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Neuroscience > journal club stuff > Flashcards

journal club stuff Flashcards

1
Q

overall glycine decarboxylase (GLDC)

effects in mice

A

causes neural tube defects

cuases features of non-ketotic hyperglycinemia

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2
Q

which mechanism is linked to human neural tube defects (NTDs)

A

aberrant folate metabolism

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3
Q

effect of Glycine decarboxylase (GLDC) on folate metabolism

A

provides the carbon units

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4
Q

what do GLDC mutations cause

A

non-ketonic hyperglycinemia

linked to NTDs

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5
Q

GLDC

A

glycine decarboxylase

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6
Q

NTD

A

neural tube defect

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7
Q

mice with reduced GLDC activity

A

develop (non-ketotic hyperglycinemia) NKH
NTDs
altered folate profiles

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8
Q

administration of formate to mice with reduced GLDC activity

A

reverses effects of NKH and NTD by providing an alternative source of carbon units and normalising folate profile

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9
Q

mitochondrial folate metabolsim is important in

A

neural tube development

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10
Q

what are drugs that target GABA signalling used for

A 
anti-anxiety
anti-convulsants
analgesic
anaesthetics
muscle relaxants
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11
Q

GABAa receptors

A

pentometric
ligand-gated ion channels
diverse subunit composition mixture

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12
Q

different subunit compositions of GABAs receptor s

A

confer different receptor properties

give different physiological effects

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13
Q

different physiological effects of GABAa receptors

A

drugs have different binding affinities for GABAa receptors

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14
Q

GABAa binding sites

A

2 orthosteric binding sites
1 allosteric binding/modulatory site

also a possible alternative site

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15
Q

muscimol

A

selective agonist for GABAa receptor

binds to the orthosteric site

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16
Q

fluni-traz-epam

A

benzodiazepine

binds to modulatory/allosteric site

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17
Q

allosteric modulator

A

substance which directly influences the effects of a receptor agonist or inverse agonist at its receptor target

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18
Q

where do allosteric modulators bind

A

a site distinct from the orthosteric site where a receptor agonist would normally bind

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19
Q

effect of allosteric modulator on structure of receptor

A

usually induce a conformational change within the protein strucutre

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20
Q

EC10

A

concentration of an agonist that produces 10% of the maximal possible effect of that agonist

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21
Q

docking binding energy

A

a measure of how well the ligand binds the receptor binding site

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22
Q

more negative docking binding energy

A

the better the ligand ‘fits’ the receptor binding site

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23
Q

DCUK-OEt

A

subunit-selective positive allosteric modulator at the GABAa receptor

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24
Q

where does DCUK-OEt bind to GABAa receptors

A

appears to act at a site distinct from the benzodiaepine site

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25
Q

example of a monosynaptic pathway

A

Schaffer Collateral Commissural pathway

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26
Q

Schaffer Collateral Commissural pathway

A

links CA3 cells to CA1 cells
in hippocampus
monosynaptic pathway
neurotransmitter = glutamate

27
Q

when action potential arrives via CA3 cells…

A

voltage gated Ca2+ entry
triggers Glu release at synapses
EPSP induced in CA1 cells

28
Q

measurements taken in CA1 cells

A

EPSP recorded with appropriately placed extracellular electrode

29
Q

how are action potentials evoked in CA3 axons

A

standard stimulating electrode

30
Q

how is pre-synaptic Ca2+ measured

A

using a Ca2+ sensitive fluorescent dye selectively loaded into axons by a local injection

31
Q

aim of measuring Ca2+ in pre-synaptic neuron

A

measure Ca2+ transient produced by pre-synaptic action potential
relate this to the post-synaptic response measured electrically

32
Q

how is the fluorescence from Ca2+ captured

A

with a photodetector

33
Q

higher probability of release means that

A

the electrical response is bigger when Ca2+ entry is promoted

34
Q

effect of width of action potential

A

wider AP is better at turning on V.G. Ca2+ channels and leaving them open longer

more Ca2+ entry

35
Q

how do you manipulate pre-synaptic action potential width

A

use a drug 4AP which blocks some of the K+ channels involved in AP repolarisatoin

36
Q

effect of adenosine on Ca2+ entry

A

acts as an agonist of Gi/o signalling

depresses Ca2+ entry

37
Q

when was LTP discovered

A

late 1970s

38
Q

what is LTP a good model of

A

how the brain forms and stores new memories

39
Q

why would a one-trial inhibitory avoidance learning procedure be used

A

to show that learning can induce changes to synaptic strength

40
Q

IA learning

A

inhibitory avoidance learning

41
Q

effect of IA learning on Glu receptors

A

induces phosphorylation of specific resideus of GluR1 and GluR2 subunits
suggests learning is inducing changes to post-synaptic receptors

42
Q

what leads us to believe that subpopulations of synpases are functionally altered following learning

A

multi-electrode recording reveals that only some recording locations are significantly changed by IA-learning

43
Q

what do neuro-imaging techniques rely on

A

the fact that more active areas of the brain require more energy so they need more oxygen and glucose

44
Q

3 types of neuro-imaging

A

Arterial spin labelling (ASL)
Blood Oxygen Level Dependent (BOLD)
Magento-encephal-ography (MEG)

45
Q

features of Arterial spin labelling (ASL)

A

fMRI technique
doesnt require contrast agent
non-invasive

46
Q

method of arterial spin labelling (ASL)

A

modify the magnetization of arterial blood
measure the delivery of
the magnetically tagged blood to target tissues

47
Q

when is an image acquired in ASL

A

when the magnetically tagged blood has reached the target tissue

48
Q

blood oxygen level dependent (BOLD) fMRI

A

assesses changes in oxygenation in the blood

49
Q

method of blood oxygen level dependent (BOLD) fMRI

A

detects differences in magnetic properties of oxyhaemoglobin vs deoxyhaemaglobin

50
Q

why does magentoencephalography (MEG) work in the brain

A

synchronised neuronal currents induce weak magnetic fields

51
Q

what do MEG and EEG signals derive from

A

the net effect of ionic currents flowing in the dendrites of neurons during synaptic transmission

52
Q

Maxwell’s equations

A

any electrical current will induce a magnetic field

53
Q

how many active neurons are needed to generate a detectable signal

A

50,000

54
Q

ASL noise compared to BOLD noise

A

ASL noise is a lot whiter than BOLD signals

55
Q

main feature of ASL

A

does not require contrast agents

56
Q

changes in perfusion seen in ASL

A

more localised to parenchyma

57
Q

changes in perfusion seen in BOLD fMRI

A

changes are tied to veins and venules

58
Q

time to collect ASL image

A

takes longer than BOLD

59
Q

time to collect BOLD images

A

can get images in less tahan 500 msec

60
Q

slices in ASL

A

fewer at a time with ASL

slices are thicker

61
Q

challenges with controlling neuroimaging studies in humans

A

stable baseline measurements
individual differences
specificity of measurements
resolution

62
Q

potential medical benefits of LSD

A

reduce anxiety, pain, depression and anorexia nervousa

63
Q

ethical implication of LSD study

A

could potentially cause harm
not hypothesis driven
effects variable and not clearly documented

Neuroscience (14 decks)

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