmitter
endogenous chemical messenger that conveys neuronal information from a pre-synaptic terminal to its post synaptic target
29
neurotransmission process- where are enzymes for the synthesis of NTs produced?
neurone cell body and move down the axon on microtubules
30
neurotransmission process- what are NTs produced from?
precursors in the pre-synaptic terminal which is then stored in vesicles
31
neurotransmission process after action potential reaches the pre synaptic terminal
3. When an action potential reached the terminal, the membrane is depolarised which causes voltage gated calcium channels to open 4. Ca2+ makes the NT vesicles fuse with the membrane (calcium sensing) 5. The NT is released into the synaptic cleft (exocytosis) 6. It binds to receptors on the post synaptic neurone 7. Enzymes break down the NT and its constituents are taken up into the pre-synaptic terminal for re-use 8. A new empty vesicle is pinched off the membrane into the pre-synaptic terminal (endocytosis) 9. This is filled with NP (loading) for the next AP
32
Ionotropic receptors
fast ligand-gated ion channels that open when the NT binds
33
Metabotropic receptors
slow because they activate a second messenger system (via GPCRs)
34
molecules that increase excitability of the post-synaptic neurone
acetylcholine, noradrenaline and glutamate
35
molecules that decrease excitability of the post-synaptic neurone
GABA and glycine
36
integration of signals allows
EPSPs to add up and if the threshold potential is met, generate an AP
37
production of EPSPs
At an excitatory synapse, if sufficient NT binds to NA+ ionotropic receptors the membrane will depolarise to produce an excitatory post-synaptic potential (EPSP)
38
production of IPSPs
occur at inhibitory synapses because Cl- channels are opened instead, further polarising the membrane (making it more negative instead of reversing the voltage, so it is harder to generate an action potential)
39
Spatial summation
when a neurone combines multiple EPSPs from different synapse connections
40
Temporal summation
when a neurone combines multiple consecutive EPSPs from the same synapse
41
Nicotinic receptors
ionotropic receptors that respond to acetylcholine (Ach), are agonised by nicotine and antagonised by curare
42
Muscarinic receptors
metabotropic Ach receptors, are agonised by muscarine and antagonised by atropine
43
GABA inhibitory receptors
agonised by ethanol and other depressants that reduce stimulation
44
Somatic motor fibre
one nerve fibre that connects CNS to the skeletal muscle it innervates
45
relationship of axial and distal muscle neurones
- Axial muscle neurones are medal to those of distal muscles
46
relationship of flexor and extensor muscle neurones
- Flexor muscle neurones are dorsal to extensor muscle neurones
47
The motor end plate
pre-synaptic terminal for one skeletal muscle fibre. Many motor end plates split off from one nerve so that it can innervate the whole muscle and coordinate its contraction
48
Motor unit
alpha motor neurone form the spine and fibres of the muscle that it innervates (causes to contract) which then splits into many synapses (motor end plates)
49
Motor neurone pool
set of alpha motor neurones that innervate one muscle, so damage to a single motor unit will not prevent normal muscle activity
50
what does the autonomic nervous system do?
controls involuntary reactions and innervates smooth muscle, cardiac muscle and gland cells
51
where are the cell bodies of ANS neurones?
cluster in ganglia which run down beside the spinal cord
52
Components of the autonomic nervous system
sympathetic and parasympathetic nervous systems
53
adrenaline pathway
- Pre-ganglionic neurones release Ach and post-ganglionic release noradrenaline (NA) so receptors in the ANS are known as adrenoreceptors
54
Ach pathway
- All neurones in this system release Ach and neurones travel long distances to target organs since most original in the cranial (neck) spinal cord
55
Contraction of muscles leads to
shortening of muscle fibres
56
areas where smooth muscle is present
in blood vessel wall and the digestive tract lining
57
Neuromuscular junction-
synapse between the neurone and the muscle fibre
58
action of acetylcholine to imitate contraction and degradation
Ach crosses NMJ and stimulates receptors to initiate contraction then is degraded by acetylcholinesterase enzymes so that acetic acid and choline (products) diffuse back to the pre-synaptic neurone to be resynthesized into Ach.
59
muscle contraction- movement of myosin and actin
1. The EPSP generated in the post-synaptic membrane (sarcolemma) travels through T-tubules (transverse tubules) into the fibre 2. This causes Ca2+ of the sarcoplasmic reticulum to open up 3. Ca2+ diffuses into the sarcoplasm and binds to troponin C so that the myosin heads are free to attach to binding sites on the actin filament 4. This binding causes a conformation change in the heads which pivot and slide the actin filament along the myosin filament to shorten the sarcomere 5. ATP is hydrolysed so the head detaches and swings back into its original position, ready to repeat the process for as long as APs and Ca2+ are present
60
Reflex
involuntary movement in response to a stimulus, instead of being processed by the brain and producing a conscious response, they travel through a reflex arc as far as the spinal cord and back
61
Myotatic reflex
in antagonist pairs of muscles, they are innervated so that one is inhibited when the other is excited to allow movement eg. in knee reflex jerk so that extensors contract, flexors relax
62
Cross extensor reflex
one leg extends when one flexes so gives stability when one leg is moved from pain
63
Vestibulo-ocular reflex
when the head is rotated, extraocular muscles (around the eyes) are inhibited on one side and excited on the other to fix the position of eyes- line of sight
64
hyponatremia
Less Na+ so less excitability, can be caused by diuretics cirrhosis ect., symptoms= cramps, fatigue, weakness
65
hypernatremia
More Na+ so more excitability, causes: water loss, renal failure ect. symptoms: Tremor, seizures, hyper-reflexia, thirst
66
hypokalaemia
Less K+ so less excitability Causes: Diuretics, cirrhosis, renal disease, malnutrition, malabsorption in GI tract, Symptoms: Mild: weakness, fatigue, constipation, arrhythmias Sever: paralysis of muscles including vital systems
67
hyperkalaemia
Less K+ so less excitability | causes: drug interactions with kidney function, symptoms: Impaired vital organ systems
68
channelopathies
diseases which affect ion channels (eg. mutations) and thus depolarisation/repolarisation of cells
69
demyelinating diseases examples
damage the Schwann cell insulation of neurones so lower AP conduction eg. multiple sclerosis, Guillain Barre syndrome (autoimmune)
70
myasthenia gravis
the immune system attacks Ach receptors so signals can’t be sent at the neuromuscular junction leading to weakness and fatigue