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MEDICAL BIO > WEEK 9 - neuronal communication > Flashcards

WEEK 9 - neuronal communication Flashcards

1
Q

the case of patient H.M.

A
  • HM had normal intelligence, no problem other than epilepsy
  • bilateral removal of 8cm of medial temporal lobe
  • developed severe and permanent inability to acquire new information
  • short term memory ok, no LONG TERM MEMORY
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2
Q

the case of patient RB

A

RB has an ischemic episode (loss of blood to brain) which caused anterograde and retrograde amnesia

damage only included a subset of cells in the hippocampus

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3
Q

what did the cases of patient H.M. and R.B. tell us

A

memory is located in the medial temporal lobe, and particularly in the hippocampus

but damage to the thalamus, caused by stroke, tumours or chronic alcoholism, also cause amnesia:
- memory systems

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4
Q

modular organisation of the brain
removal of frontal lobe

A

aggression

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5
Q

modular organisation of the brain
removal of prefrontal lobe

A

unawareness of danger

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6
Q

modular organisation of the brain
removal of hippocampus

A

retrograde and anterograde amnesia

alzheimer’s disease

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7
Q

modular organisation of the brain
substantia nigra damage

A

parkinsons’ disease

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8
Q

modular organisation of the brain
removal of thalamus

A

amnesia

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9
Q

modular organisation of the brain
cutting the corpus callosum

A

split-brain patients

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10
Q

how do neurons communicate
what are neurons

A

neurons are polarised cells that transmit in one direction

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11
Q

how do neurons communicate
neurotransmission

A

electric impulse travels down axon

triggers the release of neuro-transmitter at the synapse

binding of the neurotransmitter to a receptor in the dendritic membrane triggers the opening of ion channels

this provokes influx of Na+ ions

influx of Na+ ions creates an electric impulse that travels down the axon

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12
Q

how do neurons communicate
the membrane potential

A

higher concentration of K+ inside the cell and Na+ out

other ions too negative to the inside

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13
Q

how do neurons communicate
concentration gradient

A

will drive K+ out and Na+ in

Membrane potential
Na-K ATPase pump (maintains gradient)
- Kin Nout
- 2 potassium in 3 sodium out
- So neuron always retains a negative charge inside

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14
Q

how do neurons communicate
voltage gradient

A

more negative in the inside, will drive both K+ and Na+ in

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15
Q

how do neurons communicate
equilibrium potential for an ion

A

the votage at which there is no net flow of hat particular ion
e.g. for K+ in mammalian cells -120mV
- at 120mV the tendency of K+ to move out of the cell will be exactly offset by the attraction of K+ to enter the cell due to their positive charge and the negative charge inside the cell

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16
Q

how do neurons communicate
the sodium pump

A

OR Na+/K+ ATPase

maintains the Na+ and K+ gradients

  • the ionic concentration gradients are maintained by the sodium pump
  • this pumps Na+ out of the cell and replaces them with an influx of K+ ions
  • 3Na+ are replaced with 2K+, giving the inside of the cell negative charge
  • against the natural conc gradients requiring ATP
    –> cells use 30% of ATP for this pump
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17
Q

how do neurons communicate
the action potential

A

resting potential: the inside of the axon is -50 to 70mV inside the cell

start: all Na+ channels are closed

electrical current causes inside of the cell to become less negative, opening Na+ channels and letting Na+ in

more Na+ channels begin to close and K+ channels begin to open, letting K+ escape
K+ channels open slowly and stay open for longer

another action potential cannot occur in the refractory period
membrane potential restored

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18
Q

how do neurons communicate
the action potential
all or nothing

A

Action potential
- All or nothing
- Once over threshold depolarisation will happen

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19
Q

how do neurons communicate
saltatory conduction

A

speeds up transmission in long axons

the larger axons in vertebrates are surrounded by myelin

at regular intervals, the nodes of Ranvier, the sheath is interrupted and the axon membrane exposed

the sodium channels are restructed to these odes, thus ionic currents jump from one node to the next

this results in a higher conduction velocity to 50m/sec

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20
Q

summary neurotransmission
Na+ channels

A

closed in resting state
fast opening with electrical impulse
fast closing: inactivated state, responsible for the refractory period

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21
Q

summary neurotransmission
K+ channels

A

closed in resting state
delayed opening
slower closing

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22
Q

summary neurotransmission
can only go in

A

one direction

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23
Q

summary neurotransmission
saltatory conduction

A

myelination and jumping at nodes of ranvier

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24
Q

how do neurons communicate
neurotransmitters

A

neurotransmitters are released when synaptic vesicles fuse with the presynaptic plasma membrane

