5. Nerve/Synapse Flashcards
(113 cards)
1
Q
Central Nervous System (CNS) components
A
brain + spinal cord
2
Q
Peripheral Nervous System (PNS) components
A
neurons (motor + sensory) and autonomic fibers
3
Q
motor neurons
A
efferent fibers that give out information to muscles
4
Q
sensory neurons
A
afferent fibers that receive information
5
Q
autonomic fibers
A
connect spinal cord to visceral organs
6
Q
synapse
A
specialised site of communication between neurons
7
Q
neuron physical characteristics
A
- cell body = soma
- branching dendrites
- a single axon
8
Q
the action potential starts at the… and propagates down the…
A
initial segment
axon
9
Q
resting membrane potential
A
small excess of negatively charged ions inside the membrane of neuron
10
Q
resting membrane potential =
A
-70mV
11
Q
what creates the resting membrane potential?
A
- concentration gradients for various ions
- selective permeability of membrane to K+ ions
12
Q
membrane potential at rest:
A
- neuronal membrane highly permeable to K+ but less permeable to other ions
- K+ leak out of the cell down their concentration gradient
- unpaired (-) ions accumulate inside the cell, creating an electric gradient: K+ ions pulled back into cell
13
Q
at equilibrium: electrochemical gradient
A
chemical gradient = electrical gradient
14
Q
Nernst Equation describes…
A
the membrane potential at equilibrium
15
Q
Nernst Equation (E)
A
61/z * log([ion]o/[ion]i)
16
Q
main factor determining the neuron resting membrane potential
A
equilibrium potential for K+
17
Q
equilibrium potential for K+
A
-90mV
18
Q
leak channels
A
proteins (ion channels) that form K+ selective pores through the membrane, always open
19
Q
equilibrium potential for Na+
A
+70mV
20
Q
equilibrium potential for Cl-
A
-80mV
21
Q
why is the resting membrane potential slightly more + than the equilibrium potential for K+?
A
small inward leak of Na+
22
Q
sodium-potassium pump
A
pumps 3 Na out and 2 K in against their concentration gradients by using energy produced by ATP hydrolysis
23
Q
action potential
A
brief electrical impulse that travels down the axon
24
Q
action potential spike/peak
A
membrane potential approaches Na equilibrium potential but very briefly
25
depolarisation
when membrane potential peaks at 30mV as sodium channels open
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repolarisation
membrane potential returning to its resting potential after having spiked
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hyperpolarisation
when membrane potential decreases below its resting potential
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when is an action potential initiated?
when the membrane potential depolarises to a threshold level, influenced by voltage-gated sodium channels
29
can the magnitude of action potential increase/decrease?
no, the action potential is an all or nothing mechanism
30
3 critical properties of voltage-gated sodium channels
- closed at resting membrane potential: open when repolarising
- selective for Na+
- open channel rapidly inactivates, stopping the flow of Na+ ions
31
absolute refractory period
sodium channels are inactive and the membrane is completely unexcitable for a few seconds after an action potential
32
what does speed of propagation depend on?
how fast the Na+ channel can be converted back to its closed configuration after repolarisation
33
relative refractory period
membrane potential overshoots its resting potential, making the axon less excitable and unlikely to fire an action potential
34
action potential is a positive or negative feedback mechanism?
positive
35
action potential steps
1. depolarisation of membrane to threshold activates small fraction of sodium channels: Na+ flows in membrane
2. inside of neuron gets more positive, further depolarising the membrane: more sodium channels open
3. all sodium channels open: peak reached
4. sodium channels inactivated
5. membrane relaxes back to resting potential
36
which ion channel is more present in the axon membrane?
voltage-gated sodium channels
37
what is the dominant permeability at action potential peak?
Na+
38
rising phase of action potential:
- sodium channels open
- potassium channels still closed
39
falling phase of action potential
- sodium channels close
- potassium channels open (takes longer)
40
which ion channels have delayed activation?
voltage-gated potassium channels -> take longer to open
41
when are potassium channels maximally open?
during repolarisation phase: K+ can flow out faster to bring membrane potential back to -70mV
42
Action potential propagation steps
1. depolarisation: sodium ions flow in
2. (+) charge in this region attracted to - charge in adjacent segment
3. (+) charge flows into next axon segment
4. propagation down axon continuously like a wave
5. (+) charge can only move forward due to rapid sodium channel inactivation
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how do neurons send information?
through means of frequency and pattern of action potentials
44
what do neurotoxins target?
sodium channels
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tetrodotoxin (TTX)
produced by puffer fish, extremely potent sodium channel inhibitor
46
batrachotoxin
secreted by frogs, deadly sodium channel activator: irreversibly opens sodium channels so constant AP being fired
47
drugs that can also block sodium channels
local anesthetics and antiepileptics
48
local anesthetics
injected into the nerve to block its sodium channels so the pain information will be blocked from going up to the brain at this point
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examples of local anesthetics
lidocaine, benzocaine, tetracaine, cocaine
50
anti epileptics
prophylactic drugs taken everyday to prevent seizures (without putting you to sleep) by blocking sodium channels
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anti epileptics examples
phenytoin (Dilantin), carbamazepine (Tegretol)
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propagation rate of action potential is proportional to...
axon diameter and myelination
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Wider axon propages slower or faster?
faster
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How can thinner axons propagate faster?
surrounded by Myelin sheets
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Myelin formed by: (2)
- Schwann cells in PNS
- oligodendrocytes in CNS
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nodes of Ranvier
periodic gaps in myelin sheets
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nodes of Ranvier contain a high concentration of...? why?
voltage-gated sodium channels to enable signal to be regenerated at periodic intervals due to sodium influx
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cause of multiple sclerosis
loss of myelin due to immune system attacking myelin made by oligodendrocytes
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white matter
regions of the brain and spinal cord containing mostly myelinated axons
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grey matter
comprises cell bodies, dendrites and synapses
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3 main types of synapses
- axodendritic
- axosomatic
- axoaxonic
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axodendritic synapse
between axon and dendrites (most common)
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2 types of axodendritic synapses
- spine synapse = mainly excitatory
- shaft synapse = mainly inhibitory
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axosomatic synapse
on neuron body (soma)
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axoaxonic synapse
axon synapses with the axon of another neuron
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presynaptic refers to...
everything upstream a synapse
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postsynaptic refers to...
everything downstream a synapse
68
divergence
a single neuron makes synapses with many other neurons through its branching axon
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presynaptic vesicles
contain neurotransmitters
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synaptic cleft
narrow space between presynaptic terminal and postsynaptic spine
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active zone
vesicles docked to the membrane adjacent to synaptic cleft, ready to be released
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postsynaptic density
darker spots on postsynaptic spine, containing proteins for neurotransmitter reception
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Calcium concentration inside neuron is very...
low
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what triggers neurotransmitter release?
activation of voltage-gated calcium channels
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neurotransmitter release steps
1. action potential invades presynaptic terminal, depolarising the membrane
2. calcium channels open so Ca moves into presynaptic terminal
3. synaptic vesicles fuse with presynaptic membrane
4. neurotransmitters released into synaptic cleft
5. transmitter activates receptors in the postsynaptic membrane, opening ligand-gated ion channels
76
calcium-dependent fusion of synaptic vesicle at active zone
1. action potential activates voltage-gated calcium channels so Ca enters neuron
2. calcium binds to receptor on presynaptic terminal
3. vesicle fuses with the membrane
4. transmitters in vesicles released into synaptic cleft
5. membrane reforms
77
toxins that can act on calcium-dependent fusion of synaptic vesicle at active zone
- tetanus
- black widow spider toxin: too many vesicles fuse with the membrane
- botox: proteins responsible for neurotransmitter reception chewed up
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Excitatory Postsynaptic Potential (EPSP)
depolarises the postsynaptic membrane, making it more likely to fire an AP
-> involves excitatory synapse
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Inhibitory Postsynaptic Potential (IPSP)
hyperpolarises the postsynaptic membrane, making it less likely to fire an AP
-> involves inhibitory synapse
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glutamate
main excitatory neurotransmitter in the brain
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ionotropic receptors
ion channels that open in response to binding of neurotransmitters to receptor sites on their external surfaces
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2 types of ionotropic glutamate receptors
- AMPA receptors
- NMDA receptors
--> ligand-gated ion channels
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receptors involved in excitatory transmission
- AMPA receptors
- NMDA receptors
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AMPA receptors
responsible for fast EPSP at excitatory synapse
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AMPA receptor activation
1. Glu released from vesicles and diffuse across synaptic cleft
2. Glu bind to AMPA receptors, opening its ion channel
3. AMPA is permeable to sodium so Na+ flows into postsynaptic spine, depolarising the post-synaptic cell
86
NMDA receptors
have their pore blocked by Mg2+ at resting membrane potential so they can't conduct current
87
NMDA receptor activation
1. depolarisation expels Mg2+ so pore can conduct
2. open pore is highly permeable to Ca2+ and noncovalent cations: Calcium flows into neuron
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2 conditions required for NMDA receptor activation
glutamate binding and postsynaptic depolarisation
89
synaptic plasticity
idea that synapses can change and become stronger (larger EPSP)
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Long-Term Potentiation (LTP)
model of synaptic plasticity in experimental context
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3 phases of LTP
1. Control: a single action potential stimulates Glu release
2. Induction: high frequency action potentials depolarise post-synaptic cleft so Calcium can be conducted, leading to more Glu release
3. LTP: hours after induction, a single action potential triggers a bigger/stronger EPSP
92
excitotoxicity
high concentrations of glutamate are toxic to neurons
93
how is excitotoxicty likely to contribute to neuronal degeneration after a stroke?
