1
Q
what is the central nervous system
A
brain and spinal cord
2
Q
what is the peripheral nervous system
A
the sensory and motor nerves
3
Q
what are the
sub-categories of the peripheral nervous system
A
somatic nervous system (voluntary) - controls skeletal muscle
autonomic nervous system - controlling things you don’t think about (e.g blood pressure)
4
Q
what are the ‘hills’ and ‘grooves’ in the brain called
A
hills are gyrus
grooves are sulcus
5
Q
how many pairs of cranial nerves are there and what do they do
A
12 pairs
they take sensory information and direct into the brain or out of the brain
6
Q
how many pairs of spinal nerves are there
A
31 pairs
- 8 cervical
- 12 thoracic
- 5 lumbar
- 5 sacral
- 1 coccygeal
7
Q
where are the sensory cell bodies located
A
dorsal root ganglion (the bulge before the dorsal root)
8
Q
what happens in the dorsal horn
A
the sensory axons continue in region called dorsal horn and there they make synapses with other neurones and eventually control the activity of motor neurones
9
Q
where are the cell bodies of motor neurones
A
ventral horn
10
Q
where are motor axons sent out
A
sent out through ventral root and then join up with a spinal nerve so you have a mixed spinal nerve going out to its targets in the periphery
11
Q
what does white matter contain
A
lots of spinal tracts
- spinal tracts could be taking information up to the brain or sending information down from the brain (telling motor neurones what to do)
- grey matter in middle white matter more on the outside
12
Q
what bit of a neuron contains the nucleus
A
cell body
- sometimes called soma
13
Q
what bit of the neuron cell receives information
A
dendrites
14
Q
what part of the neuron triggers axon potential
A
initial segment
- sometimes called axon hillock
15
Q
what part of the neuron sends the action potential
A
axon
16
Q
what happens at axon (presynaptic) terminals
A
transmitter is released
17
Q
what are the three types of neurones
A
- afferent (sensory) neurones (PNS)
- interneurones (CNS)
- efferent (motor) neurones (PNS)
18
Q
how do the three types of neurones (sensory, inter, motor) work together
A
afferent neurone will have sensory receptor out in periphery responding to something like touch
- afferent neurones are a bit weird where their axon runs right past the cell body so the axon comes in at the dorsal horn
- then it will release a neurotransmitter and it’ll act on the interneurones and they’ll decide whether this needs a motor repsonse
- motor neurones have their cell bodies in the ventral horn and they travel out by ventral root
19
Q
what are glia
A
non-neuronal cells of the central nervous system
- 90% of cells in the CNS
20
Q
what are the four types of glia
A
- astrocytes
- oligodendrocytes
- microglia
- ependymal cells
21
Q
what do astrocytes do
A
- type of glia
- maintain the external environment for the neurones
- surround blood vessels and produce the blood brain barrier
22
Q
what do oligodendrocytes do
A
- type of glia
- form myelin sheaths in the CNS (Schwann cells in the PNS)
23
Q
what do microglia do
A
- type of glia
- phagocytic hoovers mopping up infection
24
Q
what do ependymal cells do
A
- type of glia
- produce the cerebrospinal fluid
25
what are the three types of potentials that neurones use to send electrical signals
action potentials - transmit signals over long distances
graded potentials - decide when an action potential should be fired
resting membrane potential - keeps cell ready to respond
26
what is usually the resting membrane potential in cells
-70mV
27
how do we get the resting membrane potential
- difference in voltage created by sodium potassium pump is very little
- resting membrane potential is due to leaky K+ channels
- K+ leaks out through these channels down its concentration gradient and as it leaks it builds an electrical gradient
- an equilibrium is reached when the electrical gradient is equal and opposite to the concentration gradient
- that is the resting membrane potential
28
what do the Nernst and Goldman-hodgkin-katz (GHK) equations do
Nernst equation predicts the equilibrium potential for a single ion species
Goldman-hodgkin-katz equation predicts the equilibrium potential generated by several ions
29
where is there a high K+ concentration - inside or outside the cell
inside
30
where is there a high Na+ concentration - inside or outside the cell
outside
31
where is there a high Cl- concentration - inside or outside the cell
outside
32
what is the function of a graded potential
to depolarise the cell to threshold by opening channels
| can also hyperpolarise - make more negative
33
what are some examples of graded potentials
generator potentials - at sensory receptors
postsynaptic potentials - at synapses
endplate potentials - at neuromuscular junction
pacemaker potenitals - in pacemaker tissues
34
what does it mean by graded potentials are graded
- a small stimulus will open few channels and evoke a small response (cell will depolarise slightly - become a bit more positive)
- a large stimulus will open many channels and evoke a large response (cell will depolarise quite a bit)
35
what does it mean by graded potentials are decremental
- they get smaller as they travel along the membrane
- think like water leaking out a hose
- your axons are very leaky so graded potentials are only useful over short distances
- this is why graded potentials are also called local potentials
