Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Clinical Neuroscience > Session 2: The Role of Neurones and Glia > Flashcards

Session 2: The Role of Neurones and Glia Flashcards

1
Q

Types of glial cells.

A

Astrocytes

Oligodendrocytes

Microglia

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

Functions of oligodendrocytes

A

Insulators providing the myelin sheath for axons

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

Functions of the microglia.

A

Immune response

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

The role of the astrocytes.

A

Structural support for neurons

Help to provide nutrition for neurones via the glucose-lactate shuttle.

Removal of neurotransmitters by taking up glutamate.

Maintain ionic environment by K+ buffering.

Help to form the blood brain barrier.

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

Explain the energy provision to neurones by astrocytes.

A

Can be either by a direct pathway where glucose goes from blood into neuron directly.

or

By glucose lactate shuttle where glucose enters the astrocyte and is formed into glycogen.

The glycogen then turns into pyruvate and then into lactate.

The lactate then is transported out of the astrocyte and into the neuron where the lactate is transformed into pyruvate again.

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

Explain astrocytes removal of neurotransmitters.

A

They have transporters for transmitters and especially glutamate.

Glutamate is toxic in high concentrations which means that it needs to be taken up somehow and that is done via the astrocytes.

This helps to keep the extracellular concentration low.

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

Explain how astrocytes work as buffers for K+ in the brain ECF.

A

As neuronal activity increases in the brain there will be an influx of Na+ and to combat that influx there is an efflux of K+.

This leads to a rise of K+ extracellularly and hyperkalaemia can ensue. In order to compensate for this rise in K+ the astrocytes will take up K+.

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

How does myelination increase conduction velocity?

A

By a large increase in membrane resistance

By a large decrease in membrane capacitance

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

What is capacitance?

A

The membrane’s ability to store charge

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

Explain the role of microglia.

A

Immunocompetent cells which recognise foreign material.

This causes phagocytosis to remove debris.

This is the brain’s main defence.

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

Explain the purpose of the blood brain barrier.

A

Limits the diffusion of substances from the blood to the brain ECF.

It maintains the correct environment for the neurones.

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

Explain the relation between the brain capillaries and the blood brain barrier.

A

There are tight junctions between the endothelial cells.

There is also a basement membrane surrounding the capillaries.

And end feet of astrocyte processes.

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

Give examples of substances that can be transported across the BBB.

A

Glucose

Amino acids

Potassium

CO2

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

Explain the typical neuronal structure.

A

Four main sections:

Cell soma

Dendrites

Axon

Terminals

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

Briefly explain the neurotransmitter release at the synapse.

A

Depolarisation causes Ca2+ ions to enter the terminal.

The Ca2+ causes the vesicles to fuse with the membrane and release the transmitters.

The neurotransmitters diffuses acrsos the synaptic cleft and binds to receptors on the postsynaptic membrane causing an action potential.

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

What does the postsynaptic response depend on?

A

The neurotransmitter

The receptor (ligand-gated or g-protein)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the main groups of neurotransmitters in the CNS?

A

Amino acids

Biogenic amines

Peptides

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Give example of NT amino acids.

A

Glutamate

GABA

Glycine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Give examples of NT biogenic amines.

A

ACh

NA

Dopamine

Serotonin

Histamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Give examples of NT peptides

A

Substance P

Somatostatin

Cholecystokinin

Neuropeptide Y

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Give examples of excitatory amino acids as NTs.

A

Mainly glutamate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Give examples of inhibitory amino acids NTs.

A

GABA

Glycine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Give examples of the main glutamate receptors.

A

Ionotropic receptors

Metabotropic receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Give the subreceptors of ionotropic glutamate receptors.

