Brainscape's Knowledge GenomeTM

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


See full index

PHRM > L12 - Glutamate > Flashcards

L12 - Glutamate Flashcards

1
Q

Besides Glu, what other a.acid acts at Glu receptors

A

Aspartate

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

How closely related to other NT are GluR?

A

Not very

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

Is astrocyte more important for Glu or GABA?

A

Glu

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

Co-agonist of NMDA receptor?

A

Glycine

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

NMDA channel blockers - list 2

A

Phencyclidine (PCP) and ketamine

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

Glycine site antagonist

A

Kynurenate

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

Polyamine site antagonist

A

Ifenprodil

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

iGluRs - subunits?

A

Pentameric structure but subunits don’t have 4 TM domains

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

iGluRs are split into 2 major divisions

A
  • NMDA R are voltage-dependent, mediate slower responses (synaptic plasticity), effects mediated by Ca2+ entry
  • Non-NMDA (AMPA, kainite) mediate fast excitatory transmission
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Phencyclidine (PCP) effects

A

Disorientation, agitation, amnesia, euphoria, ataxia, delirium
*cross between psychedelics and tranquilisers

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

PCP is a positive/negative allosteric modulator of NMDA receptors and works by?

A

Negative, blocks receptor to decrease Ca2+ influx

*A negative modulator (NAM) reduces the effects of the orthosteric ligand

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

PCP is potentially neuroprotective but what’s the issue?

A

You might get anaesthesia and psychosis and may disrupt necessary excitatory transmission

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

Ketamine is developed as an anaesthetic alternative to ?

A

PCP

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

Why is ketamine a unique drug?

A

Combines hypnotic, analgesic, amnesic (no other drugs in clinical practice combines these three)

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

Ketamine side effects?

A

Impairs all senses (dissociative anaesthesia), nausea, partial depressant of the respiratory system, elevates BP and HR, anaesthetic

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

Ketamine is competitive/non-competitive NMDA receptor antagonist?

A

Non-competitive - channel blocker
*A competitive antagonist binds to the same site as the agonist but does not activate it, thus blocks the agonist’s action. A non-competitive antagonist binds to an allosteric (non-agonist) site on the receptor to prevent activation of the receptor.

17
Q

What types of opioid receptors does it bind to at high conc?

A

Mu and sigma

18
Q

mGluR _ groups _ subtypes

A

3 groups, 8 subtypes

19
Q

Conc of Glu in synapse is 1_M, in nerve is 10_M

A

Micro, milli

20
Q

Excitotoxicity involves excessive activation of?

A

iGluRs and ONLY group 1 mGluRs (Gq signalling where Ca2+ goes up, mGluR 2 and 3 are Gi)

21
Q

Riluzole

A

Anti-Glu used to treat ALS

* blocks TTX-sensitive sodium channels

22
Q

Memantine

A

Anti-parkinsonian, Inhibits NMDA receptor induced current

  • Neuroprotection by low-affinity, uncompetitive, open-channel blockade of NMDA R
  • Open channel blockade = spares normal neurotransmission
  • Neuroprotective = decreases stroke damage
  • Treats alzheimer’s disease, retinal degen/glaucoma, neuropathic pain, OCD
23
Q

Domoic acid poisoning

A
  • Produced by planktonic algae eaten by shellfish and crabs
  • Potent, selective kainate agonist in CNS and leads to sustained excitation and neurotoxicity
  • Not destroyed by cooking or freezing
  • Causes Amnesic Shellfish Poisoning in humans after ingestion
24
Q

Cycad toxicity - weak GluR agonist

A
  • Bacteria in roots of cycad plants synthesize BMAA (beta methylamino L alanine) (weakly exototoxic)
  • Implicated in “Guam dementia”: fatal, paralysing, neurodegenerative diseases like amyotropic lateral sclerosis (ALS) plus parkinsonism-dementia (PD)
  • Conc in cycad seeds too low to be toxic but flying foxes eat the seeds - concentrating BMAA
25
Q

Problems with traditional blockade of NMDA R

A
  • Normal excitatory function is vital
  • Competitive antagonists block Glu signalling at all synapses
  • Competitive antagonists most effective at low Glu conc
  • High affinity = lasting effects = coma
  • Moderate affinity = hallucination (PCP) or drowsiness (Ketamine)
26
Q

EAATs (Excitatory amino acid transporters)

A 
5 subtypes 
1,2 - glial
3-5 - neuronal
*As there are no extracellular enzymes to metabolize Glu, it must be moved into cell to be metabolised
4 - Cerebellum
5 - retina only
27
Q

What is the problem with using competitive substrate at EAATs?

A

It heteroexchanges, forcing Glu out of the cell => excitotoxicity
Hence, use a non-transportable blocker so heteroexchange doesn’t occur

28
Q

Blockade of EAATs, antisense inhibition of EAATS or genetic KO of EAATS all lead to

A

Neuronal death

PHRM (24 decks)

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