1. stroke: neurons die, releasing Glu which diffuses to surrounding regions
2. over activation of AMPA and NMDA receptors causes too much Calcium to flow into the cell
3. cell apoptis/suicide
94
2 broad functions of inhibitory synapses
- act as a break on excitatory neurons
- shape the pattern of excitatory neuron's action potential
95
which type of synapse is more local?
inhibitory synapses
96
Y-aminobutyric acid (GABA)
main inhibitory neurotransmitter in the brain
97
GABA A receptor
postsynaptic ionotropic receptor responsible for IPSP
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GABA A receptor activation
1. GABA binds to GABA A receptors, activating it
2. Influx of Cl- into cell hyperpolarises postsynaptic membrane
99
drugs that can act on GABA A receptors
- xanax makes GABA A receptors stay open longer, accentuating the IPSP and making you sleepy
- ethanol makes GABA A receptors more receptive, causing more inhibition in the brain, making you sleepy
100
synaptic integration key points (5)
- excitatory inputs usually located on dendritic spines
- inhibitory inputs usually clustered on/near cell soma
- action potential fired depending on relative balance of EPSPs and IPSPs
- each neuron is either excitatory or inhibitory
- inhibitory neuron can only inhibit other neurons by having excitatory inputs to fire action potentials
101
Metabotropic receptors (GPCRs)
- aka G-Protein Couple Receptors
- found at synapses but aren't ion channels
102
GPCR activation
1. Glu release in synaptic cleft
2. Glu binds to mGluRs (metabotropic Glu receptors), inducing a conformational change, activating mGluRs
3. 2nd messenger generated by mGluR inside postsynaptic spine
4. 2nd messenger diffuse inside cell, activating a range of cellular proteins
103
what does 2nd messenger activate when metabotropic receptors activate?
- ion channels: 2nd messenger binds to it on inside of cell, causing it to open
- protein kinases: proteins that add phosphates to another protein to activate it
- transcription factors which will regulate gene expression in the nucleus: gene transcription + protein synthesis
104
Glutamate and GABA activate what kind(s) of receptors?
both ionotropic and metabotropic receptors
105
neuromodulators
substances that aren't directly involved in fast flow of neuronal information but modulate global neural states, influencing alertness, attention and mood
106
neuromodulators interact mainly with which kind(s) of receptors
metabotropic receptors
107
neuromodulators examples
- dopamine
- serotonin
- norepinephrine
- endorphins (neuropeptide)
108
where do neuromodulators originate from?
tiny clusters of neurons in small brainstem or midbrain nuclei
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how are neuromodulators spread out?
neuron's axon in brainstem extend all the way up to cerebral cortex
110
dopamine involved in...
- addictive behaviours
- connections between + emotion and associate behaviour: reward pathway
111
serotonin influences...
mood
112
antidepressant effect on neuromodulators
affect serotonergic transmission
-> ie Prozac
113
simulants effect on neuromodulators
affect dopamine and norepinephrine transmission
-> ie amphetamines, cocaine
