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MEDICAL BIO > WEEK 9 - neuronal communication > Flashcards

WEEK 9 - neuronal communication Flashcards

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USMLE® Step 1 flashcards Biology 101 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
Q

how do neurons communicate
synaptic proteins in vesicles and their link to the action potential
synaptotagmin:

A

synaptotagmin: Ca2+ binding, fusion, endocytosis, binds lipids and SNARE
couples exocytosis to action potential

26
Q

how do neurons communicate
synaptic proteins in vesicles and their link to the action potential
synaptobrevin

A

part of SNARE complex

27
Q

how do neurons communicate
synaptic proteins in vesicles and their link to the action potential
proton pump

A

H+ electrochemical gradient enabling the neurotransmitter to get into the vesicle

28
Q

how do neurons communicate
synaptic proteins in vesicles and their link to the action potential
vesicular transporters

A

move neurotransmitters into vesicles

29
Q

how do neurons communicate
SNARE complex proteins mediate..

A

synaptic vesicle fusion

30
Q

how do neurons communicate
SNARE complex

A

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
Q

how do neurons communicate
SNARE complex
(my description)

A

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
Q

how do neurons communicate
SNARE complex
synatotagmin

A

synatotagmin is the calcium sensor that triggers vesicle fusion in response to calcium entry

33
Q

how do neurons communicate
presynaptic active zone

A

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
Q

how do neurons communicate
calcium triggers

A

synaptic vesicle fusion

35
Q

summary vesicle release
SNARE complex

A

synaptobrevin (vSNARE, on vesicle)
syntaxin (tSNARE, on membrane)
SNAP-25, anchored to plasma membrane

36
Q

summary vesicle release
proton pump and transporters

A

to load vesicles with neurotransmitter

37
Q

summary vesicle release
synaptotagmin

A

Ca2+ sensor that triggers vesicle fusion to the plasma membrane

38
Q

summary vesicle release
active zone

A

clusters vesicles and voltage gated Ca2+ channels (VGCC)

39
Q

summary vesicle release
action potential

A

opens VGCCs, triggering vesicle release

40
Q

how neurons communicate
vesicles release..

A

neurotransmitters of various types that have different functions

41
Q

how neurons communicate
neurotransmitters
classical

A

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
Q

how neurons communicate
neurotransmitters
non-classical

A

nitric oxide: gas, vasodilation

peptides

growth factors (e.g. BDNF): long-term memory, plasticity

43
Q

how neurons communicate
life cycle of neurotransmitters

A
  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
Q

neurotransmitters
what does serotonin regulate

A

mood, memory, cognition and more (e.g. vomiting)

45
Q

neurotransmitters
serotonin cycle

A

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
Q

neurotransmitters
what is glutamate

A

the main excitatory neurotransmitter in the human brain

47
Q

neurotransmitters
the tripartite synapse

A

pre and post synaptic neurons plus glia (astrocyte)

many synapses (not all) are tripartite and involve a glial cell called astrocyte

48
Q

neurotransmitters
The Glu-Gln cycle

A

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
Q

neurotransmitters
what reflects vesicle release

A

synaptic short-term plasticity

50
Q

neurotransmitters
synaptic short-term plasticity reflects vesicle release

A

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
Q

neurotransmitters
synaptic transmission occurs..

A

in ‘quanta’ each unit corresponds to one vesicle

52
Q

neurotransmitters
a give synapse can secrete…

A

variable quanta in response to different stimuli

53
Q

neurotransmitters
the strength of transmission can depend on…

A

history of synapse

54
Q

neurotransmitters
synaptic depression results from…

A

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
Q

neurotransmitters
what is essential for continual synaptic transmission

A

synaptic vesicle recycling by endocytosis

56
Q

neurotransmitters
synaptic vesicle recycling

A

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
Q

summary: neurotransmitters
examples of different functions of neurotransmitters

A

regulating arousal, mood, learning and memory, aggression and escape responses

58
Q

summary: neurotransmitters
neurotransmitters are removed..

A

quickly from the synaptic cleft to allow for the next action potential

59
Q

summary: neurotransmitters
neurotransmitters are recycled by..

A

reuptake into neuron or glial cells (astrocytes)

60
Q

summary: neurotransmitters
what factors can induce synaptic facilitation or depression

A

timing
strength
synapse
sequential stimuli

61
Q

summary: neurotransmitters
facilitation and depression reflect

A

released vesicles

62
Q

summary: neurotransmitters
what happens once synaptic vesicles are recycles

A

synaptic vesicles are recycled
loaded again with neurotransmitter
and brought back to synapses

MEDICAL BIO (12 decks)

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