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BIOM2015 > CNS > Flashcards

CNS Flashcards

1
Q

Describe the blood brain barrier and how it is different from a general capillary.

A
  • the pore is blocked with transporters

- capillary is surrounded by the end feet of multiple astrocytes

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2
Q

List the four AA CNS neurotransmitters, and whether they are inhibitory or excitatory.

A

GABA - inhibitory
Glycine - inhibitory (mainly)
Glutamate - excitatory
Aspartate - excitatory

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3
Q

Which AA is starting molecule for other compounds?

A

glutamate

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4
Q

Describe the lifecycle of Glu and Gln

A
  • released glutamte (Glu ) is captured partly by neurons and partly by astrocytes (via excitatory AA transporter)
  • astrocytes convert most of it to glutamine (Gln) via glutamine synthase -> gets out of astrocyte and into neuron by Gln transporters
  • neuron can convert Gln into Glu with glutaminase
  • Glu gets concentrated in vesicles, through the use of a pump (Glu transporter)
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5
Q

How does glycine affect NMDA receptor glutamate responses?

A
  • Gly is a positive allosteric modulator

- together Glu and Gly have a much greater response

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6
Q

What would happen if glycine site on NMDA receptor was blocked?

A

-much less responsiveness

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7
Q

How do PCP and ketamine affect NMDA receptors?

A
  • binds to site within ion channel
  • blocks ion movement down concentration gradient
  • non-competitive antagonist (dif site to Glu)
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8
Q

How does memantine affect NMDA receptors and how could it help Alz patients?

A
  • non-competitive antagonist
  • blocks ion channel
  • can help protect the surviving neurons by reducing ion flow
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9
Q

Describe the lifecycle of GABA

A
  • GABA synthesised from glutamate by GAD
  • GAT1 are reuptake transporters on presynaptic cell, and GAT2/3 on glial cells
  • recycled GABA can be degraded by GABA-T to glutamine -> easy to transport
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10
Q

How do benzodiazepines affect GABA A receptors?

What 3 other compound types have the same effect?

A
  • positive allosteric modulators
  • increase inward Cl- current
  • barbituates, neurosteroids and alcohol
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11
Q

What effect do GABA A receptors have generally?

A
  • post-synaptic
  • activation leads to hyperpolarisation due to inward movement of Cl-
  • AP less likely
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12
Q

How do GABA B receptors function generally?

A
  • activation of heterodimer inhibits adenyl cyclase via G-proteins
  • increase outward K+ and reduce inward Ca2+
  • both effects reduce post and pre-synaptic excitability
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13
Q

How does baclofen affect GABA B receptors and what condition can it treat?

A
  • baclofen is a derivative of GABA and agonist of GABA B receptors
  • can treat spasticity (involuntary tight/stiff muscles) as reinforces inhibitory input
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14
Q

Which receptors does GHB affect and how?

A

GHB is an agonist of GABA A and partial agonist of GABA B

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15
Q

How is glycine cleared from synapses?

A
  • via transporters
  • Gly T1 into astrocytes
  • Gly T2 into presynaptic neurons
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16
Q

What receptor does strychnine affect and how?

A
  • competitive antagonist for glycine receptors

- blocking inhibitory means more excitatory response

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17
Q

How does tetanus toxin effect the body and how?

A
  • toxin migrates to CNS
  • blocks glycine release from inhibitory interneurons
  • means more reflex hyperactivity and muscle spasms
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18
Q

What was HM’s accident, and what symptoms did he have?

A
  • bicycle accident at age 9
  • knocked out for 5 mins
  • minor seizures until 16
  • after this had multiple seizures and blackouts every week
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19
Q

What surgery did HM have and what changed with his symptoms?

A
  • bilateral medial temporal lobe resection (both medial temporal lobes goneskies)
  • IQ improved and epilepsy cured
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20
Q

What were the memory side effects from HM’s surgery?

A
  • profound anterograde amnesia
  • partial retrograde amnesia (up to 2 years prior)
  • short-term memory was fine until his attention shifted
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21
Q

Define the types of declarative/explicit long-term memory:

A

Declarative is things you know that you can tell others.

Episodic - events that occurred in relation to time context
Semantic - historic/facts

22
Q

Define the types of procedural/non-declarative long term memory:

A

Skill-learning: riding a bike
Priming: more likely to use a word you heard recently
Conditioning: salivating when you see a steak

23
Q

What did HM teach us about memory?

A
  • medial temporal lobs are critical for forming types of long-term memories
  • many dif kinds of memory
  • forming/consolidating new episodic memories is dependent on the hippocampus -> in the medial temporal lobe
24
Q

What is happening in the synapses to allow long term potentiate (LTP)?

A
  • increased Glu release allows more Na to enter with greater depolarisation
  • forces Mg out of NMDA pore
  • subsequent Ca flow activates protein kinases
  • protein kinase 1/CAMKII makes AMPA more sensitive to Glu
  • protein kinase 2 (via NO) triggers more Glu release
  • also get metabotrophic receptors, enzymatic and other long term changes
25
Q

How does CAMKII enzyme help LTP?

A
  • phosphorylates AMPA receptor
  • makes them more permeable to Na
  • increases resting potential of the cell making it more sensitive to incoming impulses
  • more AMPA receptors at synapse
26
Q

What is the extracellular amyloid plaque hypothesis for AD?

A
  • APP protein is broken down by series of secretases
  • AB42 forms when gamma secretase cuts 2 AA too long
  • insoluble fragments called AB42 accumulates outside cell
  • sticky AB42 forms amyloid plaques
27
Q

Describe how intracellular neurofibrillary tangles may contribute to AD?

