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Excitable cells > Lectures 18-21 > Flashcards

Lectures 18-21 Flashcards

1
Q

what is acute and chronic?

A

acute - sudden

chronic - long term

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2
Q

what is a stroke?

A

reduced blood flow and oxygen to the brain.

build up of CO2 since not removed via blood.

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3
Q

What causes a stroke?

A

athero-thrombo-embolism (clot)
embolism from heart.
intracranial small vessel disease.

brain artery blocked.
brain artery bleeds.
poor circulation.
heart failure.
drowning.
low oxygen at birth.
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4
Q

what are risk factors for a stroke?

A 
inflammation, either in the brain or outside.
atherosclerosis.
age.
diabetes.
ethnicity - african caribbean 
alcohol.
family history.
heart disease.
high bp.
high cholesterol.
obesity or unfit.
smoking.
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5
Q

what can reduce the risk of a stroke?

A

statins yo.

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6
Q

what are the symptoms of a stroke?

A 
sudden headache - usually bleeding.
dizziness/sudden falls.
difficulty speaking/understanding.
loss of vision, particularly in one eye.
weakness on one side of body.

FAST

can occur during sleep.

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7
Q

what damage does a stroke do?

A

every minute loses 2 million brain cells.

death isnt immediate however.

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8
Q

what is a “mini stroke”

A

TIA - transient ischaemic attack

no real damage.

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9
Q

what is the risk from atherosclerosis?

A

produces toxins.

can break off and block arteries - thrombus.

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10
Q

What is TPA?

A

breaks down blood clots.

quickly restores blood flow.

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11
Q

What are the side effects of TPA?

A

it can lead to bleeding.
need to be sure the stroke is caused by a clot, not by bleeding or it exacerbates it.

can cause reperfusion injury.
can cause hyperoxemia (high o2) which leads to inflammation and oxidative stress.

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12
Q

what is the ischaemic core?

A

low blood flow, affected early on, damage occurs quickly.
beyond rescuing.

surrounded by the ischaemic penumbra, slightly higher blood flow, this region will be damaged if left untreated.

it’s the dead tissue which spread toxins and causes other tissue to die.

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13
Q

Why do dead cells spread toxins?

A

K inside and Na out normally, maintained by pumps.

no o2 causes pumps to fail, cells depolarise. pumps breakdown and toxins damage healthy neurones/other cells.

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14
Q

what is damaging to the brain that’s released from neurones?

A

glutamate.
na and ca ions.
free radicals - superoxide (o2 radical).

slide on lecture 18 summarising.

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15
Q

what is inflammation?

A

response usually to infection, can occur in sterile conditions though.
heat/redness/swelling/pain/loss of function.

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16
Q

name some inflammatory mediators in the brain.

A

glial cells - astrocytes and microglia.

cytokines, free radicals and prostaglandins.

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17
Q

describe cytokines.

A

small proteins involved in all forms of disease and injury.
you don’t find them in healthy tissues, they are produced by damaged cells.

they can act on the brain, communicate between cells and activate inflammation.

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18
Q

how do cytokines effect the brain?

A

hormonal change, sympathetic NS activated, altered immune system, sleepiness, fatigue, altered appetite, weight loss, fever.

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19
Q

what is IL-1?

A

interleukin 1, cytokine.
key inflammatory mediator.
major disease target.
produced rapidly in the brain in response to an injury.

IL-1beta
IL-1alpha

acts on glia to release toxins.
active at tiny concentrations.

naturally occuring and highly selective competitive antagonist - IL-1Ra (receptor antagonist)

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20
Q

what is pro IL-1beta?

A

inactive precursor to IL-1beta.

activated by caspase-1.

21
Q

where does IL-1 target?

A

mainly glial cells to release toxins and endothelial cells to promote entry of immune cells.

22
Q

what is learning?

A

a change in behaviour as a result of experience.

acquisition of knowledge.

23
Q

what is memory?

A

the storage and retrieval of knowledge.

24
Q

what is declarative or explicit memory?

A

events or facts.

25
Q

what is non declarative or implicit memory?

A

procedural - ie skills or habits.

associative - ie pavlov doggi

26
Q

how are long term memories formed?

A

sensory input - short term memory - consolidation - long term memory.

requires protein synthesis, potentially unlimited capacity, can last a lifetime.

27
Q

what is retrograde amnesia?

