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Scientific Foundations > Neurochemistry > Flashcards

Neurochemistry Flashcards

1
Q

What are ependymal cells?

A

Cells that line the ventricles

They produce, monitor, and circulate CSF

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2
Q

What type of cell is an olfactory or retinal cell?

A

Bipolar neuron

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3
Q

What are basket cells?

A

Inhibitory interneurons that form dense plexus of terminals around the soma of target cells

Found in the cerebellum and cortex

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4
Q

What are betz cells?

A

Large motor neurons

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5
Q

What type of cell forms most of the corpus striatum?

A

Medium spiny neurons

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6
Q

What are Purkinje cells?

A

Huge neurons in the cerebellum

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7
Q

What are Renshaw cells?

A

Neurons with both ends linked to alpha motor neurons

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8
Q

What are granule cells?

A

The smallest type of neurons, found in the cerebellum

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9
Q

What are anterior horn cells?

A

Motor neurons located in the spinal cord

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10
Q

What are spindle cells?

A

Interneurons that connect widely separated areas of brain

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11
Q

What are the main types of circuits neurons can form?

A

▪️Divergence (same or multiple pathways)
▪️Convergence (single or multiple sources)
▪️Reverberating circuit
▪️Parallel after-discharge circuit

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12
Q

How are neurotransmitters transported down an axon?

A

I’m vesicles

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13
Q

What evokes the release of neurotransmitters from vesicles?

A

Influx of calcium caused by action potential

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14
Q

Where do vesicles go after releasing neurotransmitters?

A

Back up the axon to the soma

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15
Q

What are the two types of axonal transport?

A

▪️Slow (1-5mm/day)
▪️Fast (200-400mm/day)

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16
Q

What is transported via fast axonal transport?

A

▪️Neurotransmitters
▪️Growth factors
▪️Toxins/pathogens (e.g. HSV, tetanus)

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17
Q

What is slow axonal transport important for?

A

▪️Transporting complex products (e.g. axoplasm to terminals)
▪️Neuronal growth
▪️Part of mature neuron function

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18
Q

What are the 3 main types of synapses?

A

▪️Axodendritic
▪️Axosomatic
▪️Axoaxonic

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19
Q

What targets are relevant for neurotransmitters?

A

▪️Receptors (ionotropic, metabotropic)
▪️Enzymes
▪️Transporters
▪️Nuclear/mitochondrial receptors

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20
Q

What are ionotropic receptors?

A

Receptors with a channel that opens up when a ligand (NT) binds to it, changing its shape, and allowing ions to flow across the membrane.

(Aka neurotransmitter-gated or ligan-gated channels)

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21
Q

What are cations?

A

Ions with a positive charge (e.g., Na+, K+, Ca+)

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22
Q

How does the opening of an ionotropic receptor effect the membrane?

A

Has direct and fast effects of neural membrane excitability.

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23
Q

How does synaptic transmission with metabotropic receptors compare to ionotropic receptors?

A

Much slower

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24
Q

What happens when a neurotransmitter binds to a metabotropic receptor?

A

▪️ G-protein coupled with the receptor is activated and produces effector
▪️ Effector stimulates secondary messenger synthesis
▪️ Secondary messenger activates intercellular process, which opens the channel

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25
Q

What pathways can be activated by G-proteins (GPCR/7TM)?

A

▪️ Canonical pathway (which activates cyclic AMP or phosphatidylinositol pathway)
▪️ Alternative pathways (via beta-arrestins, GRKs and SrcKs)

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26
Q

Why might different molecules activating the same metabotropic receptor lead to different effects?

A

Depends on which pathway is activated (show bias for different ones)

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27
Q

What can control metabotropic receptor activity?

A

G-protein coupling

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28
Q

G-protein coupling has a _________________________

A

Dynamic equilibrium (at any one time some will be coupled and some wont, changes very quickly)

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29
Q

Which metabotropic receptors do agonists show higher affinity for?

A

G-coupled receptors (compared to uncoupled)

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30
Q

How does the affinity of antagonists at metabotropic receptors differ when it is G-coupled compared to when it is uncoupled?

A

No difference

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31
Q

What happens with chronic agonist stimulation of a metabotropic receptor?

A

Desensitisation - internalisation of receptors, some get destroyed, some get recycled but regeneration of new ones cannot keep up with the number destroyed so total amount reduces

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32
Q

What happens with chronic antagonist stimulation of a metabotropic receptor?

A

Hypersensitisation - prevents internalisation and destruction of receptors, leading to increased number of receptors on the surface

(Reaction to less stimulation to try and increase stimulation!)

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33
Q

What controls second messenger cellular concentrations?

A

Specific enzyme pathways (e.g., cyclic nucleotides)

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34
Q

What happens if there is too much secondary messenger?

A

Increase affinity of the breakdown enzyme for its substrate to increase the breakdown of the messenger

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35
Q

How might one metabotropic receptor interact with another?

A

Secondary messengers provide a path between them so activity of one can modulate activity of another

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36
Q

What is an excitatory neurotransmitter?

