Brainscape's Knowledge GenomeTM

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


See full index

Drugs and the brain > Amino acids transmitters > Flashcards

Amino acids transmitters Flashcards

You may prefer our related Brainscape-certified flashcards:
The Brain flashcards
1
Q

What are the different amino acid transmitter families?

A

Excitatory-glutamate, aspartate, N-acetylasparytyl glutamate, glycine.
Inhibitory- GABA, glycine- taurine/beta alanine.

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

When were GABA, glycine and glutamate discovered?

A

19050-1970’s
11970-1980’s
1980’s

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

Explain amino acid metabolism? What do they feed into?

A

Glutamate can be synthesises into:
- GABA-T via GAD
-glutamine via glutamine synthase and reverse back to glutamate via glutaminase.
-glutamate to alpha-ketoglutarate that enters the Krebs cycle and also can become aspartate and glycine through transaminase.

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

Explain the glutamine cycle (excitatory amino acid)?

A
  1. VGluT- metabolise glu so it can be transported.
  2. Glutaminase- gin into glu
  3. Glutamine synthetase- broken down in astrocytes so it can be recycled and reused.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the two types of glutamate recptor?

A

Ionotropic and Metabotropic.

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

Ionotropic glutamate receptors?

A

LG ion channles, fast, iglu, includes: AMPA, Kiante, NMDA. E.g. nAChR.
The iGluR subunits have 3 transmembrane domains and are tetramers with 4 agonist binding sites.

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

Explain Inotropic receptor sub unit combinations for NMDA, AMPA, Kainate.

A

NMDA:
glu N1/N2A/ 3A-B
AMPA:
GluA 1-4
Kainate:
GluK1-3
there heterotrimers
make up a variety if different r’s
splicing can increase this diversity.

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

Metabotropic glutamate receptors?

A

Family c of GPCR
slower
mGluR
3 groups
1-mGluR 1,5
2-mGluR 2,3
3- mGluR 4,6,7,8

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

Which amino acid is inhibitory?

A

GABA gamma-aminobutyric acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Key feature about GABA gamma-aminobutyric acid?

A

wide distribution in the CNS.
stored in vesicles and release when there’s influx of ca and high ca conc.
there’s transporter proteins for uptake and add to vesicular pool.
formed from glutamate by glutamic acid decarboxylase.
There’s GABA-A and GABA-B AND GABA-C families

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

What happens at the GABAergic terminal?

A

Gaba released from vesicles diffuse across the synapse to r on the post, GAT1 recycles and reuses it for use again.

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

Explain GABAergic transmission?

A

20% all neurons are GABA
20% of all CNS transmitters
short local connections
some long projections to the striatum to the substantia nigra and globus pallidus.
also in brain tissue and synapses.

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

What happens when the GABA receptor is activated?

A

GABA binds to the GABAA receptor, it opens a cl- channel allow cl- influx into the cell. So the cell increases in chloride permeability (Pcl). Ecl is close to resting membrane potential so influx stabilises membrane potential so stays near rest and leads to inhibition.

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

What are the different type of GABA rectors and how many types are in each?

A

6x Benzodiazepine, beta-carboline site
1x Typical GABA A site
5x Neurosteroid sites
4x Barbiturate, propofol, etomidate site
3x picrotoxinin site
2x agonist binding sites

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

What compounds enhance and decrease GABA A fucniton?

A

enhance- sedatives, anxiolytics, anticonvulsants.
decrease- convulsant, anxiogenics.

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

What GABA A Receptor subunit genes are there ? and how many? Which are most common?

A

alpha 1-6
beta 1-3
gamma 1-3
delta
epsilon
pi
Theta
rho 1-3 (retinal expression for GABA C.
most common are a,b,y.

17
Q

Where are the binding sites located in relation to the subunits?

A

between a1 and b2, b2,a1, a1,y2. in the interfaces. There’s also a benzodiazepine site that has high affinity but it needs a y2 subunit.

18
Q

Key features of extra synaptic GABAA receptors?

A

outside the synapses
high affinity
respond to ambient gaba to produce tonic inhibition
contain delta
insensitive to benzodiazepine
targets for alcohol, Neurosteroid and some anaesthesia
involve din brain disorders

19
Q

GABA B structure ?

A

pre or post
two subunits 1/2
GPCR family C
have VG ca channels, , open k channels and inhibit adenylyl cyclase via Gl.

20
Q

What is a main inhibitory amino acid and its fucntion?

A

Glycine- High conc in spinal cord
acts diff on a glyR( cys-loop r) compared to NMDA r
transport proteins for reuptake. Glyt1(astrocytes)/2(sc).
get from diet and serine synthesis.

21
Q

Explain the glycine receptor structure?

A

3 alpha ( sc, brain, brain), 1 beta.one is for gly and is between the a and b or 2 a.

22
Q

What are renshaw cells?

A

SC interneurons, stimulated by collateral from a motor n.
release gly to motor n
neg fdbk
reg MN
antagonist (strychnine)
agonist( gly, taurine, b-alanine)
ethanol anaesthetics modulator
treat pain, epilepsy, hyperekplexia, alcoholism.

23
Q

Structure of iGluR’s

A

Sub unit combos for NMDA: N1/2 A-D/ 3 A-B
AMPA: A 1-4
Kainate: K 1-3
4-5

24
Q

AMPA receptors

A

mediate fast syn transmission
fast EPSP, wide spread in CNS, rel perm to na, k, ca dep on sub unit
4 subunits bind glutamate,

25
Q

Kainate receptors

A

less wide spread, found on pre syn terminals, ca perm but less than AMPA. fast EPSP,

26
Q

NMDA receptors

A

highly perm to ca
blocked by mg2+ at rest mem pot
need glycine or D-serine as a coagonist- is at NMDA but not for other iGluR.

27
Q

Explain NMDA R as a drug target?

A

At RMP, mg blocks the R but when mem pot increases and receptor is bound , block is released so ions flow through and depol the cell.

28
Q

What diseases are linked to iGluR?

A

schizophrenia, AD, PD, autism, stroke, MND, depression, epilepsy, neuropathic pain.

29
Q

what are the antagonist and channel blockers for NMDA, AMPA, Kainite receptors.

A

N- ap-5/cpp/7-cholorkyn/ha466 . chan blockers- phencyclidine, ketamine, mematine, mg2+ mk801
A- nbqx/cnqx
K- nbqx/acet

30
Q

Metabotropic receptor family

A

8 families,
in family C of GPCR
in 3 groups
group 1- 1,5 - somatodendritic location, enhance NMDA Currents and inhibit K currents
group2 - 2,3 - in nerve terminals, inhib autor
group 3- 4,6,7,8- nerve term, inhib autor

31
Q

Examples for each group agonist and antagonist

A

1)DHPG/CHPG- LY36785/S4CPG- TREAT Pain, pd, epi
2) LY354740-TREAT GLU DIS
LY341195-COG ENHANCE
3)LAP4/3,4 DCPG
CPPG

Drugs and the brain (16 decks)

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