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Sem 4: Nervous System > 2a.) Neurones & Glia > Flashcards

2a.) Neurones & Glia Flashcards

1
Q

Which is more abundant in CNS: neurones or glia?

A

Glia

(~1011 neurones, ~1012 glia)

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2
Q

Describe, in general terms/briefly, the role of glia in CNS

A
  • Support neurons
  • Nourish neurons
  • Insulate neurons
  • Revmove waste
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3
Q

Neurones sense _____ and ____ with other ____

A

Neurones sense change and communicate with other neurones

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4
Q

State the 3 types of glial cells in CNS and briefly summarise each one’s role

A
  • Astrocytes (support)
  • Oligodendrocytes (insulators)
  • Microglia (immune response)
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5
Q

Which glial cell in CNS is the smallest?

A

Microglia

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6
Q

There is only one type of astrocyte found in CNS; true or false?

A

False- there are several different types of astroctyes

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7
Q

State 5 roles of astrocytes in the CNS

A
  • Structural support
  • Help to provide nutrition for neurones (glucose-lacate shuttle)
  • Remove neurotransmitters (to control neurotransmitter conc)
  • Maintain ionic environment (K+ buffering)
  • Help to form blood brain barrier
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8
Q

Why do we need astrocytes to help provide energy for neurones?

A

Neurones do no store or produce glycogen hence they don’t have an energy reserve; therefore, as well as taking up glucose via GLUT3 they can also take up lactate which is produced by the astroctyes to help supplement their supply of gluose when neuronal activity is high

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9
Q

Which transporters transports glucose into neurones?

A

GLUT 3

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10
Q

Describe the glucose-lactate shuttle

A
  • Glucose transported across blood brain barrier via GLUT 1
  • Moves into interstitial space in CNS
  • Transported into astrocyte via GLUT 1
  • Used to produce glycogen
  • Glycogen broken down in to glucose
  • Glucose further broken down into pyruvate (this releases some ATP)
  • Pyruvate converted into lactate (this uses some ATP)
  • Lactate transported out of astrocyte via MCT1 (co-transported with hydrogen ions)
  • Lactate transported into neurone via MCT1 (co-transported with hydrogen ions)
  • Lactate converted into pyruvate
  • Pyruvate used to release energy
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11
Q

Astrocytes have transporters for transmitters such as glutamate; explain why it is important that astrocytes have transporters for glutamate

A
  • Astrocytes having transporters means taht they can uptake transmitters, such as glutamate, and remove them from teh synaptic space
  • This helps to keep extracellular [glutamate] low
  • Glutamate is excitotoxic (it is the major excitatory neurotransmitter in brain and too much of it can cause excess calcium to move into post-synaptic cells and cause damage)
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12
Q

Why is it important that astrocytes are able to buffer [K+] in the brain?

A
  • High levels of neuronal activity could cause high [K+] in brain ECF (because to make action potential, upward stroke= inward movement of Na+ and downard stroke= outward movement of K+)
  • Astrocytes have multiple methods of taking up K+ to keep ECF [K+] low: K+ channels, NKCC2, Na+/K+-ATPase
  • High brain ECF [K+] can cause neuron depolarisation which could inactivate some neurons
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13
Q

What property of astrocytes further aids to re-uptake of K+ into astroctyes?

A

Astrocytes have a more -ve membrane potential (relative to ECF)???

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14
Q

What is the role of oligodendrocytes in CNS?

A

Myelinate axons/produce myelin sheath

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15
Q

Compare Oligodendrocytes (in CNS) and Schwann Cells in PNS in terms of myelination

A
  • One oligodendrocyte can wrap around, and myelinate, more than one axon
  • One Schwann cell wraps around, and myelinates, one axon
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16
Q

Describe the role of microglia in CNS

A
  • They are immunocompetent cells that can recognise foreign material (resulting in their activation)
  • They can then phagocytose foreign material and debris and act as APCs
  • They can also act as T cells

THEY ARE THE BRAINS MAIN DEFENCE SYSTEM

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17
Q

What’s the purpose of the blood brain barrier?