A
  • microtubules are railropad tracks
  • tau proteins tie together and stabilise the microtubules
  • in AD tau proteins get tangled and cluster
  • structure unstable
  • loss of axonal transport results in cell death ACh
28
Q

What is the most severely affected neuron type in AD and what drug can help?

A

-ACh neurons
-normally AChE breaks down ACh into choline and acetate in the synapse, as ACh has a short duration of action
-inhibiting AChE will increase the action of ACh in synpases
-Drug examples: donepezil, rivastigamine and galantamine
(done at the river, gal)

29
Q

How can memantine help with AD?

A
  • blocks NMDA receptor ion channel
  • noncompetitive NMDA receptor antagonist
  • at high conc can inhibit learning and memory
  • at low conc, can promote synaptic plasticity and preserve neurons -> slows entry of Ca into cells
  • minor cognitive function improvements
30
Q

What areas in the brain are mainly affected with AD?

A

-focus on language and memory (temporal lobes and hippocampi)

31
Q

What is LATE and how does it differ from AD?

A
  • another form of dementia
  • mimics symptoms of AD
  • similar symptoms but progresses more slowly
  • different protein build up -> TDP43
32
Q

What is aducanumab and how does it work?

A

-first drug to target amyloid plaques

monoclonal antibody treatment may prevent plaque formation or remove B-amyloid from brain

33
Q

What could sound waves and microbubbles do for AD?

A

-non-invasive ultrasound tech that may clear the brain of amyloid plaque and restore memory function

34
Q

What are the main features of vascular dementia?

A
  • associated with vascular risk factors
  • can co-exist with other dementias
  • depends on severity of vessel damage and the brain region affected-> but mostly frontal cortex
35
Q

How is vascular dementia treated?

A
  • some AD meds may help

- proactive CVD health factors may slow damage

36
Q

What is lewy body dementia (LBD)?

A
  • incl parkinsons and dementia with lewy bodies

- earliest symptoms differ but same changes in brain

37
Q

How is LBD different from AD?

A
  • LBD varies from day to day in severity of memory issues
  • LBD is build up of LB proteins in brain
  • LBD has flat facial expressions/no facial muscle control
  • potential for REM sleep behaviour disorder
  • AD doesnt have physical symptoms until quite late
38
Q

How is LBD treated?

A
  • AchE inhibitors may help improve alertness and reduce hallucinations
  • if moderate or severe memantine may help
  • carbidopa-levodopa reduces parkinsonian signs
39
Q

What does parkinsons have that LBD doesn’t and what are the consequences?

A
  • diminished pigment/neuron loss in the substantia niagra
  • origin of dopaminergic innervation of the striatum
  • regulates posture and muscle tone
40
Q

How does L-dopa therapy work for parkinsons and what other drug goes with it?

A
  • L-dopa is main drug bc dopamine cannot cross BBB, but l-dopa can
  • dopaminergic receptors in brain then convert it to dopamine
  • carbidopa is an enzyme inhibitor that prevents the conversion of L-dopa to dopamine before the drug reaches the brain
  • helps 10% L-dopa reach brain rather than just 1-3 % of L-dopa alone
41
Q

What is frontotemporal dementia/picks disease and its key features?

A
  • FTD affects higher order functions
  • loss of cells in frontal and temporal lobes of brain
  • key feature is behavioural
  • impulsive behaviours and disinhibition
  • change in personality
42
Q

What causes FTD/picks disease?

A
  • abnormal clumps of tau proteins called pick bodies
  • they derail transport system of microtubules in brain
  • same misfolded protein as in AD, but very different “wrong” fold
43
Q

What treatment is used for FTD?

A
  • SSRIs increase seratonin

- anti-psychotics may help behaviour; increase noradrenaline and serotonin

44
Q

Describe cell necrosis pathway

A
  • injury/disease pathology
  • cells swell
  • chromatin is digested/hydrolysed
  • cytoplasm and organelle membranes disrupted
  • entire cell lyses
  • inflammation/immune activation occurs
45
Q

How does calcium contribute to necrosis?

A
  • calpains are proteolytic (cut proteins) and are regulated by Ca conc.
  • calpains activate caspases (cleave proteins)
  • calpains activate the rupture of lysosomes and cathepsin (another protease) escapes
46
Q

What is apoptosis?

A
  • programmed cell death
  • cell shrinks
  • bubble like blebs on surface
  • break into small bubble-wrapped fragments
  • phagocytic cells engulf fragments and also secrete anti-inflammtory cytokines
47
Q

How does excitotoxicity lead to cell death and what are the consequences?

A
  • Glu binds to its receptors
  • triggers influx of Na and Ca ions along with water into presynaptic neuron
  • neurons swell and die
  • these neurons then release Glu and cycle continues
  • can play central role in ischemic stroke brain damage (downstream of blood clots)
  • starving neurons release excessive Glu
48
Q

How do telomeres contribute to aging and how can we protect them?

A
  • they are caps on end of chromosomes and protect DNA
  • when the caps disappear overtime as cells divide, cells age as DNA no longer protected
  • standard nutrition things - AOX, oily fish etc
  • physical exercise stabilises telomeres
49
Q

What vitamin can slow progress of some of AD?

A

-vitamin E can maybe prevent or delay mild cognitive impairment

50
Q

What are the receptors for glutamate?

A
  • NMDA
  • Non NMDA
  • mGlut
51
Q

What is meant by a positive allosteric modulator?

A

When one is present, it enables that receptor to respond to a greater extent

BIOM2015 (8 decks)

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