How Nerves Work Flashcards
(127 cards)
1
Q
Subdivisions of the nervous system
A
the brain
the spinal cord
the peripheral nerves
the somatic nervous system
the autonomic nervous system
the enteric nervous system
2
Q
The brain
A
- Meninges
- Gyrus vs sulcus
- Cerebellum
- Cerebrum
- Diencephalon
- Brainstem
3
Q
cerebrum contains
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- frontal lobe
- temporal lobe
- parietal lobe
- occipital lobe
4
Q
diencephalon contains
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- thalamus
- hypothalamus
5
Q
brainstem contains
A
- midbrain
- pons
- medulla oblongata
6
Q
frontal lobe is
A
the front half bit of the brain
7
Q
temporal lobe is
A
under the frontal and parietal lobe and above the cerebellum. It touches the occipital lobe perpendicularly.
8
Q
parietal lobe is
A
between the frontal and occipital lobe and above the temporal lobe.
9
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occipital lobe is
A
the very end of that touches the temporal lobe perpendicularly and also touches the back end of the cerebellum
10
Q
the forebrain contains
A
- cerebrum
- diencephalon
11
Q
The spinal cord
A
31 pairs of spinal (plus 12 pairs of cranial) nerves 8 cervical (7 vertebrae) - neck, shoulders & arms 12 thoracic (12 vertebrae) - chest & abdomen 5 lumbar (5 vertebrae) - hips & legs 5 sacral (5 fused vertebrae) - genitalia & gastrointestinal tract 1 coccygeal (4 fused vertebrae)
12
Q
very mobile vertebrae
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- cervical (neck)
- lumbar (hips and legs)
discs between lumbar vertebrae are most susceptible to wear and tear over time - cumulative strain
13
Q
discs
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- promote flexibility of spine
- act as shock absorber by preventing jarring
- reduce friction
- act as spacer between vertebrae
14
Q
afferenet is
A
sensory and on the dorsal root
note: s in dorsal means its sensory
15
Q
efferent is
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motor and on the ventral root
note: no s in ventral so its motor
16
Q
ganglion is between
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dorsal root and dorsal horn
note: dorsal also means posterior (both have s in them meaning they are sensory)
17
Q
Neurones
A
Cell body (soma) Dendrites - receive information Initial segment (axon hillock ) - triggers action potential Axon - sends action potential Axon (presynaptic) terminals - release transmitter
18
Q
Afferent (sensory) neurones send signals they receive to
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Interneurones
19
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Interneurones are found in the
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Central nervous system
20
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Interneurones send signals to
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Efferent (motor) neurones
21
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Efferent (motor) neurones are found in the
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Peripheral nervous system
22
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Afferent (sensory) neurones are found in the
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Peripheral nervous system
23
Q
the axon terminal can cause a reaction to occur in
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muscle, gland or neuron
24
Q
Glia
A
- Comprise 90% of cells in the CNS
- Astrocytes
- Oligodendrocytes
- Microglia
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Astrocytes
- maintain the external environment for the neurones
| - surround blood vessels & produce the blood brain barrier
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Oligodendrocytes
- form myelin sheaths in the CNS
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Microglia
- phagocytic hoovers mopping up infection
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Gross structure of the spinal cord
- grey (inside) vs white matter (outside)
- dorsal vs ventral horn
- dorsal root ganglion
- spinal nerves
- spinal tracts
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Action potentials
transmit signals over long distances - big all or none things that self propagate over potentially infinite distances.
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Graded potentials
decide when an action potential should be fired
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Resting membrane potential
keeps cell ready to respond
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the equilibrium potential is
the membrane potential at which the electrical gradient is exactly equal and opposite to the concentration gradient pushing the K out.
ie- the concentration gradient determines the equilibrium potential
If the concentration gradient was higher it will develop a bigger electrical potential before it is matched and so the equilibrium potential will be higher.
