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BMS11004 > BMS11004 - WEEK 4 TUESDAY, WEDNESDAY, THURSDAY > Flashcards

BMS11004 - WEEK 4 TUESDAY, WEDNESDAY, THURSDAY Flashcards

brain extracellular fluid, BBB, ventricular system, CSF, neurons, astrocytes, blood vessels

1
Q

what is the neuronal microenvironment made up of

A

glia, capillaries, other neurons, extra-cellular space

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2
Q

what is extracellular space made up of

A

extracellular matrix (structural support), BECF (brain extracellular fluid)

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3
Q

how can BECF influence, and be influenced by neuron

A

increased neuronal activity impact changes in BECF composition and continue round in loop

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4
Q

why must BECF composition need to be tightly regulated

A

neuronal dysfunction or death

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5
Q

how can neuronal activity change BECF composition

A

increased K+ conc on outside of cell
changes in Ca2+ conc
changes in O2, glucose, CO2 conc
increased H+ = acidification
NT conc

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6
Q

how could a change in BECF composition change neuronal activity

A

increased K+ conc in BECF increases resting potential bringing cell closer to threshold for firing AP
increased NT release, leading to unspecific receptor activation = unspecific neuronal activity

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7
Q

name 4 ways of regulating neuronal microenvironment, and BECF

A
  1. BBB
  2. CSF in ventricular system
  3. neurons
  4. glial cells
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8
Q

how can you study BBB in research

A

intravenous dyes injection, pass through leaky capillary and stain soft tissues but no stains in brain

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9
Q

what is function of BBB

A

protect neuron from blood-substance conc fluctuation
-increased amino acid conc post-food
-increased K+ H+ conc after exercise
-circulating hormones
-inflammatory mediators
-toxins

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10
Q

how is BBB maintained, and how can important molecules pass by

A

tight junctions between endothelial cells, astrocytic endfeet, thick basement membrane

passes via facilitated transport, exchangers, co-transporters, many mitochondria in endothelial cell (more ATP), diffusion of small uncharged lipid soluble molecules

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11
Q

what are transport exchangers

A

proteins moving ions in opposite direction

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12
Q

what are co-transporters

A

proteins moving ions together

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13
Q

where are leaky regions of BBB

A

choroid plexus (ventricular system = where CSF made), circumventricular organ

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14
Q

what do leaky regions of BBB allow

A

hormone release, osmoreceptors (OVLT, subfornical organ, hypothalamus) detect osmolarity of blood and cytokines, activating temp control centre so brain can directly analyse blood for infections

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15
Q

explain layout of cavities and ventricles in ventricular system in brain

A

4 cavities
2 lateral ventricles in cerebral hemispheres, come down meet 3rd ventricle and cerebral aqueduct into 4th ventricle to brain stem (medulla, pons, cerebellum)

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16
Q

what does CSF do

A

physical buffer for protection
maintains ion levels between intra/extracellular fluid and BECF
remove waste product

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17
Q

what is in CSF

A

similar to blood (no RBC, platelets)
less K+, amion acids, protein

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18
Q

what is exchanged form CSF to BECF

A

macronutrients eg; glucose
micronutrients eg; vitamins
ions eg; HCO3-

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19
Q

what is exchanged from BECF to CSF

A

metabolic waste products eg; CO2
NTs which are not recyled

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20
Q

outline flow of CSF

A

secreted by choroid plexus, circulate around ventricles, down to central canal and foramen
absorbed from subarachnoid space to venous blood system at superior sagittal sinus

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21
Q

how much CSF produced per day

A

500 mls

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22
Q

how it extracellular fluid prevented from accessing CSF

A

tight junctions and selective absorption of substances into CSF across choroidal epithelial cells (AT/facilitated diffusion)

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23
Q

name 3 type of meninges

A

pia mater
arachnoid mater
dura mater

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24
Q

give properties of pia mater (inner)

A

soft, pliable, thin membrane, quite permeable

25
Q

give properties of arachnoid mater (middle)

A

under subarachnoid space, has tight junctions

26
Q

give properties of dura mater (outer)

A

thicker, important for structure

27
Q

where is CSF forced out of arachnoid granulations into

A

superior sagittal sinus

28
Q

outline details of arachnoid membrane envaginations

A

arachnoid granulations (up to 1cm)
arachnoid villi (smaller)
many tight junctions to prevent things moving in between cell

29
Q

outline bulk movement of CSF out of subarachnoid space

A

via vesicle across membrane into venous sinus

30
Q

how does more CSF move across into venous sinus

A

increased absorption with increased intracranial pressure
more CSF made, more pressure is generated in subarachnoid space, so more CSF moved across into venous sinus

31
Q

how is hydrocephalus created

A

too much CSF production (not enough absorption)
dilation of ventricular system
obstruction in ventricular system/interrupted CSF absorptions
increased intracranial pressure
loss of brain cell, loss of brainstem relfex

32
Q

where do neurons and astrocytes terminate neurotransmission

A

tripartite synapse

33
Q

what ions does neurons and astrocytes remove from extracellular space, and how

A

K+, via pump into cell to keep intracellular K+ greater than in extracellular, to maintain equilibrium