36
what does it mean by graded potentials can summate
a single neuron will have lots of synapses evoking their own postsynaptic potential, if two occur at the same time they can add together
37
how do you generate a graded potential
- you open/sometimes close particular ion channels (e.g K+, Na+, Cl-, Ca2+ although Ca2+ has lots of unintended consequences so tend not to use that) (remember to think about concentration gradient AND electrical gradient)
- e.g. if you wanted to hyper polarise the cell you would open K+ channels so it would leak out
38
how do you hyper polarise (make more negative) postsynaptic potentials
```
fast IPSP (inhibitory postsynaptic potential) via inotropic receptor - neurotransmitter binds to Cl- channel and it opens very quickly and Cl- comes into cell making it more negative
slow IPSP - there is separate receptor and channel, neurotransmitter is released and binds to receptor (metabotropic) then G protein will open channel and in this case it is K+ leaky channel so cell becomes more negative. takes the G protein some time to find its target this is why it's slow
```
39
how do you depolarise (make more positive) postsynaptic potentials
```
fast EPSP (excitatory postsynaptic potential) - neurotransmitter binds to receptor and opens channel. this channels lets through anything with a charge of +1 (so will let some potassium out but Na+ coming through means K+ is near equilibrium anyway)
slow EPSP - obvious one is to block leaky K+ channels. neurotransmitter binds to separate metabotropic receptor and G protein closes channels
```
40
where do you get a stronger graded potential on a neurone
if you stimulate a receptor on the end of a dendrite you will get a smaller response. (so might not reach action potential) if you stimulated one closer to the initial segment you would get a larger response
41
what is spatial summation
- in graded potentials
- two different inputs on neuron are stimulated at approximately the same time to give graded potential. this evokes are larger response than if they were just doing it on their own
42
what is temporal summation
- in graded potential
| - the same input is stimulated twice in quick succession to reach threshold
43
what is is called when a synapse is synapsed onto another synapse which is synapsed onto the neurone
axo-axonic synapse
44
what is it called when synapse is synapsed at end of dendrite (further away from cell body)
axo-dendritic synapse
45
what's it called when a synapse is synapsed onto the cell body/at beginning of dendrite next to cell body
axo-somatic synapse
46
what are the different values in an action potential
- graded potential makes the cell depolarise to threshold (around -55mV)
- once it reaches -55mV then you get a massive depolarising phase where the inside of the cell becomes positive (around +40mV)
- but then very quickly the cell repolarises and goes back to a bit more negative than it was before (phase of hyperpolaristation) and then eventually it'll go back to resting membrane potential
47
how do we get the depolarisation in the action potential
- Na+ voltage gated channels open and the inside of the cell becomes more positive
- these open very quickly and shut very quickly
- K+ leaky channels are also still open because they are usually always open
48
how do we get the hyper polarisation (or just depolarisation) in the action potential
- the voltage gated channels from the depolarisation stage will shut
- voltage gated potassium channels (different from leaky K+ channels) will open so cell becomes more positive
- eventually those will shut too and we are back to resting membrane potential
49
what are the properties of the action potential
- have a threshold
- all or none (you either reach threshold and get action potential or you don't)
- have a refractory period (break between firing)
- they are self-propagating (grows new action potential as it continues along membrane)
- they travel slowly
- they have these properties because they are mediated by voltage gated channels as opposed to ligand ones which generate graded potential
50
why can the action potential never go backwards along axon
due to the refractory period
51
what are two ways to speed up action potential
- large axons
- myelination
self propagation of action potentials is very slow but these two methods speed it up
52
how do large axons speed up action potential
- just like how water flows more easily through a bigger tube
- electric current flows more easily down a large axon (axial resistance is lower)
- large axon allows Na+ channels to be more spaced out along axon so requires fewer channels
- mammals don't have large axons but squids are very good at it
53
how does myelination speed up action potential
- Schwann cells in PNS and oligodendrocytes in the CNS
- myeline increases membrane resistance and reduces membrane capacitance (so less capacity for ion channels and more of them shut too)
- so less current is wasted, the axons are less leaky
54
what are the consequences of demyelination
- multiple sclerosis in the CNS
- Guillain-barre syndrome in the PNS
- they attack the myeline sheath
- membrane resistance is decreased and capacitance is increased
- more current is lost and conduction fails
55
what is the compound action potential
- humans have small and large unmyelinated and myelinated axons, all conducting at different velocities