A

memory loss for event prior to trauma.

28
Q

what is anterograde amnesia?

A

inability to lay down new memories.

29
Q

how does pavlov show learning pathways?

A

a conditioned stimulus leads to a response, the conditioned stimulus becomes associated with an unconditioned one and a new pathway is formed.

30
Q

what is Hebb’s rule?

A

when an axon of cell A is near enough to excite cell B and repeatedly takes part in firing it, some growth process or metabolic change takes place in one or both cells such that A’s efficiency to fire B increases.

When pre- and post-synaptic neurons are simultaneously and strongly or repeatedly activated, the synaptic connection between them becomes enhanced/strengthened.

31
Q

what is activity dependence?

A

animals deprived of experience during development, less neuronal branching occurs.
less dense AMPA receptors in mice in hippocampus.

32
Q

where is the hippocampus located?

A

temporal lobes, part of the limbic system.

33
Q

what does the hippocampus do?

A

involved in memory processing, severely affected in Alzheimers.

34
Q

what did Bliss & Lomo show?

A

Brief high-frequency electrical stimulation of the input pathway produces long-lasting enhancement of the strength of the input-output synapse.

very short tetanus can cause an increased amplitude for weeks after. The basis of memory.

35
Q

what is tetanus?

A

very quick succession

36
Q

how are AMPA and NMDA receptors stimulated tetanically?

A

more glutamate is released, causes activation of AMPA receptors which depolarises the post-synaptic cell due to Na influx.
This drives off Mg block on NMDA and allows ca to enter the post synapse, this activates protein kinases and memory.

NMDA associates depolarisation and the arrival of glutamate, stronger like pavlov.

37
Q

What is the long term effects of tetanic stimulation?

A

more AMPA receptors on post synaptic cell, more glutamate is released.
protein kinases release a retrograde messenger (NO) which causes more glutamate to be released.

38
Q

what experiment was evidence of LTP?

A

long term potentiation.
Morris water maze with rats.

learn to find hidden platform underwater using landmarks.

39
Q

what disrupts spatial learning?

A

Bilateral hippocampal damage.
NMDA-receptor blockers (e.g APV [drug]).

Deletion of Calmodulin-dependent protein kinase II (CaMKII) gene blocks hippocampal LTP and spatial learning. But – this gene is widespread.

Deletion of NMDA-receptor gene specifically in CA1 neurons blocks hippocampal LTP and spatial learning.

Mice with extra CA1 NMDA receptors show enhanced learning ability.

40
Q

what are the learning mutants of drosophilia melongaster?

A

can’t learn association, due to a cAMP.

41
Q

what does the aplysia californica show?

A

studied by eric kandel.
a sea hare/slug.

shows habituation, sensitisation and classical conditioning.

gill withdrawal as a protective reflex.

42
Q

describe how the withdrawal response in aplysia californica works.

A

in abdominal ganglia.

sensory input innovates the siphon, motor nerves go out to the gill for the withdrawal response.

43
Q

what is synaptic depression?

A

habituation - less of a response from post synaptic neurone.

repeated stimulation induces less Ca influx per AP, so less NT.

44
Q

describe presynaptic facilitation

A

interneuron joins to pre synaptic sensory neuron.

??

45
Q

how does short term memory occur in the slug babes?

A

5-HT receptors are GPCR, release adenylyl cyclase –> cAMP.
this activates protein kinase A which inhibits voltage gated K channels.

this leads to a longer repolarisation phase since less K efflux.
increased NT release.

46
Q

how does long term memory work in slug babies?

A

multiple shocks causes more cAMP activated, you get changes in gene expression and structural changes.

persistent kinase A inhibits K channels for long periods of time.

47
Q

describe the sensitisation of the gill withdrawal response.

A

Increased neurotransmitter release at sensory neuron  motoneuron synapse (functional plasticity)
Activation of cAMP signalling cascade, leading over the long term to changes in gene expression
Increased number and area of active synaptic zones (structural plasticity)

48
Q

why does classical conditioning increase the gill withdrawal response?

A

When CS and US are paired, there is greater activation of adenylyl cyclase in the presynaptic terminal than with either stimulus by itself.

This is because the CS action potential admits Ca2+ into the presynaptic terminal. The Ca2+ (by interacting with a protein called calmodulin) increases the response of adenylyl cyclase to G-proteins.

Excitable cells (6 decks)

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