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25
how do neurons communicate synaptic proteins in vesicles and their link to the action potential synaptotagmin:
synaptotagmin: Ca2+ binding, fusion, endocytosis, binds lipids and SNARE couples exocytosis to action potential
26
how do neurons communicate synaptic proteins in vesicles and their link to the action potential synaptobrevin
part of SNARE complex
27
how do neurons communicate synaptic proteins in vesicles and their link to the action potential proton pump
H+ electrochemical gradient enabling the neurotransmitter to get into the vesicle
28
how do neurons communicate synaptic proteins in vesicles and their link to the action potential vesicular transporters
move neurotransmitters into vesicles
29
how do neurons communicate SNARE complex proteins mediate..
synaptic vesicle fusion
30
how do neurons communicate SNARE complex
links vesicle to plasma membrane - the vesicle that contains Ca2+ synaptobrevin (vSNARE) binds Syntaxin (tSNARE) and SNAP-25, which is anchored to the plasma membrane tetanus toxin and botulinum toxin cleave the SNARE complex proteins and block synaptic transmission
31
how do neurons communicate SNARE complex (my description)
SNARE complex fuses vesicle containing ca2+ ions to fuse with the membrane - This releases the ca2+ ions - Ca2+ fuses with the receptor on (post)synapse causing it to open - Influx of cations - Continued depolarisation Electrical signal --> chemical signal --> electrical signal
32
how do neurons communicate SNARE complex synatotagmin
synatotagmin is the calcium sensor that triggers vesicle fusion in response to calcium entry
33
how do neurons communicate presynaptic active zone
the presynaptic active zone is highly organised structure voltage gated calcium channels are concentrated in the active zone facilitating vesicle fusion and neurotransmitter release synaptotagmin in vesicles is the calcium sensor
34
how do neurons communicate calcium triggers
synaptic vesicle fusion
35
summary vesicle release SNARE complex
synaptobrevin (vSNARE, on vesicle) syntaxin (tSNARE, on membrane) SNAP-25, anchored to plasma membrane
36
summary vesicle release proton pump and transporters
to load vesicles with neurotransmitter
37
summary vesicle release synaptotagmin
Ca2+ sensor that triggers vesicle fusion to the plasma membrane
38
summary vesicle release active zone
clusters vesicles and voltage gated Ca2+ channels (VGCC)
39
summary vesicle release action potential
opens VGCCs, triggering vesicle release
40
how neurons communicate vesicles release..
neurotransmitters of various types that have different functions
41
how neurons communicate neurotransmitters classical
inhibitory: GABA hyper-polarises synapses, silencing transmission excitatory (depolarizing): - Glu main in brain - Ach mian for motorneurons catecholamines: - dopamine: arousal, reward, learning and memory - adrenaline: visceral - noradrenaline: flight or fight, mobile body for action - serotonin: mood, cognition
42
how neurons communicate neurotransmitters non-classical
nitric oxide: gas, vasodilation peptides growth factors (e.g. BDNF): long-term memory, plasticity
43
how neurons communicate life cycle of neurotransmitters
1. amino acid precursor in neuron 2. precursor metabolised 3. vesicular transported 4. release and binding to post synaptic receptors 5. auto-receptors to regulate release synthesis, firing 6. termination: plasma membrane transporter 7. termination: diffusion 8. termination: glial membrane transporter 9. inactivation
44
neurotransmitters what does serotonin regulate
mood, memory, cognition and more (e.g. vomiting)
45
neurotransmitters serotonin cycle
tryptophan (Trp) in neuron is metabolised by TrpOHase and LAADC to produce Serotonin (5-HT) 5-HT in vesicles by vesicular mono-amine transporter 5-HT released binds with post-synaptic receptors (15v types) and pre-auto-receptors 5-HT is taken up by SERT, goes back into vesicles or metabolised by MAO in mitochondria
46
neurotransmitters what is glutamate
the main excitatory neurotransmitter in the human brain
47
neurotransmitters the tripartite synapse
pre and post synaptic neurons plus glia (astrocyte) many synapses (not all) are tripartite and involve a glial cell called astrocyte
48
neurotransmitters The Glu-Gln cycle
many synapses (not all) are tripartite and involve a glial cell called astrocyte astrocytes provide neurones with lactate for energy and take up Glu via Excitatory Amino Acid Transporter (EAAT) astrocytes covert Glu to Gln, and give Gln back to the pre-synaptic neuron neuron converts Gln and Glu again
49
neurotransmitters what reflects vesicle release
synaptic short-term plasticity
50
neurotransmitters synaptic short-term plasticity reflects vesicle release
closely spaced stimuli facilitate as the interval between stimuli increases facilitation diminishes facilitation can accumulate during a train of stimuli more realistic: at most synapses both facilitation and depression occur
51
neurotransmitters synaptic transmission occurs..
in 'quanta' each unit corresponds to one vesicle
52
neurotransmitters a given synapse can secrete...
variable quanta in response to different stimuli
53
neurotransmitters the strength of transmission can depend on...
history of synapse
54
neurotransmitters synaptic depression results from...
vesicle depletion is vesicle pool is large and probability of fusion is low: NO DEPRESSION if the vesicles pool is small and the probability of fusion is high: STRONG DEPRESSION i.e. the second stimulus releases half as many quanta
55
neurotransmitters what is essential for continual synaptic transmission
synaptic vesicle recycling by endocytosis
56
neurotransmitters synaptic vesicle recycling
kiss and run fusion with plasma membrane and clathrin endocytosis to vesicle pool fusion with membrane and endocytosis to endosome vesicles need to be refilled with neurotransmitter
57
summary: neurotransmitters examples of different functions of neurotransmitters
regulating arousal, mood, learning and memory, aggression and escape responses
58
summary: neurotransmitters neurotransmitters are removed..
quickly from the synaptic cleft to allow for the next action potential
59
summary: neurotransmitters neurotransmitters are recycled by..
reuptake into neuron or glial cells (astrocytes)
60
summary: neurotransmitters what factors can induce synaptic facilitation or depression
timing strength synapse sequential stimuli
61
summary: neurotransmitters facilitation and depression reflect
released vesicles
62
summary: neurotransmitters what happens once synaptic vesicles are recycles
synaptic vesicles are recycled loaded again with neurotransmitter and brought back to synapses
63

MEDICAL BIO (17 decks)

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