- extracellular recording from a nerve (bundle of axons) will therefore generate a 'compound' action potential
- this gives classification of axons based on their conduction velocity and this correlates with their anatomy and their function
- e.g. large myelinated will have a larger velocity than small unmyelinated
56
what is the neuromuscular junction
the synapse between the motor neurone and skeletal muscle
57
how is the action potential in the neuromuscular junction generated
- the action potential in motor neuron opens voltage gated Ca2+ channels in presynaptic terminal
- this triggers fusion of vesicles containing ACh (Ca2+ dependent exocytosis)
- acetylcholine is released (ACh) and diffuses across synaptic cleft
- ACh binds to ACh receptors (nicotinic) on post synaptic plate
- this opens Na+/K+ ligand gated channels
- this evokes a graded potential (the end plate potential) which ALWAYS depolarises membrane to threshold
- this opens voltage gated Na+ channels and evokes new action potential
- ACh is removed by acetylcholinesterase
58
what does the ligand-gated Na+/K+ channel do in the neuromuscular junction
evokes the graded potential which is unusually large and ALWAYS REACHES THRESHOLD
59
what do the voltage gated Na+ channels on the post synaptic plate do
generate the new action potential
60
is there synaptic integration in the neuromuscular junction's new action potential
no
- there are post-junctional folds that pack voltage gated Na+ channels close to where the graded potential is evoked so no synaptic integration
61
so what are the order of the ion channels which open in the neuromuscular junction
1. voltage gated calcium channels open (pre-synaptic)
2. acetylcholine binds to nicotinic receptors post-synaptically after diffusing across synapse
3. ligand gated sodium potassium channel opens (triggers graded potential)
4. voltage gated sodium channel opens (triggers action potential)
5. Act removed by acetylocholinesterase
62
what are the differences between the CNS synapses and the neuromuscular junction
- same sequence of events but range of neurotransmitters
- range of post-synaptic potentials
- small post-synaptic potentials (synaptic integration)
- anatomical arrangement of synapses different (axon-dendritic, axon-somatic, axon-axonal)
- synaptic connectivity (convergence, divergence, feedback inhibition, monosynaptic and polysynaptic pathways)
- synaptic plasticity
63
what are some of the common neurotransmitters in CNS synapses
- most important excitatory one in CNS is glutamate (mediates nearly all fast excitatory transmission in CNS)
- most important inhibitory would be GABA (mediates nearly all fast inhibitory transmission in the CNS)
- glycine=mediates all fast inhibitory in spinal cord
- nitric oxide is transmitter that doesn't go in vesicle because too liipophilic
64
what is the difference between the post synaptic potentials in the CNS and the neuromuscular junction
- in CNS there is range of post synaptic potentials (fast and slow EPSP, fast and slow IPSP) whereas in the NMJ you just have one massive fast EPSP (endplate potential)
- also in CNS post synaptic potentials are small and often have to be added together=synaptic integration (why CNS synapse is less predictable, might not always reach threshold unlike NMJ)
65
what are the different types of anatomical arrangements of synapses in the CNS
- axo-dendritic
- axo-somatic
- axo-axonal
- in the NMJ there is just the motor neurone synapsing directly onto skeletal muscle
66
what is convergent synaptic connectivity in the CNS
- activity of one cell if being influenced by activity of lots of cells
67
what is divergent synaptic connectivity in the CNS
- one neuron is synapsing onto several different ones and affecting the activity of several different post synaptic neurones
(you get this is in the NMJ too because one motor neurone will synapse onto several different muscle fibres and activate them all and form the motor unit
68
what is feedback inhibition in synaptic connectivity in the CNS
- action potential initiated at axon hillock, send action potential down neurone
- sometimes on the way there is axon collateral which when activated activates an inhibitory interneurone
- inhibitory transmitter released which hyperpolarises the cell
69
what are monosynaptic and polysynaptic pathways
monosynaptic = simple reflex activités could be mediated by a pathway of just two neurones
polysynaptic = most of our reflexes, can turn excitatory reflex into inhibitory one by turning one of the many neurones into an inhibitory neurone
70
what is synaptic plasticity in the CNS
- using synapse intensively can change their strength
- can effect long term depression
- one of the reasons neurones tend no to use calcium to depolarise cells
principles of normal function
flashcards
Decks in class (15)
# Cards
-
week 168
-
week 2 forces acting across membranes48
-
week 2 intro to blood27
-
week 2 immunology57
-
week 3 proteins and enzymes44
-
week 3 nitrogen17
-
week 4 how nerves work70
-
week 4 skeletal, smooth (and cardiac) muscle54
-
week 4 essential pharmacology11
-
week 4 sensory receptors and reflexes52
-
week 4 autonomic nervous system27
-
week 4 pharmacology on NMJ and ANS22
-
week 3 carbs revised50
-
week 3 citric acid cycle & terminal respiration (revised)35
-
week 3 lipids (revised)58