34
Q

what does increased K+ cause astrocyte to start

A

increase glucose metab to help neuron
shuttle lactate to neurons and allow pumps to keep pumping more K+ into cell (using ATP conversion)
increased K+ uptake

35
Q

what is equilibrium potential for K+ in both neurons and astrocytes

A

-90mV

36
Q

what is neurons resting MP

A

-65mV

37
Q

what is astrocytes resting MP

A

-85mV

38
Q

do astrocytes or neurons have higher K+ selectivity

A

astrocytes
also has more selective membranes to K+, more extracellular K+ will influence Vm

39
Q

are astrocytic or neuronal membranes more permeable to Na+

A

neuron

40
Q

how to astrocytes communicate (chemical synapse or gap junction), and what does this create

A

use gap junctions which creates syncytium = intracellular compartments connected via gap junctions without having to release into any extracellular spaces

41
Q

what do connexins do in astrocyte

A

create pore from one astrocytic intracellylar compartment to another astrocytic intracellular compartment
if neurons create lots of K+, nearby astrocyte can uptake and pass onto others without it making contact with extracellular space, redistributing K+ to areas of decreased activity
can also transport sugars, aa, cAMP, Ca2+ through gap junction via syncytium

42
Q

what is neurovascular coupling

A

couple neuron activity to vascular activity

43
Q

how can astrocytes detect if neuron is very active

A

from dendritic spine (release lots of NT, AP) and attach themselves to arterioles to release things modulating muscles activity surround blood vessel, to relax/contract, to increase/reduce amount of O2 entry

44
Q

how does MRI work

A

3D, structural, H+ atoms align in scanner, radio wave cause H+ facing new direction. when relax and return to old position, emit resonance

45
Q

how strong is MRI

A

0.5-3T, 60T in research

46
Q

what do radio frequency coil in MRI do

A

radio frequency coil directs wave, detect bounce back wave

47
Q

what do gradient coils in MRI do

A

other magnets, lower strength, adjusts field

48
Q

how does PET work

A

label glucose, injects radioactive tracer, absorbing into bloodstream and measure volume in brain to show active area

49
Q

Neuron A has an axon twice as wide as neuron B’s axon. If everything else is same between 2 neurons, how long is neuron A’s space constant compared to neuron B’s space constant?

A

A’s space constant is sqrt (2)times (ie. 1.4 times) longer than B’s space constant

50
Q

What’s wrong with this statement? “If myelin makes AP go faster by insulating axon, AP would go even faster if entire axon is insulated, even Nodes of Ranvier”

A

Nodes of Ranvier are necessary for voltage-gated Na+ channels, to allow the propagation of signal (signal needs generation by sodium channel)

51
Q

What would happen to neuronal conduction speed if you insert a lot of K+ leak channels into membrane (ie. K+ channels that are open at resting potential)

A

decrease: membrane resistance goes down, shorter space constant

52
Q

Given [Ca2+]I = 0.0001mM, [Ca2+]o = 1mM, what is Nernst potential of [Ca2+]

A
  • ECa2+ = 61.54mV log Ca2+ outside/Ca2+ insideECa2+ = (61.54/2) log (1/0.0001)ECa2+ = +123.08 mV
53
Q

Why does botulinum toxin cause paralysis?

A
  • targets and destroys SNARE proteins, (these are ‘zippers’ for movement of NT) therefore cannot move chemicals into vesicles for pre-synaptic transmission exocytosis, resulting in signal not travelling, and therefore paralysis
  • blocks release of Acetylcholine
54
Q

If you block vesicle endocytosis, how would this affect release of small molecule vs peptide neurotransmitters?

A

block releases of small molecule NT (no vesicle recycling) but not peptides (secretory granules are ‘one and done’)

55
Q

If AMPA receptors are permeable to both Na+ and K+, why does activating them cause depolarisation?

A
  • receptors reverse potential is 0mV so opening channels move membrane potential closer to 0 (depolarised)
  • at rest, membrane is only permeable to K+. even if you increase permeability to both Na+ and K+ (using an AMPA receptor,) Na+ permeability is proportionally higher than at rest
  • by opening AMPA receptors, increasing relative permeability for Na+, compared to K+
56
Q

What would happen if GABA opens a GABA-A receptor and membrane potential is below chloride’s Nernst potential? Would you get net inflow or outflow of chloride ions?

A
  • if below Cl- Nernst Potential. opening chloride conductance depolarises cell (positive current going in, or negative currents go out)
  • below Cl- Nernst potential, negative potential pushing Cl- out overwhelms concentration gradient pushing Cl- in
57
Q

Why is atropine used to treat nerve gas poisoning?

A
  • nerve gas Acetylcholine, by blocking Acetylcholinesterase
  • atropine blocks muscarinic acetylcholine receptors
58
Q

Why is an excitatory synapse on soma more effective in evoking AP in postsynaptic neuron than an excitatory synapse on tip of a dendrite?

A
  • less distance to axon hillock
  • EPSP decays as it propagates from tip of dendrite to soma

BMS11004 (29 decks)

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