nerves Flashcards
(112 cards)
1
Q
what are nerves
A
Nerves are a bundle of fibres that transmit impulses from various parts of the body to the brain or spinal cord and back. They also transmit impulses within different brain regions
2
Q
how the nervous system is split image
A
into the PNS and CNS and so forth
3
Q
The afferent/sensory system transmits information about senses from and to
A
sensory organs to other parts of the body.
4
Q
the efferent (motor) system is comprised of?
A
the somatic and autonomic systems.
5
Q
The somatic nervous system directs contraction of what muscles
A
skeletal muscles. It is important for the voluntary contraction of muscles.
6
Q
The automatic nervous system is responsible for regulating what activity?
A
the involuntary activity of visceral organs, such as the heart and gastrointestinal tract, blood vessels and certain glands.
7
Q
what is the enteric nervous system
A
element of the PNS which exists entirely within the gastrointestinal tract.
8
Q
there are 2 cell types in the nervous system: they are?
A
neurons and glia
9
Q
- examples of glia in the CNS
A
ASTROCYTES and OLIGODENDROCYTES
10
Q
examples of glia in the PNS
A
schwann cells
11
Q
what roles do glia play to neurones
A
a more supportive role both structurally and metabolically to neurons.
Schwann cells and oligodendrocytes are important in the conduction of nerve impulses, as they provide insulation, wrapping themselves around a neurone to support sending impulses over long ranges.
12
Q
what do neurons do
A
these are the cells that generate and send impulses
13
Q
neurons know the general structure
A
14
Q
neurons characteristics / structure
A
- a soma (cell body)
- axons
- dendrites
15
Q
whats a soma
A
[containing a nucleus and other organelles, such as mitochondria and endoplasmic reticulum, which are responsible for its general metabolic functions]
16
Q
what are the dendrites
A
[the points of contact for axons from other neurons. In essence, dendrites form the receptive area of a neuron].
17
Q
why are axons important
A
only neurons have it
18
Q
where do axons leave the soma at before they travel to the target?
A
axons leave the soma at the AXON HILLOCK then travel to target (another neuron or a muscle, for example) where the AXON TERMINAL, or pre-synaptic terminal, forms a synaptic connection.
19
Q
A
20
Q
what do axons contain?
A
Axons contain an AXON INITIAL SEGMENT near the axon hillock where digital signals known as ACTION POTENTIALS are initiated. In most neurons, the axon branches to create several terminals.
21
Q
what are mammalian axons:
A
have narrow diameters, just a few μm, and are relatively short in the CNS (mm) compared with most axons in the PNS. The latter tend to be grouped together to form nerve trunks which are sheathed in connective tissue to provide protection.
22
Q
neuron function image
A
https://www.notion.so/nerves-15300bb3982d8014a6d8f72feab44468?pvs=4#15300bb3982d80f6927fc5621f20d100
23
Q
what do neurons convey
A
action potentials
24
Q
what do neurons release and where
A
NEUROTRANSMITTERS, at SYNAPSES they make with other neurons.
25
what do these neurotransmitters do?
bind to receptors on dendrites and form a drug-receptor complex, resulting in the trigger of signals within neurons. The signals are transferred to the soma.
26
neuron cell membrane image
https://www.notion.so/ion-and-electric-gradients-in-neurons-15300bb3982d80c6b6b5fcac4968bf70?pvs=4#15300bb3982d809bb2abdd9658b2540e
27
what is the extracellular Na+ concentration like?
is very high (~150 mM) whereas that in the cell is low (~15 mM)
28
what is the extracellular K+ concentration like?
is low (~5 mM) and the intracellular K+ concentration is high (~140 mM)
29
what is Ca2+ concentration inside the cell like versus outside ?
inside is also very low (~100 nM) whereas outside the cell, Ca2+ concentration is very high (1.3 mM).