A

Limit diffusion of substances from the blood to the brain ECF to help maintain the correct environment for neurones

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18
Q

Describe three structural features of the blood brain barrier that help it limit diffusion

A
  • Tight junctions between endothelial cells
  • Basement membrane surrounding capillary
  • End feet of astrocyte processes
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19
Q

Provide some exampels of substances that can move across blood brain barrier

A

*NOTE from the diagram that substances don’t move paracellulary due to presence of tight junctions between endothelial cells

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20
Q

The CNS is often described as immunocompromised; explain what we mean by this and why it is important for the CNS to be immune specialised

A
  • Microglia can act as APCs and present antigens to T cells. T cells can then enter CNS. However, CNS inhibits the initiation of the pro-inflammatory T cell-response- this inhibits inflammation
  • This is important in CNS as the rigid skull will not tolerate too much volume expansion (which could be caused by inflammation)
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21
Q

If you gave someone a brain transplant, would there be rapid rejection of the allograft?

A

No, because the CNS is immune privelaged/specialised

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22
Q

Describe the typical structure of a neuron

A
  • Celll soma (body)
  • Dendrites (receive incoming signals)
  • Axons (propagates action potential)
  • Terminals (connect with other neurons or the effector cell)
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23
Q

One axon can have many terminals; true of false?

A

True

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24
Q

If an axon is synapsing with another neuron, it can synapse with the dendrites of the other neurone or the cell body of the other neurone. Most of the axons synapsing at cell body of other neurone are what type of neuron?

A

Inhibitory neurones

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25
Q

Briefly describe neurotransmitter release at the synapse

A
  • Action potential arrives and causes depolarisation of pre-synaptic neuron
  • Opens voltage-gated Ca2+ channels in pre-synaptic neuron
  • Ca2+ influx into cell
  • Ca2+ causes vesicles to fuse with membrane and release neurotransmitter
  • Neurotransmitter diffuses across synaptic cleft and binds to receptors on post-synaptic membrane
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26
Q

The post synaptic response depends mainly on what 2 things?

A
  • Nature of neurotransmitter (is it excitatory or inhibitory)
  • Nature of receptor (ligand-gated ion [fast] or GPCR [slow])
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27
Q

How many neurotransmitters are in the CNS?

A

>30 have been identified

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28
Q

Neurotransmitters in CNS can be divided into three chemical classes; state the three classes and provide examples of neurotransmitters in each

A
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29
Q

Out of the amino acid neurotransmitters in CNS; state which one is excitatory and which two are inhibitory

A
  • Excitatory: glutamate
  • Inhibitory: GABA & glycine
30
Q

State the main/major excitatory neurotransmitter in CNS

A

Glutamate

(over 70% of all CNS synapses are glutamatergic hence glutamate is not only major excitatory neurotransmitter it is also the major neurotransmitter)

31
Q

Glutamate receptros can be divided into two classes; state these two classes and briefly describe what each class is

A
  • Ionotropic: have an associated integral ion channel hence act quickly
  • Metabotropic: have a GPCR hence are slower
32
Q

State the 3 ionotropicglutamate receptors and state what each on transports

A
33
Q

Briefly describe how ionotropic glutamatergic receptors work

A
  • Ligand binds to receptor
  • Activation of receptors causes influx of Na+ (and Ca2+ in case of NDMA receptros) and efflux of K+
  • This causes depolarisation
  • This increases excitability
34
Q

Briefly descibe how metabotropic glutamatergic receptors work

A
  • Ligand binds to receptor
  • Causes conformational change in shape so now G-protein can bind to GPCR

….. usual steps

  • Can be linked to either changes in IP3 and Ca2+ mobilisation
  • Or can be linked to inhibition of adenylate cyclase and decreased cAMP levels
35
Q

Give an example of metabotropic glutamatergic receptor in CNS

A
36
Q

Briefly describe the mechanism behind fast excitatory responses

A
  • Excitatory neurotransmitters bind to post synaptic cell
  • Activate ligand-gated ion channel
  • Causes influx of Na+ (and Ca2+ in NMDA) and efflux of K+ to cause depolarisation
  • This generates more action potentials
37
Q

Glutamatergic synapses have two receptors; what two recepotrs are present at glutamatergic synapses?

