Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

neuroanatomy > Signalling > Flashcards

Signalling Flashcards

1
Q

What receptors are there for Glutamate?

A

ionotropic and metabotropic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what is glutamate?

A

main excitatory neurotransmitter in the BRAIN
released in half of the neurones
non-essential amino acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

where is glutamate synthesised?

A

synthesised locally in the brain as can’t cross the BBB

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what are glutamates action?!

A

calcium influx = causing action potential

role in plastic changes with memory, learning, and development

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what are glutamate’s ionotropic receptors?

A

AMPA
NMDA - requires glycine co-agonist
kainate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is NMDAs purpose?

A

calcium influx related to synaptic plasticity in memory and learning - NMDA is opened with a high increase in EPSPs - unblocks in LTP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is AMPAs purpose?

A

plasticity and synaptic transmission

in LTP more of these are inputted in post synaptic membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What happens when there’s too much Glutamate?

A

excessive influx of Ca2+ which can lead to cell death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what cell pathways are effected in glutamate excitotoxicity?

A
  • membrane breakdown (phospholipase)
  • cytoskeleton alteration
  • generation of nitrogen oxide free radicals
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

If GluR2 is non-editing in an adult what disease may it imply?

A

MND

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is Glutamates PD pathology?

A
  • balance between NMDA excitation and D2 inhibition
  • in PD loss of D2 results in over-activation of glutamate receptors (plastic changes)
  • causes excitotoxicity in PD
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What does activation of NMDA receptors enhance in AD?

A

Production of amyloid beta plaques and phosphorylates tau

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What pharmacological evidence is there for glutamate mediated damage in AD?

A

memantine (NMDA antagonist) leads to functional improvement in AD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the distribution of muscarinic recpetors?

A

midbrain, medulla and pons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the distribution of nicotinic receptors?

A

sub nig, locus coerleus, septum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

where are both muscarinic & nicotinic?

A 
putamen
caudate 
cortex
hippocampus
thalamus
hypothalamus 
cerebellum
17
Q

How is ACh used in the sympathetic nervous system?

A

preganglionic (nicotinic)

18
Q

How is ACh used in the parasympathetic nervous system?

A

pre (nicotinic) and post ganglionic (muscarinic)

19
Q

What are the 2 types of ACh receptors?

A

Nicotinic - ionotropic

Muscarinic - metabotropic

20
Q

What is the pathophysiology of Mysthenia Gravis?

A
  • Autoimmune
  • autoantibodies against nicotinic ACh receptors on the post synaptic membrane of the NMJ
  • error in transmission of signal from neurone to muscle cell
  • Muscle can’t contract
21
Q

Name 3 possible affected proteins in MG.

A

Nicotinnic ACh Receptors
MUSK - muscle specific kinase
lipoprotein related protein 4

22
Q

How does nerve agent cause damage?

A

blocks activity of acetylcholinesterase
causing accumulation in the synaptic cleft
=chronic depolarisation

23
Q

What symptoms would be expected from Acetylcholinesterase inhibitors (over activation of acetlycholine) ?

A

SLUDGEM

salivation, lacrimation, urination, defecation, Gastro pain, emesis, miosis.

24
Q

3 drugs that treat opioid poisoning + there action.

A

atropine - antagonist of muscarinic
diazepam - reduces release of Ach
pralidoxime - reactivation of AchE

25
Q

How are Acetylcholinesterase inhibitors used in MG?

A

prolong Ach in the NMJ to improve transmission

26
Q

Action of Acetylcholinesterase inhibitors in AD.

A

increases levels of ACh in the synapse improving deficit but DOES NOT alter disease course

27
Q

What is the significance of GluR2 subunit being edited or none edited?

A

GluR2 when non-edited it causes the glutamate receptor to be more permeable to Ca2+ therefore the more non-edited GluR2 receptors of a neurone means they’re more prone to the effects of excitotoxicity

neuroanatomy (21 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions