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CNS > Neurochemistry 1 > Flashcards

Neurochemistry 1 Flashcards

1
Q

Name the different types of glial cells

Which are the most abundant

A
  • Astrocytes
  • Oligodendrocytes
  • Schwann cells
  • Microglia

Astrocytes are the most abundant

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2
Q

Function of microglia

A

Immune cells

Secrete cytokines - when they become activated this increased inflammatory cytokines and cause inflammation

this is seen a lot of people with neuro degenerative diseases

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3
Q

Define synapse

A

Specialised sites where neurons communicate with other cells via NTs

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4
Q

Name the 4 steps in neurotransmission

A
  1. NT synthesised and stored in high conc in nerve terminals, in synaptic vesicles
  2. Released upon stimulation of nerves
  3. Stimulates target organs/cells
  4. Active mechanisms to terminate its effect
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5
Q

Name the 3 classifications of NTs

GIve examples

A

Classical (small molecule) NTs

Neuropeptides (non-classical NTs) - short peptides (3-36 AAs long) that are neuroactive

Unconventional - NO (cannot be stored in nerve terminal), CO (cannot be stored in nerve terminal), arachidonic acid (not easily stored in nerve terminal)

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6
Q

Name the 3 small molecule NTs that are derived from tyrosine

A

Dopamine

Norepinephrine

Epinephrine

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7
Q

As a general rule, what do classical NTs have in common

A

Either AAs or derived from AAs (except ACh)

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8
Q

What is serotonin derived from

What is its synonym

A

Tryptophan

5-hydroxytryptamine

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9
Q

What is histamine derived from

A

Histidine

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10
Q

What is GABA derived from

Name its synonym

What is unique about GABA

A

Derived from glutamate

γ-aminobutyric acid

Non-typical but still has an amino grp and a carboxylic acid grp

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11
Q

What do ACh, glycine and glutamate have in common

A

All classical (small molecule) NTs

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12
Q

In step 1 of neurotransmission, synthesis and storage of NT in high conc in nerve terminals, where does the synthesis usually occur

A

Cytosol

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13
Q

How is NT transported into synaptic vesicles

A

Dependent on 2 proteins:

  • H+-ATPase (proton) pump - creates H+ gradient (by pumping H+ INTO vesicle) across vesicle membrane, pumping
  • H+/NT antiporter - uses the energy stored in this H+ gradient so H+ leaves and a NT enters
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14
Q

What is step 2 in neurotransmission

A

Release of NT upon stimulation of the neuron

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15
Q

How is NT released

A

Exocytosis of synaptic vesicles is tightly coupled to arrival of an AP at the axon terminus

Also dependent on Ca2+ influx into the presynaptic nerve terminal

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16
Q

Define AP

What is its speed

A

Electrical signal that travels from neuronal cell body down the axon to the axon terminus

Characterised by high speed (up to 120 m/s) with no loss of signal over long distances

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17
Q

What structures wrap around the axon

A

Oligodendrocytes/Schwann cells

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18
Q

What is the composition of myelin

A

70-80% lipid

20-30% protein

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19
Q
A
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20
Q

Role of Ca2+ in NT release

A

This electrical signal must be converted into a chemical signal - Ca2+

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21
Q

As a result of the opening of the VG Ca2+ channels, how does [Ca2+] change

A

80-100 nM → 1-100 uM

Increase in Ca2+ is highly localised

22
Q

How is a low Ca2+ conc maintained in the axon

A

Ca2+ pumps pump Ca2+ back out to maintain low conc in cytosol

Mitochondria also have a Ca2+ uptake system

23
Q

Name 2 SNARE proteins

A

SNAP25 and Synaptobrevin

24
Q

Function of Synaptotagmin

A

Ca2+ sensing

25
Q

Function of Synapsin

A

Links proteins to cytoskeleton and keeps vesicles in place

26
Q

What does the V-ATPase do

A

Pumps H+ into cell

27
Q

Name the SNARE protein present on the VESICULAR membrane

A

Synaptobrevin

28
Q

Name the SNARE protein present on the plasma membrane

A

Syntaxin

29
Q

Name the SNARE protein present on both membranes

A

SNAP-25

30
Q

Function of SNARE proteins

A

Control fusion of 2 membranes

31
Q

Describe the structure of synaptotagmin

A

Made up of long alpha helices - bind and become intertwined with each other - stable complex, that is highly resistant to degradation

32
Q

What does the SNARE complex look like

A
33
Q

MOA of action of synaptotagmin

A

Affinity for Ca2+ = 1uM

Binding of Ca2+ to synaptotagmin changes its confirmation and it pulls the vesicle closer to the mebrane

this then stimulates the fusion of the 2 membranes and NT is exocytosed into the synaptic cleft

34
Q

What diseases affect the presynaptic terminal - give an example

What are the symptoms

What is it caused by

A

Some myasthenic syndromes e.g. the autoimmune disease Lambert-Eaton myasthenic syndrome (LEMS) - attacks presynaptic Ca2+ channels

Present as muscle weakenss that worsens with exertion

Caused by abnormal transmission at neuromuscular synapses

ALSO clostridium bacterial toxins (even if you stimulate this neuron it cannot change the voltage)

35
Q

Describe the vesicle cycle

A

Loaded with NT

Move into reserve pool

Linked via synapsin to cytoskeleton

AP arrives they become mobilised to nerve terminal pre-synaptic membrane

Docked onto membrane and primed

Linkages to membrane are shown

Ca2+ influxes into cell and then get fusion with the plasma membrane and exocytosis of its contents

The membrane that was part of the vesicle gets re-taken up - clatherin coating

Empty vesicle then gets reloaded with NT

36
Q

Where does botulinum toxin come from

Describe its structure

A

From clostridium botulinum, which causes food poisoning and paralysis

Heavy chain involved in entry into neurons in NMJ

Light chain has protease activity

37
Q

Why does BOTOX have an effect on muscles

A

Attracted to neurons at the neuromuscular junction

38
Q

Distinguish between the heavy and light chain in botulinum toxin

A

Heavy chain - involved in entry into neurons in the NMJ

Light chain - protease activity

39
Q

How can toxins affect transmitter release

A

Because the light chain has protease activity, it degrades the snare proteins and the snare complex cannot form => vesicle will not be able to fuse with the plasma membrane and there will be no NT release

Nerve terminals can grow new ones but takes months

40
Q

Medical uses of Botox

A

Strabismus (crossed eyes)

Blepharospasm (uncontrolled blinking)

Hyperhidrosis (excessive sweating)

Glabellar frown lines

Chronic migraines

41
Q

What is step 3 in neurotransmission

A

When it is released into the synaptic cleft, the NT binds and activates receptors on the post-synaptic cell membrane

42
Q

Name the 2 types of NT receptors

A

Ionotropic - ligand gated ion channel

Metapotropic - GPCR

43
Q

What receptors do classical NTs bind to

A

Both to specific ionotropic and metabotropic receptors

44
Q

What is the defining feature of ionotropic receptors

A

Generally heteromeric - individual receptors are made of multiple subunits

45
Q

Name the glutamate receptors

A
46
Q

Overview of subunits for the different types of receptors

A
47
Q

MOA of heteromeric ion channels

A

NT are binding to 1 or 2 of these subunits - we notice that certain subunits have a higher affinity of binding than others

Change the conformation and opens channel in the interior pore formed by the 5 subunits

This allows flux of certain ions

Signal is transduced into post-synaptic cell

48
Q

Describe metabotropic receptors

Give examples

What sort of response do they elicit

A

7 transmembrane domain

e.g. Adenylate cyclase, phospholipase C or A, ion channels

Responses tend to be slower than for ionotropic receptors and of longer duration

49
Q

What are the different receptor classes and their receptor subtypes

A
50
Q

Step 4 in neurotransmission

A

Termination of the effect of the NT

51
Q

Name the main mechanisms for termination response

A
  1. Enzymatic degradation
  2. Uptake into 1) neuron via specific membrane transport protein, then uptake into synaptic vesicles, 2) surrounding astrocytes
  3. Diffusion away from synaptic cleft

CNS (36 decks)

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