A
  • AMPA
  • NDMA
38
Q

Describe why glutamatergic synapses need both AMPA and NMDA receptors

A
  • AMPA receptors mediate the initial fast depolarisation (activiation causes influx of Na+ and efflux of K+)
  • NDMA receptors, however have Mg2+ ions sitting in and hence blocking their pore. In order to remove the Mg2+ ion and unblock the pore the post-synaptic cell has to be depolarised. Activation of AMPA causes the depolarisation of the post synaptic cell which then causes Mg2+ move and hence unblocks the NMDA pore. NMDA pore now permeable to Na+ and Ca2+ and can hence cause further depolarisation
39
Q

Glutamate receptors are thought to have an importnat role in what…?

Explain how

A
  • Learning and memory

How:

  • Activation of NMDA receptors (and mGluRs) can upregulate AMPA receptors
  • Strong, high frequency stimulation then causes long term potentiation (LTP)
  • Ca2+ influx through NMDA receptors is important for the induction of LTP
40
Q

What amino acid neurotransmitter acts as a co-agonist for NMDA?

A

Glycine

*NDMA has receptor for both glutamate and glycine

41
Q

This image helps summarise long term potentiation

A
42
Q

What is long term potentiation?

A

Long-term potentiation (LTP) is a persistent strengthening of synapses based on recent patterns of activity. These are patterns of synaptic activity that produce a long-lasting increase in signal transmission between two neurons

43
Q

GABA and glycine are the inhibitory amino acid neurotransimtters; state where each one predominatly acts

A
  • GABA: main inhibitory transmitter in brain
  • Glycine: inhibitoy neurotransmitter mostly in brainstem and spinal cord
44
Q

Describe how GABA and glycine receptors acts as inhibitory receptors

A
  • GABAA and glycine receptors have integral Cl- channels
  • When ligand binds to these receptors it opens Cl- channel causing influx of Cl-
  • This causes hyperpolarisation of post-synaptic cell
  • This causes inhibitory post-synaptic potential which decreases action potential firing
45
Q

State two classes of drugs which bind to GABAA receptors

A
  • Barbiturates
  • Benzodiazepines
46
Q

Describe how barbiturates and benodiazepines acting on GABAA receptors work

A

Bind allosterically to GABAA receptors and increase the probability of channel being open. This causes more Cl- to move into post-synaptic cells, causing hyperpolarisation, and decreasing action potential firing

47
Q

State what the following drugs are used for:

  • Barbiturates
  • Benzodiazepines
A
  • Barbiturates: anxiolytic & sedative actions however not used for this now as there is risk of fatal overdose, dependence and tolerance. They are sometimes used as anti-epileptic drugs
  • Benzodiazepines: anxiolytic & sedative effects hence used to treat insomnia, anxiety and epilepsy
48
Q

In this diagram of knee jerk reflex, which synapse will have glycine as the neurotransmitter?

A

The inhibitory interneuron in spinal cord (which is acting to inhibit the contraction of hamstrings resulting in relaxation of hamstrings so quadriceps can contract)

**Remember: glycine is the main inhibitory neurotransmitter in the brainstem and spinal cord

49
Q

We know that glutamate is the major excitatory neurotransmitter in CNS and that GABA & glycine are main inhbitory neurotransmitters in CNS; what is the role of the other transmitters then (since we know there are >30 neurotransmitters in CNS)?

A

Other transmitters have more of a modulatory role in CNS or are involved in discreet pathways

50
Q

Discuss Acetylcholine as a neurotransmitter, include:

  • Where it is used as a neurotransmitter (think about autonomic nervous system aswell as brain)
  • What receptors it acts on
A

ACh in autonomic nervous system:

  • All pre-ganglionic synapses use ACh which bind to nACh receptors
  • Post-ganglionic synapses of parasympathetic which bind to mACh receptors

ACh in somatic:

  • No ganglia, just use ACh acting on nACh receptors

ACh in central nervous system:

  • Acts on both nACh and mACh receptors in brain
  • Mainly excitatory
  • Receptors often present on pre-synaptic terminals to enhance the release of other transmitters
51
Q

ACh is mainly excitatory in CNS; true or false?