A

One that enhances the probability of an action potential

Depolarises or increased probability of depolarisation

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37
Q

What is an inhibitory neurotransmitter

A

Hyperpolarises the membrane and reduces probability of action potential

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38
Q

Can the same neurotransmitter have both excitatory and inhibitory effecrs?

A

Yes! - depending on the circuit and the receptor it binds to

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39
Q

What controls neurotransmitter release?

A

▪️ Activity (e.g., change in neuronal firing rate modulated by somatodendritic auto-receptors)
▪️ Synaptic neurotransmitter concentration
▪️ Other neurotransmitters released from other terminals that activate pre-synaptic hetero-receptors

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40
Q

What modulates synaptic membrane excitability and local neurotransmitter release?

A

Pre-synaptic auto-receptors

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41
Q

What terminates neurotransmitter activity?

A

▪️ Dissociation of NT from receptor
▪️ Receptor internalisation (typically in response to agonist binding for metabotropic receptors)
▪️ Synaptic “free” NT concentration drops

42
Q

What causes synaptic “free” NT concentration to drop?

A

▪️ NT diffuses away
▪️ Re-uptake into pre-synaptic terminal or glia via re-uptake transporters
▪️ Catabolism by extracellular (e.g., acetylcholinesterase, COMT) or intracellular enzymes (e.g., MAO)

43
Q

What are the main modulatory monoamines?

A

▪️ Dopamine
▪️ Noradrenaline
▪️ Histamine
▪️ Serotonin (5-HT)

44
Q

What type of molecule is glutamate, GABA, and glycine?

A

Amino acids

45
Q

What constitutes the majority of neurotransmitters in the brain?

A

Glutamate and GABA

46
Q

What is GABA?

A

▪️ Principle inhibitory NT
▪️ Typically acts on ionotropic receptors attached to chloride channels
▪️ Increase of chloride ions = increasingly negative potential (hyperpolarisation)

47
Q

What is glutamate?

A

▪️ Principle excitatory NT
▪️ Typically acts on receptors coupled with cation channels - depolarisation!

48
Q

What is glutamate involved in?

A

Cognition, memory, and learning

49
Q

What are the main glutamatergic ionotropic receptors?

A

NMDA, AMPA, and kainate

50
Q

What role does glutamate play in neurodegenerative disease?

A

Insult to brain = increased glutamate release = excitotoxicity = cells self-destruct

51
Q

What are the most prominent glutamate pathways?

A

▪️ Cortico-cortical
▪️ Thalamo-cortical
▪️ Cortico-striatal

(also pathways been cortex, substantia nigra, subthalamic nucleus, and pallidum)

52
Q

What does GABA regulate?

A

▪️ Neuronal excitability
▪️ Muscle tone
▪️ Levels of alertness

53
Q

What are the two main types of GABA receptors?

A

▪️ GABA a = ionotropic (opens Cl- and K+ channels)
▪️ GABA b = metabotropic (works via GPCRs)

54
Q

Where is GABA taken into and what is it converted to?

A

▪️ Astrocytes
▪️ Converted into glutamate and glutamine

55
Q

What happens to glutamine when it is released by astrocytes?

A

▪️ Taken up by neurons
▪️ Converted into glutamate and then GABA

56
Q

What are the two acetylcholine receptors?

A

▪️ Nicotinic (typically excitatory)
▪️ Muscarinic (either excitatory or inhibitory)

57
Q

What is the main role of acetylcholine?

A

Cognitive function - possible role in AD/AD treatment

58
Q

What is the monoamine synthetic pathway?

A
  1. L-tyrosine
  2. L-DOPA
  3. Dopamine
  4. Noradrenaline
  5. Adrenaline
59
Q

Where are the cell bodies for dopamine synthesis?

A

Midbrain nuclei - substantia nigra, ventral tegmental area

60
Q

What are the main functions of D1 and D5 receptors?

A

▪️ Excitatory
▪️ Increase cAMP which enhances cation channel opening

61
Q

What are the main functions of D2, D3, and D4?

A

▪️ Inhibitory
▪️ Decrease cAMP

62
Q

How many dopamine receptors are there and what kind of receptor are they all?

A

▪️ 5
▪️ All GPCRs (metabotropic)

63
Q

How is dopamine taken back into presynaptic terminals and what can inhibit this?

A

▪️ Via dopamine transporters (DAT)
▪️ Inhibited by amphetamine, cocaine, and methylphenidate - increase reward!

64
Q

How are dopamine and noradrenaline catabolised?

A

▪️ By MAO-A in the neurons
▪️ By MAO-B in glial
▪️ By COMT extracellularly

65
Q

What conditions are associated with abnormal dopamine?

A

▪️ Schizophrenia (increased in PFC)
▪️ ADHD (decreased)
▪️ Parkinson’s (severe deficiency due to cell death in substantia nigra)

66
Q

Why is Parkinson’s treated with L-DOPA instead of dopamine?

A

Dopamine cannot cross the BBB and has severe adverse cardiac effects

67
Q

Where is noradrenaline synthesised?

A

Noradrenergic neurons in locus coeruleus

68
Q

Where does noradrenaline take effect?

A

▪️ Brain stem
▪️ Spinal cord
▪️ Cerebellum
▪️ Hypothalamus
▪️ Amygdala
▪️ Neocortex

69
Q

What are the two types of CNS noradrenaline receptors?

A

▪️ Alpha-2 = inhibitory
▪️ Beta-2 = excitatory

70
Q

Where else are noradrenaline receptors typically found?

A

On vasculature

71
Q

How are dopamine, noradrenaline, and serotonin transported?

A

In synaptic vesicles by vesicular monoamine transporter (VMAT)

72
Q

What is the main role of adrenaline?

A

Attention and focus

73
Q

What conditions have been associated with abnormal noradrenaline in the brain?

A

▪️ ADHD
▪️ Depression
▪️ Schizophrenia

74
Q

What is serotonin derived from?

A

Tryptophan

75
Q

What neurons are modulated by serotonin?

A

Glutamatergic and GABAnergic

76
Q

Where are serotonergic cell bodies found?

A

Raphe nuceli

77
Q

How many receptors are associated with serotonin?

A

17

78
Q

What type of receptor are serotonin receptors?

A

All metabotropic (GPCRs) except for 5-HT3 which is a ligand-gated ion channel

79
Q

How is serotonin taken back into pre-synaptic terminals?

A

Via serotonin transporters (SERT)

80
Q

What inhibits serotonin reuptake?

A

▪️ MDMA
▪️ Amphetamine
▪️ Cocaine
▪️ Tricyclic antidepressants
▪️ SSRIs

81
Q

How is serotonin catabolised?

A

By MAO-A

82
Q

What role does serotonin play physiologically?

A

▪️ Well-being
▪️ Happiness
▪️ Mood
▪️ Appetite
▪️ Sleep

83
Q

What conditions have been associated with abnormal levels of serotonin?

A

▪️ Depression
▪️ Anxiety
▪️ Eating disorder
▪️ Parkinson’s disease?

84
Q

What are the main histamine receptors in the CNS?

A

H1 and H3 (all metabotropic)

85
Q

How is histamine formed and where?

A

▪️ By decarboxylation of L-histidine
▪️ In the tuberomammillary nuclei in posterior hypothalamus

86
Q

What is physiological role of histamine?

A

Regulation of sleep, appetite, and body temperature

87
Q

What conditions have been associated with abnormal histamine levels?

A

Schizophrenia

88
Q

What are the main purines in the brain?

A

Adenosine and ATP

89
Q

What is the main role of adenosine receptors?

A

Co-localise with other receptors, such as D2, affecting their function

90
Q

What can block adenosine 2A receptors and what is the effect of this?

A

Caffeine - decreases function of D2 thus increases the effect of dopamine

91
Q

What do endorphins do?

A

▪️ Generally inhibitory
▪️ Act via opioid receptors
▪️ General pain control and feelings of happiness

92
Q

How are endocannabinoids transported through the cytoplasm?

A

Via endocannabinoid transporter proteins (eCBTs) because they are very hydrophobic

E.g., heat shock proteins, fatty acid binding proteins

93
Q

What are the two main endocannabinoids?

A

▪️ Anandamide
▪️ 2-Arachidonoylglycerol

94
Q

What are the two main cannabinoid receptors?

A

▪️ CB1 - one of the most abundant of all CNS receptors
▪️ CB2 - mainly on activated glia, role in immune activation?

95
Q

How are cannabinoids broken down?

A

▪️ Fatty acid amide hydrolase (FAAH)
▪️ Monoacyl glycerol lipase (MAGL)

96
Q

What are the main physiological roles of cannabinoids?

A

▪️ Feeding behaviour
▪️ Motivation
▪️ Pleasure

97
Q

What is the Hebbian theory of neuronal plasticity?

A

Circuits that get used often will be reinforced, making it easier for those cells to communicate

Conversely, connections used less often will die off

98
Q

What is long-term potentiation?

A

Persistent strengthening of synapses:

▪️ Strong depolarisation leads to removal of NMDAR Mg2+ block
▪️ Rapid flow of Ca2+ into the cell
▪️ Activation of protein kinases
▪️ Trigger insertion into postsynaptic membrane

99
Q

What is the cellular basis of synaptic plasticity?

A

▪️ At resting potential, ion flow through NMDAR is blocked by extracellular Mg2+
▪️ Mg2+ is displaced by depolarisation of post-synaptic membrane
▪️ Pattern of this and presynaptic glutamate release determines extent of NMDAR activation and Ca2+ influx
▪️ Ca2+ activates second messenger pathways
▪️ Pathways enable easier activation of pathway with lower amounts of glutamate

100
Q

What is long-term depression?

A

Synapses become less efficient

▪️ Weka depolarisation leads to lesser degree of removal of NMDAR Mg2+ block
▪️ Modest increase in Ca2+
▪️ Activation of protein phosphatases
▪️ Trigger removal from postsynaptic membrane

101
Q

How is the best way to measure in vivo neurochemistry?

A

▪️ PET
▪️ SPECT

102
Q

What is SV2A used for?

A

A marker of synapses, giving a measure of synaptic density

Scientific Foundations (27 decks)

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