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Higher [K+]
- Reduces concentration gradient
- Sustains a smaller electrical gradient at equilibrium
- RMP is reduced (ie cell depolarises) fires action potential
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The blood brain barrier
- Capillaries of the brain are especially “tight”
- Due to astrocytes & tight junctions between endothelial - cells
- This protects the brain from changes in plasma [K+]
The heart is not so lucky and therefore hyperkalemia causes ventricular fibrillation as there is no heart blood barrier to stop the K reaching excitable cells in the heart.
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ventricular fibrillation
s a heart rhythm problem that occurs when the heart beats with rapid, erratic electrical impulses. This causes pumping chambers in your heart (the ventricles) to quiver uselessly, instead of pumping blood around the body.
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why is RMP close to K equilibrium
At rest there is lots of open K channels.
| There is also some open Na and open Cl channels but because permeability is lower they have a smaller effect on RMP.
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if you poison the Na/K pump,
cells only depolarise a few mV. You have to wait for concentration gradient to run down before you lose the RMP.
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The RMP is dominated by the
resting permeability to K which is why the RMP is close to the K equilibrium potential. This in turn depends on the K concentration gradient that has been set up by the Na/K pump.
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Open (more) K channels and
and K flows out and cell hyperpolarises.
This happens as there is less K outside the cell due to the Na/K pump. Think of the "leaky" K channels that are concentration gradient of K.
The electrical gradient is opposite to this as k is positive and cell is negative but concentration wins.
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Open Na channels and
Na flows in and cell depolarises.
This happens as there is less Na inside the cell due to the Na/K pump. Opening Na channels means passive transport and so more Na goes inside cell.
The electrical gradient is same as this as Na is positive and cell is negative.
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Open Cl channels and
Cl flows in and cell hyperpolarises.
This happens as there is less Cl inside the cell.
Opening Cl channels means passive transport and so more Cl goes inside cell.
The electrical gradient is opposite to this as Cl is negative and cell is also negative but concentration wins.
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Open Ca channels and
Ca flows in and cell depolarises.
This happens as there is less Ca inside the cell.
Opening Ca channels means passive transport and so more Ca goes inside cell.
The electrical gradient is same as this as Na is positive and cell is negative.
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Hyper means
over
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hypo means
under
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depolarisation
Anything towards zero
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overshoot
Over zero
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repolarisation
Back to original
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hyperpolarisation
Below resting membrane potential
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Potassium increase causes
neurons to depolarise
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what makes a neurones decide to fire an action potential
the resting membrane potential has to be depolarised to a magic threshold - about -55mV.
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what makes it depolarise?
External stimuli acting on specific sets of ion channels to create graded potential where the size of the potential is related to the size of the stimulus.
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Junction between two neurones - the synapse - where Action Potential releases
transmitter molecules, they activate (pharmacological) receptors on second cell which open ion channels and create another graded potential.
It could:
- try and make the cell fire = EPSP (excitatory post-synaptic potential)
- stop it reaching threshold = IPSP (inhibitory post-synaptic potential)
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Graded potentials could occur
out in the terminals of sensory nerves - say in response to pressure on the skin. Called a generator potential (Vander calls it a receptor potential – confusing).
If the graded potential is big enough it will reach threshold and make the cell fire an action potential (or more)
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At neuromuscular junction,
motoneurone depolarises the muscle to threshold by evoking a graded potential = endplate potential
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Examples of graded potentials
- Generator potentials
- Postsynaptic potentials
- Endplate potentials
- Pacemaker potentials
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Generator potentials
- at sensory receptors
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Postsynaptic potentials
- at synapses
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Endplate potentials
- at neuromuscular junction
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Pacemaker potentials
- in pace maker tissues
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Graded potentials
determine when an action potential is fired
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Graded potentials are also known as
- electrotonic potentials
- decremental potentials
- non-propagated potentials
- local potentials
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some local stimulus (could be pressure on a touch receptor or a neurotransmitter on a postsynaptic membrane) causes channels to open. Let's say they are Na channels.
what happens?
Current flows across membrane and creates a potential difference (V=IR, membrane potential, draw it). That current leaks out along the rest of the membrane.
As you go further away, more current has already leaked out so you get a smaller and smaller membrane potential (draw it). In that sense they are decremental and non propagated. They can only operate very locally.
For long distance transmission you need the action potentials that come later.
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Graded potentials are graded therefore
can signal stimulus intensity in their amplitude.
If there is a stronger stimulus at the beginning (bigger pressure or more neurotransmitter) you get more channels opened, bigger current flow, and therefore a bigger potential.
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Graded potentials can be
- depolarising
- hyperpolarising
Firing an action potential depends on reaching a firing threshold and therefore graded potentials can excite or inhibit a cell.
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Hyperpolarising postsynaptic potentials
Opens Cl- channels - or open even more K+ channels.
Takes them away from threshold and so is inhibitory.
Hence called IPSPs.
And this is what GABA and Glycine do.
Cl entering cell causes fast IPSP.
K leaving cell causes slow IPSP.
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Depolarising postsynaptic potentials
To depolarise cells, transmitters tend to open the type of channels permeable to Na and K (= non-specific monovalent cation channels), but more Na gets in than K gets out, so it depolarises. Causes fast EPSP.
Or block some of those leaky K channels. Causes slow EPSP.
If glutamate was released it would bind and cause another channel to open.
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ligand-gated ion channels
Postsynaptic potentials are produced by a neurotransmitter opening or closing ion channels
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voltage-gated ion channels
Actions potentials are produced by depolarisation of the membrane potential opening ion channels
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Graded potentials are important in synaptic integration as they can
summate (add to each other).
This whole process is called integration - just means looking at all the inputs (synapses or physical stimuli) and deciding whether or not to send one of those long distance signals (an action potential).
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temporal summation.
One stimulation on its own does this. Stimulate it again quickly and the next EPSP adds on to it.
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spatial summation.
Or you can do the same with two stimulation, eg- red and blue.
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If initial segment reaches threshold,
cell fires an action potential.
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EPSP is
decremental so it gets smaller as it travels
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imagine this, a is further away from axon hillock so it decays more than b.
Neither on its own reaches threshold.
Stimulate b twice, what will happen?
temporal summation that reaches threshold.
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Imagine this, a is further away from axon hillock so it decays more than b.
Neither on its own reaches threshold.
If you stimulate a and b, what will happen?
spatial summation that reaches threshold.
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spatial summation cannot happen without
temporal summation
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Synaptic integration
The process of summing all inputs in space and time, to determine whether or not the initial segment reaches threshold.
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Anything closer to the axon hillock have
a bigger EPSP than those that are far away as the EPSP is decremental and so gets smaller as it travels.
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And you also get IPSPs that
tend to stop the cell reaching threshold.
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EPSP and IPSP are ___ _______
pre-synaptic
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if an IPSP directly touches the dendrite area then it can
inhibit all input as it is non-specific. eg- if someone has already eaten then why buy the sandwich
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if an IPSP indirectly touches the dendrite area (by touching one EPSP) then it can
inhibit just that one input as it is specific. eg- sandwich contains everything a person likes except tomatoes.
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EPSPs act by
- opening Na+/K+ channels
| - closing K+ channels
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IPSPs:
- opening Cl- channels
| - opening K+ channels
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action potential steps
- RMP sitting at -70mV, reaches threshold for some reason - usually about -55mV.
- Sudden massive depolarsiation and overshoot to +30. - - - Only last about 1 msec, then rapid repolaristion beyond resting level.
- After repolarising it will hyperpolarise and go back to stable state
note: its much bigger, but shorter lasting than most graded potentials
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Ionic basis of the action potential
At RMP:
- Na permeability is very low, K is higher because of those leaking channels.
During depolarisation:
- Voltage dependent Na channels open almost immediately, Na floods in and depolarises cell. Massive increase in permeability = decrease in resistance.
Example of positive feedback
During repolarisation:
- K+ permeability slowly rises as more K+ channels (this time the voltage dependent ones) open.
- Cause repolarisation and after hyperpolarisation.
- Eventually they shut and we are back to where we started.
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Absolute refractory period
The voltage gated channels need some time to rest.