30
how are ionic concentrations maintained
using PUMPS expressed in the bilayer
31
how does the Na+/K+ ATPase Pump/Transporter work
1. This pump binds a molecule of ATP together with 3 Na+ ions inside the neuron.
2. The ATP is hydrolysed leading to the phosphorylation of the pump at a highly conserved aspartate residue.
3. This leads to a conformational change in the pump such that the Na+ ions are exposed to the outside of the membrane. Phosphorylation also reduces the affinity of the pump for Na+ and so the ions are released.
4. The change in conformation reveals binding sites for 2 extracellular K+ ions which causes the dephosphorylation of the pump so that it reverts to its original conformation thus transporting the ions into the neuron.
32
There are also other ATPases to maintain the concentrations like what?
the Na+ Ca2+ exchanger.
33
what are ion channels
these are macromolecular structures/proteins that form pores in the membrane which allow the exchange of ions
34
why are the ion channels pores special
These pores are highly selective for particular ions.
35
therefore K+ channels only allow what ions, and Na+ channels only allow what ions?
So, K+ channels allow only K+ to pass through whilst Na+ channels allow only Na+ ions to pass
36
Some ion channels allow multiple ions to pass through and are named accordingly. Most of these ion channels are closed normally.
- neurons have K+ channels in their membrane which are open at rest and allow K+ to flow out of the cell down the concentration gradient.
→ These leak K+ channels together with the Na+/K+ ATPase maintain the ion channel gradient
across the membrane.
37
Ions carry a charge. Since there is a difference in the concentrations of ions between the inside and outside of the cells, what is generated?
membrane potential
This is typically in the order of −65 mV to −80 mV (on average - 70 mV).
38
The membrane potential is the sum of?
individual ion gradients
39
As the ions are charged, this results in an electrical gradient in addition to the concentration gradients. What does this cause?
electro-chemical gradient across the membrane for each ion.
40
what is the NERNST equation used to calculate
the equilibrium potential of the ion
41
what is the NERNST equation
https://www.notion.so/ion-and-electric-gradients-in-neurons-15300bb3982d80c6b6b5fcac4968bf70?pvs=4#15300bb3982d80e18e06e178c9c03e4e
RT/ZN x ln([ion]out / [ion]in)
42
what are voltage gated ion channels
those that respond to voltage changes across the cell membrane
43
to understand how a neuron regulates it’s activity, we need to understand how ions move across a membrane: what can this be via
ion channels
44
A special characteristic of voltage gated ion channels is?
that they have a ‘voltage-sensor’, a series of charged amino acids. Thus, these channels will only open during a range of potentials. Hence, these channels are not open at rest and do not contribute to the resting membrane potential of neurons.
45
voltage gated ion channels have 3 diff states which are
Three different states: open, closed and inactivated.
inactive doesn’t mean closed!
46
The channel opening = time-dependent. what does this mean?
= open for a period of time and then go into an inactivated stated followed by a closed state.
47
where are ion channels distributed?
throughout the neuron (i.e. they are present in soma, dendrites and axons)
48
different types of ion channels are not evenly distributed - for example?
e.g. axon initial segment has a high density of Na+ channel
49
what do dendrites do
express a significant number of receptors and ion channels
50
their anatomy makes them best placed to do what?
receive the most signals from other neurons
51
what is glutamate
most common neurotransmitter
52
what does the release of glutamate onto dendrites activate?
ionotropic receptors
these receptors are linked to ion channels
53
glutamate binding to these ionotropic receptors causes what?
the ion channels to open and Na+/Ca2+ ions to flow into the dendrite.
54
what do the positive ions moving into the dendrites cause?
the membrane potential to become more positive (or depolarise) and produces an EXCITATORY POST-SYNAPTIC POTENTIAL (EPSP)
55
Many EPSPs are generated and these travel where?
to the soma
56
what happens when EPSPs sum up
the membrane potential depolarises more.
57
The voltage change spreads and reaches where?
the axon
58
If the membrane voltage reaches -55 mV or so, what does this lead to and mean?
leads to Na+ channels which are highly concentrated in the axon initial segment open and generate an ACTION POTENTIAL.