A

True

52
Q

Where do the neurones responsible for cholinergic pathways in CNS originate?

Where are local cholinergic interneurones found?

A
  • Basal forebrain- nucleus basalis & septohippocampal nucleus (project mainly to cortex and to hippocampus respectively)
  • Brainstem- pedunculopontine & laterodorsal tegmental nuclei

Local cholinergic interneurones found in many places but particulary in the corpus stratium

53
Q

What is the full name of the cholinergic nucleus basalis…?

A

Nucleus basalis of Meynert

54
Q

What 3 things are cholinergic pathways in CNS involved in?

A
  • Arousal
  • Learning & memory
  • Motor control
55
Q

Degeneration of what neurones in what nucleus of brain is associated wtih Alzheimer’s disease?

A

Degeneration of cholinergic neurones in the nucleus basalis

56
Q

What mediation can we use to alleviate symptoms of Alzheimer’s disease?

A

Cholinesterase inhibitors

57
Q

State the three dopaminergic pathways in the CNS

A
  • Nigrostriatal pathway (75% of dopamine in brain, cell bodies in substantia nigra)
  • Mesocortical pathway (cell bodies in midbrain ventral tegmental area)
  • Mesolimbic pathway (cell bodies in midbrain ventral tegmental area)
58
Q

State which dopaminergic pathways in CNS are involved in:

  • Motor control
  • Mood, arousal, reward
A
  • Motor: nigrostriatal pathway
  • Mood, arousal, reward: mesocortical & mesolimbic pathway
59
Q

What condition is associated with a loss of dopaminergic neurones?

A

Parkinson’s disease (decreased input from substantia nigra to corpus striatum)

60
Q

What condition is associated with the release of too much dopamine?

A

Schizophrenia

61
Q

What medications can we use to treat schizophrenia?

A

Dopamine D2 receptor antagonists

62
Q

What affect does amphetamines have on CNS and hence behaviour?

A
  • Amphetamine causes dopamine and noradrenaline release
  • Produces schizophrenic like behaviour
63
Q

What drug can we use to treat Parkinson’s disease (which is due to loss of dopaminergic neurones)?

Explain how it works

A

Levodopa

  • Dopamine cannot penetrate blood brain barrier so we cannot just give dopamine
  • Levodopa is a dopamine precursor that can cross the BBB via the LNAA transporter
  • Once it crosses blood brain barrier it is converted to dopamine by AADC (dopa decarboxylase/aromatic amino acid decarboyxlase)
  • We give a selective extracerebral decarboxylase inhibitor e.g. carbidopa at same time to prevent levodopa being converted into dopamine in periphery
64
Q

What receptors does NA operate through?

A

G-protein coupled alpha and beta receptors

65
Q

Where are cell bodies of noradrenergic neurons found in CNS?

Where do they release NA to?

A

Found in small clusters in pons & medulla (Most prominent cluster is Locus coeruleus)

Diffuse release of Na throughout cortex, hypothalamus, amygdala, cerebellum (and spinal cord)

66
Q

Most NA in brain comes from a group of neurones in which nucleus?

Discuss when these neurones are most active

A
  • Locus Coeruleus (LC)
  • LC neurones inactive durign sleep, activity increase during behavioural arousal (which can increase alertness)
67
Q

A deficiency in NA can be associated with…?

A

Depression

68
Q

Where are cell bodies of serotonergic neurones found in CNS?

A

In pons & medulla; they are often referred to as the raphe nuclei

69
Q

State two functions of serotonergic pathways in CNS

A
  • Sleep/wakefulness
  • Mood
70
Q

What medications are given to treat depression & anxiety disorders?

A

SSRIs (serotonin selective reuptake inhibitors)

71
Q

Too much calcium entry through NMDA receptors can cause…?

A

Excitotoxicity

72
Q

What does increased levels of dopamine in the periphery cause?

A

GI upset

Sem 4: Nervous System (21 decks)

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