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Voltage gated potassium channels are
slower to open and close and so stay open longer
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voltage gated sodium channels
are quicker to open and close and so stay open for a short period of time.
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Poisoning the pump produces a
```
delayed effect. It takes time for the gradients to run down.
Local anaesthetics (procaine/lidocaine) block those voltage dependent Na channels. So APs cannot be transmitted.
```
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Properties of action potentials
- They have a threshold
- They are all or none
- They cannot encode stimulus intensity in their amplitude, only in their frequency
- Self propagate
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Self-propagation of APs
Action potentials have a threshold and therefore are all or none. They cannot encode stimulus intensity in their amplitude but can do this in their frequency of action potentials fired.
Local current flow also spreads back, but this does NOT evoke a new AP because those channels are in their refractory state - hence the depolarisation (the action potential) can only keep sweeping forward down the axon and so on - until the electrical signal gets to the end of the axon where it may make a muscle twitch or another neurone do something
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Properties of action potentials
- mediated by voltage-gated channels
- have a threshold
- are all-or-none
- can only encoded stimulus intensity in their firing frequency, not amplitude
- are self-propagating
- have a refractory period
- travel slowly
- conduction velocity can be improved by big axons or
- myelination
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large axons increase conduction velocity as
A bigger axon has a lower axial resistance – that means the depolarisation evoked at one channel can spread further – it does this passively, but VERY quickly.
That means you can spread you Na+ channels out further and the depolarisation from one will still be big enough by the time it gets to its neighbour to reach threshold and make its neighbour open.
It is the opening of the voltage gated channels that takes the time – so the less of that and the more of the passive spread you can have, the better it is.
Big fibres are good, but if you have may of them you have nerves the size of tree trunks.
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what forms myelin?
Folds of membrane from:
- Schwann cells (in PNS)
- Oligodendrocytes (in CNS)
form the myelin sheath
Gaps = nodes of Ranvier
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Graded potentials summate (integrate) trigger
an AP at the axon hillock/initial segment by reaching threshold.
Na channels are only present at the nodes, so it cannot propagate as normal, but because myelin increases resistance of membrane it allows the AP to spread like a local current, to the next segment, with little decrement.
Evokes a new AP there.
And the next, and the next.
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The signal (AP) cannot go back because of the
refractory period (recovery period).
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Absolute refractory period is when
the neuron cannot be excited to generate a second action potential (no matter how intense the stimulus)
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Relative refractory period is when
a stronger than normal stimulus is needed to initiate a new action potential.
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Saltatory conduction (to hop or leap) is the
propagation of action potentials along myelinated axons from one node of Ranvier to the next, increasing the conduction velocity of action potentials.
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Effect on myelination on APs:
| The depolarisation evoked by voltage-gated Na channels at one node of Ranvier spreads as a
local circut and while this is decremental (i.e. non- propagated), it travels further than in an un-myelinated axon because less current is wasted leaking out of the membrane or charging up the capacitance. This means it is still big enough by the time it reaches the next node to reach threshold and trigger another action potential.
And you can tell how important it is because of the effects of de-myelinating diseases – e.g. multiple sclerosis (problems with vision, arm or leg movement, sensation or balance)
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Effect on demyelination on APs:
- Big local current decays quicker
- Does not depolarise to next node to threshold.
- And conduction fails.
eg
- Multiple sclerosis
- Guillain-Barre syndrome
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compound action potential
Mammals have small and large unmyelinated and small and large myelinated axons. Therefore extracellular recording from a bundle of axons (a nerve trunk) evokes a “compound” action potential
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Fibres vary in sensitivity to pressure
Big ones go first ie A>B>C
| that is why you arms goes numb and useless when you sleep on it - but it does not necessarily hurt.
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And in their sensitivity to anaesthetics
small ones go first which is handy.
