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CNS > Neurochemistry 2 > Flashcards

Neurochemistry 2 Flashcards

1
Q

Where does the synthesis of ACh take place

A

In cytosol of nerve terminal

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2
Q

Where is choline acetyltransferase only found

A

In the nerve terminals of cholinergic neurons

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3
Q

Overview of synthesis of ACh

A
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4
Q

How id Acetyl CoA formed

Where is it generated

A

Oxidative decarboxylation of pyruvate

Generated in mitochondria but also in the cytosol by LCFAs and certain AAs that are present everywhere

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5
Q

Where is there a high conc of choline

Where is there a high uptake system for choline

A

High conc in blood system

Most cells have an uptake system for choline but only cholinergic systems have this high uptake system

they can concentrate a lot of choline into the nerve terminals

once it is synthesised it goes to the vesicles

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6
Q

What 2 receptor types can ACh bind to

A

IONOTROPIC - nicotinic

METABOTROPIC - muscarinic

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7
Q

What is the structure of the nicotinic ACh receptor channel

What are its subunits

A
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8
Q

How does the nAChR complex bind ACh

A

each complex has 2 binding sites for ACh

Mostly on alpha subunits, though partial involvement of δ and γ subunits

Ligand binding opens channel and allows influx of Na+

Alpha chains that line the transmembrane region have large amounts of negatively charged AAs, making the pores of the channel -vely charged and it will attract +vely charged ions

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9
Q

Define antagonist

A

Compound which binds to the receptor

Lacks intrinsic activity

Instead it blocks the activity of the physiological ligand

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10
Q

Agonists that bind to the nAChR, including the endogenous agonist

A

ACh = endogenous agonist

Nicotine = an agonist of ACh ionotropic receptor - a plant alkaloid

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11
Q

Antagonist of nAChR

A

α-bungarotoxin

An antagonist of ACh ionotropic receptor

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12
Q

What do M1, M3 and M5 mAChRs activate

A

Phospholipase C (PLC) via G0 or Gq

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13
Q

MOA of M2 and M4 mAChRs

A

Inhibit adenylate cyclase via Gi

Stimulate a K+ channel via Gs

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14
Q

Where are mAChRs present

Functions

A

In striatum and in peripheral nervous system

Also mediate autonomic functions acting on the heart, SM and exocrine glands

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15
Q

Agonists that bind to mAChRs

A

Muscarine - fungal alkaloid that binds with high affinity

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16
Q

Antagonists that bind to mAChRs

A

+ => inhibited by

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17
Q

Summary of ligands for ACh receptors

A
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18
Q

Activators of nicotinic receptors

A

ACh

Nicotine

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19
Q

Inhibitors of nicotinic receptors

A

a-bungarotoxin

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20
Q

substances that do not bind to nicotinic receptors

A

Muscarine

Atropine

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21
Q

Activators of muscarinic receptors

A

ACh

Muscarine

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22
Q

Inhibitors of ACh receptors

A

Atropine

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23
Q

Substances that do not bind to muscarinic receptors

A

Nicotine

a-bungarotoxin

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24
Q

How is ACh inactivated

How is Choline taken back up

A

ENZYMATIC DEGRADATION

Degraded by acetylcholinesterase in synaptic cleft where ACh is at high conc

Catalytic rate of enzyme = 104-105 mols/s

one of the most rapid enzymes known - why ACh is used at NMJs so that we have good control over muscles

Choline is taken back up into the nerve terminal by high affinity Na+ dependent uptake system

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25
Inhibitors of acetylcholinesterase Sarin nerve gas - lethal dose = 0.5mg Neostigmine
26
Localisation of AChesterase
27
MOA of myasthenia gravis (autoimmune disorder causing muscle weakness)
Patients sera contain antibodies directed against their own nAChRs results in a decreased number of functional AChRs on muscle cells Defective NM transmission leading to muscle weakness
28
Neostigmine as an inhibitor of ACh
29
What are the excitatory AAs (EAAs)
Glutamate Aspartate Homocysteic acid (sulfur containing) Produce an EXCITATORY response in neurons - neuron is more likely to send an AP
30
What is the most important NT for normal brain function
Glutamate Nearly all excitatory neurons in CNS are glutamatergic glutamate is present in all cells
31
Synthesis of glutamate What happens to glutamate once it has been released
Glutamate is synthesised from glutamine by glutaminase Glutamate that has been released is taken up by astrocytes Here it is converted back to glutamine by glutamine synthetase
32
Ionotropic receptors and their subtypes
Glutamate binds to all
33
Metabotropic Glu EAA receptors and their subtypes
34
Consequence of switching from NR2B to NR2A (NMDA ionotropic glu EAA receptor subtype) What is it regulated by
Learning capability is diminished NMDA and AMPA receptors are key receptors in the formations of memories Glu R1 and Glu R2 used when we're learning something, but when its consolidated it switches to Glu R2 and Glu R3
35
For the receptor AMPA, 1. Ions flux through open channel 2. Opening of channel is triggered by
1. Influx of Na+ only 2. Glu binding
36
For the receptor Kainate, 1. Ions flux through open channel 2. Opening of channel is triggered by
1. Influx of Na+ only 2. Glu binding
37
For the receptor NMDA, 1. Ions flux through open channel 2. Opening of channel is triggered by
1. Influx of Na+ and Ca2+ 2. Glu binding + mebrane depolarisation
38
What are the subunits of ionotropic Glu (or EAA) receptors derived from
A different ancestral gene than AChR
39
Name the NMDA receptor antagonists What is their MOA
D-AP5 MK801
40
How are NMDA receptors different from others
EC portion of the receptor is much larger than it is for the nicotinic ACh receptor
41
Role of glycine with the NMDA receptor
Regulates its activity by keeping the channel open for longer
42
When is Mg2+ found in an NMDA receptor
in the CLOSED state blocks the flow of Na+ and Ca2+ into the cell and it has to be removed before Ca2+ and Na+ can be allowed in
43
How do AMPA and NMDA receptors (found in close proximity in the same post synaptic membrane) act together
AMPA receptor opens quickly upon Glu binding (\< 1 ms) NMDA receptor opens slowly (\> 2ms) Ligand gated =\> Glu must bind Voltage dependent =\> there must be entry of Na+ to change the transmembrane potential This removes the Mg2+ block from the channel
44
Structure of metabotropic Glu receptors how are the different groups different
7 membrane spanning peptide at least 8 sutypes, mGluR1-8, have been cloned 3 CLASSES Group 1 - mainly postsynaptic Group 2 and 3 - mainly presynaptic (glutamate can act on the neuron that released it)
45
Describe Group I metabotropic Glu receptors
Mainly POSTSYNAPTIC
46
Describe Group II and III metabotropic Glu receptors
Mainly PRESYNAPTIC Glu can act on the neuron that released it
47
Different classes of metabotropic receptors
48
What important function do metabotropic Glu receptors play a role in
Memory function mGluR inhibitors block memory formation at some synapses (especially grp 1 as they can potentiate the NMDA receptor opening) NMDA receptor activation potentiates signalling via mGluRs
49
MOA of excitatory AA receptors and neuronal cell death in stroke
ISCHAEMIA Block in blood supply Excessive Glu release causes over-stimulation of NMDA receptors - excess Ca2+ influx into post synaptic neurons Leads to excitotoxic cell death
50
Effect of Ca2+ on excitotoxicity
Large influx of Ca2+ * Can activate calpains, phospholipases, NOs (ox damage), nucleases etc that can lead to very rapid cell death by necrosis * Ca2+ is sequestered into mito. resulting in swelling and rupture of mito. - delayed cell death (window for treatment) * NMDA-R antagonists D-AP5 and MK801 provide protection in models of ischaemia
51
What substances provide protection in models of ischaemia
NMDA-R antagonists D-AP5 and MK801
52
Name the inhibitory AA NTs
GABA Glycine
53
MOA of inhibitory NT receptors
Influx of -vely charged ions - Cl- Inside of cell becomes MORE -ve HYPERPOLARISATION of post-synaptic cell making it less likely to initiate an AP
54
MOA of excitatory NT receptors | (NMDA, AMPA, nicotinic AChR)
Influx of +vely charge ions - Na+ Inside of the cell becomes LESS -ve Depolarisation of post-synaptic cell makes it more likely to initate an AP
55
What proportion of synapses uses GABA How is it synthesised presence of what substance indicates a GABAergic neuron
33% of synapses in brain use GABA - main inhibitory NT in the brain Synthesised from glutamate // glutamic acid decarboxylase Presence of GAD indicates a GABAergic neuron
56
Name the main NT in the spinal cord
Glycine
57
How is GABA deactivated
By being taken up into nearby glial cells also taken up by presynaptic neuron and recycled into synaptic vesicles
58
Ionotropic GABA receptors
GABAA GABAC
59
Metabotropic GABA receptors
GABAB
60
What is the GABAA receptor structurally related to What is the ion channel selective for How is it inactivated
Structurally related to nAChR Ion channel is selective for Cl- ions Inactivated - GABA is removed from synaptic cleft by transporters
61
How does Valium (diazepam) act
Through modulating GABA-A receptor signalling Cl- enters the cell =\> hyperpolarisation Benzodiazepines (e.g. diazepam) and barbituates enhance the hyperpolarising effect of GABA
62
What compounds enhance the hyperpolarising effects of GABA
Benzodiazepines (eg diazepam) and barbituates
63
MOA of presynaptic inhibition
Inhibitory NT binds to receptors on the presynaptic cell Reduction in depolarisation of the presynaptic nerve terminal Less Ca2+ influx Less excitatory NT release
64
Overview of NT receptor classification

CNS (36 decks)

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