59
what also receive signals that cause the membrane to become more negative (or hyperpolarize).
The soma and dendrites
60
in terms of glutamate: common in the brain: this is espectially relevant to the esps pic above: when released, it binds to…?
receptors present on the dendrites (the 2 ionotropic ones - these are coupled to iron channels)
61
Na is + so makes cell membrane more positive =
excitatory response: so when AMPA receptor opens - cell membrane = more positive
62
glutamate can also bind to nmda one receptors to open the permeable to Na/Ca2+ channel: what effect does this have?
so the membrane potential is more positive as more pos ions go into the cell.
- therefore, EPSP is released!
63
why is this effect transient (temporary)
as glutamate can unbind from the receptor, so then ion channels close, and membrane channels go back to rest after the EPSP is released.
64
- EPSP’s generated in the dendrite travel to where, to do what
the soma and summate
65
what happens after EPSP’s summate?
they become a single EPSP of a bigger amplitude/voltage, which spreads over the axon: when this reaches a certain membrane potential, generates an impulse/action potential.
this is how action potentials are generated!
66
if you had lots of action potentials all the time, what would be caused.
epilepsy
67
therefore the opposing mechanism to relax this are ?
IPSPs: GABA, acting on GABAa receptors.
68
In adult neurons, these inhibitory signals are normally generated by what neurotransmitter?
GABA, the major inhibitory neurotransmitter, acting on its receptors.
also transient (short time/time dependent) response
69
how does GABA also act on ionotropic receptors?
results in the opening of an ion channel that is permeable to Cl- ions.
70
As Cl- is a negatively charged ion, the influx of Cl- into the cell causes the membrane to hyperpolarize. what does this do to neuronal activity?
This will dampen neuronal activity as it will oppose the initiation of action potentials.
71
resting potential of Cl-
-80mV
72
how are action potentials generated?
left = near the soma and cell body, the first thing near is the axon initial segnament (AIS). depolarisation reaches here, and at -55mV (threshold, sodium channels open up)
73
The action potential or nerve impulse is the means by which information is passed along from axons to
to the terminals.
74
When neurons receive excitatory inputs that sum up and depolarize the axon initial segment to -55 mV or so, what opens?
voltage-gated Na+ channels open rapidly.
75
what is known as the action potential threshold?
The membrane potential at which the Na+ channels open at the axon initial segment
76
The opening of voltage-gated Na+ channels allows Na+ influx down its concentration gradient which, in turn, does what to the membrane potential and channels?
depolarises the membrane potential and promotes more channels to open
77
this depolarisation = rapid - how quick?
less than 1 ms.
78
The Na+ equilibrium potential is +60 mV so what does the membrane do to
approach this
depolarizes rapidly
79
This potential is still not reached - why?
because voltage-gated Na+ channels become inactive and voltage-gated K+ channels open at potentials of -30 mV or so.
80
the voltage gated K+ channels open slower than Na+ channels but the K+ influx out of the cell prevents the membrane potential from depolarizing beyond +40 mV. What happens as more K+ channels open up?
The membrane potential then starts to fall rapidly
ACTION POTENTIAL REPOLARISATION PHASE.
81
The membrane potential is then restored by what?
the pumps (Na+/K+ ATPASE) and voltage-gated K+ channels closing.
81
The membrane potential in fact becomes more negative than the resting membrane potential
(known as the AFTERHYPERPOLARIZATION) and approaches what?
EK, the K+ equilibrium potential.
82
why is the after hyperpolarization and restoration of the resting membrane potential important
as they allow Na+ channels to become available again to generate a new action potential, should the membrane depolarize again.
83
The period during the hyperpolarisation phase is called what?
the relative refractory period:
84
- is the action potential quick or slow
very rapid
85
Unlike synaptic potentials, this is an “all or nothing” event and is often described as a digital signal. Thus, information is coded in
the frequency of action potentials, not their amplitude.