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There is another classification system that originated in sensory nerve fibres:
Ia muscle spindle annulospiral ending = A alpha
Ib golgi tendon organ = A alpha
IIb muscle spindle flower spray ending = A beta
III pain and cold = A delta
IV pain and heat = C
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Action potentials:
- mediated by voltage-gated channels
- Encode stimulus intensity by frequency
- Cannot summate so are are all-or-none
- Evoked at threshold
- Refractory period
- Self-propagating
- Depolarising
- Sends electrical signal over long distances
- have a refractory period
- travel slowly
- conduction velocity can be improved by big axons or by myelination
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Graded potentials:
- Graded
- Encode stimulus intensity by amplitude
- Can summate
- Has no threshold
- No refractory period
- Decremental (signal can decay)
- De- or hyper-polarising
- Ligand-gated channels
- “Decides” if a cell will fire an action potential
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Ionic basis of the action potential is
mediated by voltage-gated channels
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But how does AP in neurone evoke contraction in muscle?
Contraction is triggered by AP in sarcolemma.
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The neuromuscular junction (first half that happens in the sarcolemma):
Action potential in motor neurone
- Opens voltage-gated Ca2+ channels in presynaptic terminal
- Triggers fusion of vesicles
- Acetylcholine (ACh) released
- Diffuses across synaptic cleft
- Binds to ACh (nicotinic) receptors
- Opens ligand-gated Na+/K+ channels
- Evokes graded (local) potential (end plate potential)
- Always depolarises adjacent membrane to threshold
- Opens voltage-gated Na+ channels - evokes new AP
- ACh removed by acetylcholinesterase
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The neuromuscular junction:
| tetrodotoxin
blocks Na+ channels and so blocks the action potential
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The neuromuscular junction:
| joro spider toxin
blocks Ca2+ channels and so stops transmitter release
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The neuromuscular junction:
| botulinum toxin
disrupts the release machinery and so blocks transmitter release
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The neuromuscular junction:
| curare
blocks Ach receptors and so prevents the end plate potential
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The neuromuscular junction:
| anticholinesterases
block ACh breakdown and so increase trasnmission at the NMJ
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Central nervous system synapses:
| Action potential reaches axon terminal
- Opens voltage-gated Ca2+ channels in presynaptic terminal
- Calcium enters axon terminal and to active zone
- neurotransmitter release and diffusion
- neurotransmitter binds to postsynaptic receptors
- neurotransmitter removed from synaptic cleft
118
Central nervous system synapses:
| Range of neurotransmitters
- Acetylcholine
- Norepinephrine
- Dopamine
- Serotonin (5HT)
- Histamine
- Glutamate
- GABA
- Glycine
- Peptides
- ATP
- Adenosine
each have several receptors
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Central nervous system synapses:
| Range of postsynaptic potentials
- Fast EPSPs (ionotropic)
- Slow EPSPs (metabotropic)
- Fast IPSPs
- Slow IPSPs
Enables complex synaptic integration
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NMJ postsynaptic potentials
big endplate potential
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Central nervous system synapses:
| Anatomical arrangement of synapse
- Axo-somatic
- Axo-dendritic
- Axo-axona
this has significant effects on their function.
122
Anatomical arrangement of NMJ
does not change.
123
Central nervous system synapses:
| Synaptic connectivity
- convergence
- divergence
- feedback inhibition
- monosynaptic vs polysynaptic pathways (Polysynaptic pathways are much more open to modulation at each synapse)
note: Stick an inhibitory interneurone in the polysynaptic chain and the effect changes entirely.
124
Synaptic connectivity of NMJ
always motorneurone-muscle cell – a bit of divergence to make a motor unit, but otherwise that is it.
125
CNS more complex than NMJ because:
- Range of neurotransmitters
- Range of postsynaptic potentials
- Small potentials (hence synaptic integration)
- Variations on anatomical arrangement
- Variations on “connectivity” of neurones
126
NMJ as a simple synapse
presynaptic vesicle, Ca2+-dependent ACh release, postsynaptic receptors, endplate potential, “safe” transmission, acetylcholinesterase
127
Comparison with CNS synapses
recognise why CNS synapses are so much more complicated; ie range of transmitters & receptors, fast and slow PSPs, EPSPs and IPSPs, small PSPs, synaptic integration, types of synapse, neuronal connectivity
