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BioMed Season Finale Part 1 > CNS Disorders > Flashcards

CNS Disorders Flashcards

1
Q

what are the different methods of studying CNS disorders

A

imaging
post-mortem
indirect neuropharmacological markers
genetics-linkage analysis
animal models

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2
Q

what are the different imaging techniques for studying CNS disorders

A

computerized tomography - CT
Magnetic resonance imaging - MRI
functional MRI - fMRI

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3
Q

what is the spatial resolution of a CT scan

A

several mm

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4
Q

what is MRI technology based on an its spatial resolution

A

oxyhaemoglobin has a different magnetic resonance than deoxyhaemoglobin
less than 1mm

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5
Q

what is the basis of how fMRI’s work

A

visual stimulation utilises oxygen
microvasculature responds by increasing blood flows to specific brain regions
leads to increase in the oxyHb to deoxyHb ratio

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6
Q

function of diffusion tensor imaging

A

mapping pathways and investigating aberrant pathways

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7
Q

what is the difference between a PET and a SPET scan and what is the advantage and what do they both do

A

SPET uses single positron emissions and doesn’t need a cyclotron
reveal activity in the brain and estimate receptor levels

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8
Q

what are other non-invasive imaging techniques

A

electroencephalography
magnetoencephalography

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9
Q

when detecting for indirect markers where would you search

A

cerebrospinal fluid
plasma
urine
binding to platelets

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10
Q

what is an indirect marker for depression

A

platelet binding - binding to monoamine transporter

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11
Q

what are the disadvantages of using indirect markers for CNS disorders

A

proteins are labile - may degrade
patient may be taking medication

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12
Q

what does genetic-linkage analysis detect

A

RFLPs - restriction-fragment length polymorphisms

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13
Q

what does RFLPs require and what is its purpose in genetic-linkage analysis

A

requires family pedigree of the genetic disease
easiest to study in genetically isolated communities
detects whether the RFLPs and the disease are linked

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14
Q

why might genetic-linkage analysis using RFLPs not be effective with some diseases

A

may involve multiple genes
or involve mitochondrial DNA

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15
Q

what are the dis/advantages of using animal models

A

advantage - drug screening for therapies
disadvantage - not an exact phenocopy of the disease

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16
Q

where is ayahuasca derived from and what is the active psychomimetic ingredient

A

obtained from vines
harmaline

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17
Q

what is the active constituent in peyote

A

mescaline

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18
Q

why might lysergic acid diethylamide (LSD) be so potent

A

act very specifically at receptors sites in the brain

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19
Q

what does the cross-tolerance between LSD and mescaline suggest

A

they both act on the same class of receptor site

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20
Q

what is the structure of LSD and mescaline similar to

A

5-HT - seretonin

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21
Q

what does LSD act as in terms of 5-HT receptors

A

interacts with 5-HT receptors in peripheral vasculature
in the periphery it acts as a 5-HT2 receptor antagonist
in the brain it acts a 5-HT receptor agonist/partial agonist

22
Q

what does the effects of LSD suggest it alters

A

primary somatosensory cortex
thalamus

23
Q

what is the function of raphe neurones and how does LSD effect them

A

send extensive projections to the forebrain
decreases their firing rate

24
Q

what did lesioning the raphe nucleus in rats tell us about the effects of decreased firing rate of raphe neurones via LSD

A

that they did not exert the hallucinogenic effects
rats were able to distinguish saline from LSD

25
Q

what does LSD increase activity in

A

locus coeruleus neurones
also increases activity in subsets of neurones in the cortex

26
Q

where are 5HT2A receptors present

A

temporal cortex
prefrontal cortex
thalamus

27
Q

function of the thalamus

A

processes somatosensory information and receives information from the locus coeruleus

28
Q

if 5HT2A receptors mediate hallucinogenic action then what is the rationale behind testing for different hallucinogen potency

A

that drugs with higher 5HT2A affinity will produce more potent hallucinogenic effects and vice versa

29
Q

where 5HT2A receptors expressed

A

pyramidal neurones in the cortex

30
Q

how does LSD effect the cortex

A

increases activity of layer V pyramidal neurones in the cortex

31
Q

what do imaging studies of LSD suggest

A

higher cortical activity

32
Q

what is phencyclidine (PCP)

A

a dissociative anaesthetic
same class as ketamine

33
Q

what does phencyclidine induce

A

causes a catatonic like state without muscle relaxation

34
Q

what do radioligand studies of PCP show it interacts with

A

sigma opiate receptors - modulates NAdr release
non-competitive antagonist of glutamate receptors (NMDA)

35
Q

what are the features of addiction

A

compulsion to take drug
tolerance to drug
withdrawal symptoms - opposite effects to those in presence of drug

36
Q

what is an operant chamber

A

an environment that allows a rat to self administer a drug

37
Q

what is the evidence that suggests that dopamine pathways are important for reinforcing

A

administration of spiroperidol - a DA antagonist and 6A-OH-DA lesions both block reinforcement

38
Q

where do Da/NAdr/5-HT pathways originate from and what are they implicated in

A

midbrain/medulla - medial forebrain bundle
mood/behaviour

39
Q

where do dopamine axons project from and too

A

the medial forebrain bundle
nucleus accumbens

40
Q

what is the evidence for specific transporters in the reinforcing properties of cocaine

A

Mice with DA transporter knockout have chronically elevated synaptic dopamine
cocaine administered to these animals produces no change in base-line DA
these animals will still administer cocaine there may be another reinforcing stimulus other than DA

41
Q

what is the function of F105

A

important for high affinity binding of cocaine but not for DA transport

42
Q

what was the effect of cocaine in mice with knock-in mutant dopamine transporter

A

did not elevate extracellular dopamine or increase locomotion

43
Q

affect of ethanol on dopamine release

A

increases DA release in the nucleus accumbens

44
Q

effect of dopamine transporter antagonist in animal models

A

blocks ethanol self-administration

45
Q

effect of opiates on the limbic system

A

increases dopaminergic activity

46
Q

function of fluoromethylspiroperidol

A

used to label dopamine receptors in PET scans

47
Q

in terms of genes what is the long-term effect of addiction

A

increase in DA leads to increase in cAMP leads to activation of CREB which leads to immediate early gene expression

48
Q

what may the addiction induced immediate early gene expression cause

A

changes in receptor levels

49
Q

what was found in rat models to be associated with high alcohol preference

A

innate/acquired hyperactivity of extrahypothalamic CRF systems

50
Q
A

BioMed Season Finale Part 1 (13 decks)

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