86
where are axon potentials initiated
at the axon hillock
87
where do axon potentials move down after being initiated?
down the axon towards the axon terminals, away from the soma.
88
what does axon potentials moving down require
the depolarisation to spread along the axon such that the threshold can be reached in another part of the axon to generate the next action potential and so on.
89
what is depolarisation
Depolarisation is the result of Na+ ion influx creating an electrical current.
90
what is the limiting factor of depolarisation
how far the current can spread through the axonal cytoplasm before leaking out through the membrane
91
what do thin axons have little of, which means there will be more current leak?
relatively little cytoplasm compared with the surface area of the membrane thus there is likely to be more current leak:
the opposite is true in axons with larger diameters.
92
in both cases, however, there is a limit to how far current can flow before it dissipates. This has the additional effect of limiting what?
the conduction velocity; that is the speed at which action potentials travel along an axon.
93
how do we overcome a limited conduction velocity?
To overcome this, some axons are wrapped in a myelin sheath which acts as an electrical insulator
94
what are schwann cells responsible for?
for myelinating axons in the PNS whilst oligodendrocytes perform this function in the CNS
95
what does myelin do?
prevents the leakage of current through the membrane allowing it to spread through the cytoplasm below.
96
myelin sheath structure
- due to schwann cells
- not continuous
- regular gaps called nodes of ranvier
97
whats clustered on the nodes of ranvier
the voltage-gated ion channels are clustered so it is where the action potentials are generated
98
what is saltatory conduction
how in myelinated axons the action potential jumps from node to node
99
do myelinated or unmyelinated neurons have higher conduction velocities
Myelinated axons, such as those of α motor neurons, also have much higher conduction velocities (30-120 ms−1) than unmyelinated ones (0.5-2 ms−1), such as C-fibres involved in pain perception.
100
the action potential @ diff mV’s image
https://www.notion.so/action-potential-generation-in-neurons-15300bb3982d8092bb1ae121f3376f01?pvs=4#17200bb3982d80388b97db74deab6388
101
once generated, the axon potential moves down the end of the axon to
the terminals
102
from axon initial segment → end steps
- all along the axon = high conc of Na+ channels: once depolarisation occurs, it spreads from the next part of the axon etc, causing the sodium ion channels there to open up and generate an action potential again
- this happens if the axon is unmyelinated!
- the action potential depends on the spread of depolarisation and opening of subsequent sodium channels along the axon.
- the sodium influx generates a small electric current, which travels along the axon. but @ some point leakage occurs of it. if enough leakage = wont reach end of axon
- passive spread is of this electrical current
103
what are the main class of clinically used drugs that affect action potential generation?
local anaesthetics
104
how do anaesthetics work/where can they be applied (general)
used to block the sensation of pain, for example during dental procedures or childbirth, and can be applied topically, injected or infiltrated into the spinal cord (epidural).
105
anaesthetics example
lidocaine
106
does lidocaine work quickly? how long does it last
effects are rapid. in onset (~2 min) and last for up to an hour.
107
Note the amide group in lidocaine/some other anaesthetics structure. why is this key?
Drugs which lack this group, for example procaine, are susceptible to metabolism by non-specific plasma esterase which means that it has a much slower rate of onset (~20 min) and higher doses must be administered.
108
are local anaesthetics acids or bases?
weak bases
109
Lidocaine has a pKa of 7.9 so at physiological pH (7.4) approximately how much of the drug is ionised.
75%
110
why is whether or not lidocaine is ionised or not key?
Only the unionised form can permeate the axonal membrane.
111
- Once inside the cell, a proportion of the drug molecules become ionised. why is that key for binding
It is in this form that they bind to voltage-gated Na+ channels. Binding to the channel prevents Na+ ions from passing through the channels thus inhibiting the firing of action potentials. Some local anaesthetics bind preferentially to channels in the open state and therefore act more rapidly on axons that are generating action potentials