A

AMPA receptors

Kainate receptors

NMDA receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Explain how the ionotropic receptors work.
They are ion channels receptors and cause an increase in the permeability of Na+ and K+ (also Ca2+ in the case of NMDA receptors). This causes **depolarisation** and **increased excitability.**
26
Explain how the metabotropic receptors work.
G-protein coupled receptors Ip3 and Ca2+ increase or inhibition of adenylate cyclase and decreased cAMP.
27
Explain the fast excitatory reponses.
Excitatory neurotransmitters cause **depolarisation** of the postsynaptic cleft by acting on **ligand-gated** ion channels (ionotropic). This causes excitatory postsynaptic potential (EPSP) and the depolarisation causes more action potentials
28
What kind of receptors are found on glutamatergic synapses?
They have both AMPA and NMDA receptors. The AMPA receptors mediate the **initial fast depolarisation** and the NMDA receptors are permeable to Ca2+.
29
Explain how the NMDA receptors work.
The receptors need glutamate to bind and the cell to be depolarised to allow ion flow through the channels. It also works with glycine as a co-agonist.
30
Explain the glutamate receptors role in learning and memory.
There is activation of NMDA receptors which can **up-regulate** the **AMPA** receptors. The strong and high frequency of stimulation causes a **long term potentiation** called LTP. Ca2+ entry through NMDA receptors are important for induction of LTP.
31
In the case of too much Ca2+ entry through the NMDA receptors, what may happen?
It can cause excitotoxicity by too much glutamate.
32
What is the main inhibitory transmitter in the brain? (AA)
GABA
33
Where does glycine act as an inhibitory NT?
Mostly in brainstem and spinal cord.
34
Explain how the GABA and glycine receptors work.
They have integral Cl- channels which when they open causes **hyperpolarisation** and an **inhibitory post-synaptic potential** and a **decrease in action potential firing.**
35
Give examples of drugs that bind to GABA (A) receptors.
Barbiturates and Benzodiazepines.
36
Explain the action of barbiturates. Risks as well
Enhance the response to GABA. They have an **anxiolytic** (inhibits anxiety) and **sedative** action. Not really used for it but **can be used as an anti-epileptic drug**. There is a risk of fatal overdose Dependence Tolerance **They have largely been replaced by benzodiapezines**
37
Explain the action of benzodiapezines.
Enhance the response to GABA Sedative and anxiolytic effects that is used to treat **anxiety, insomnia and epilepsy**.
38
What releases glycine?
Inhibitory interneurones in the spinal cord.
39
What role do other amino acid transmitters have that are not glutamate, GABA or glycine?
Modulatory role and discreet pathways.
40
Where does ACh act?
Neuromuscular junction Ganglion synapse in ANS Postganglionic parasympathetics **Central neurotransmitter** **Nicotinic and muscarinic** receptors in the brain It is **mainly excitatory** and the receptors often present on the presynaptic terminals to enhance the release of other transmitters.
41
Explain briefly the cholinergic pathways in the CNS.
They **originate** in the basal forebrain and brainstem. They then give diffuse projections to many parts of the **cortex** and **hippocampus**. E.g. Septohippocampal pathway.
42
What are local cholinergic interneurones?
Found in the CNS and are not pathways but act locally like the **corpus striatum**.
43
What are the cholinergic pathways mainly involved in?
Arousal Learning Memory Motor control
44
Explain how Alzheimer's disease relate to cholinergic pathways.
Degeneration of cholinergic neurones in the nucleus basalis.
45
What is used to alleviate symptoms of Alzheimer's disease?
Cholinesterase inhibitors
46
Give examples of dopaminergic pathways in the CNS.
Tubero-hypophyseal pathway Nigrostriatal pathway Mesocortical pathway Mesolimbic pathway
47
Main function of nigrostriatal pathway.
Involved in motor control (substantia nigra to dorsal striatum)
48
Main function of the mesocortical pathway.
Involved in mood, arousal and reward.
49
Main function of the mesolimbic pathway.
Involved in mood, arousal and reward.
50
Give examples of conditions associated with the dopamine pathway.
Parkinson's Schizophrenia
51
Briefly explain Parkinson's diease.
Associated with loss of **dopaminergic neurones.** This is at the input of **substantia nigra** (pars compacta) to the **corpus striatum**.
52
What is Parkinson's treated by?
**Levodopa** L-dopa is converted in to the desired **dopamine** via **DOPA decarboxylase** also called AADC
53
Explain how schizophrenia can be related to dopamine.
May be due to release of **too much** dopamine. **Amphetamine** releases **dopamine** and NA. This produces schizophrenic like behaviour**.**
54
What is given in the case of Schizophrenia?
Antipsychotic drugs such as **Dopamine D2 receptor antagonists**.
55
Carbidopa is a drug that is given to inhibit AADC from converting L-DOPA into Dopamine, why is this given in Parkinson's?
Because Carbidopa only inhibits L-Dopa conversion into Dopamine **outside** of the **BBB**. This is because you don't want L-DOPA to be converted outside of the brain ECF.
56
Why does carbidopa not convert L-DOPA into Dopamine in the brain?
Because it cannot cross the BBB
57
Roles of noradrenaline (NA)
Transmitter at postganglionic at effect synapse in ANS NT in CNS Acts via **GPCRs** and alpha+beta adrenoceptors. **Receptors in the brain for NA is the same as in the PNS**.
58
Briefly explain the noradrenergic pathways in the CNS.
Cell bodies of NA containing neurones are found (arise) from the brainstem and specifically **pons** and **medulla.** There is then a diffuse release of NA throughout the **cortex, hypothalamus, amygdala,** and **cerebellum**.
59
Where does most of the noradrenline in the brain come from?
A group of neurones in the **locus ceruleus**.
60
Give examples of how the locus ceruleus neurones can differ in activity.
**Inactive** during sleep **Increased** activity during behavioural arousal **Increased** activity due to amphetamines. (Also increase dopamine release)
61
Expain the relationship between mood and state of arousal.
Depression may be associated with a **deficiency** of NA.
62
Briefly explain the Serotonergic pathways in the CNS.
Serotonin and 5-HT have a similar distribution to noradrenergic neurones. The functions are **sleep/wakefuness** and **mood**.
63
Give example what can be given in treating depression and anxiety disorders relating to the serotonergic pathways.
SSRIs (Serotonin selective reuptake inhibitors)
64
What structure produces dopamine?
Substantia nigra
65
What structure produces serotonin?
raphe nuclei
66
What structure produces noradrenaline?
Locus coeroleus
67
Explain glycine's role in the patellar tendon reflex.
Hitting the patellar tendon causes spindle fibres to activate and afferents activate with glutamate as their NT. This produces an **excitatory response** of the quadriceps to jerk the knee upwards (knee extension). Glutamate also excites an **interneuron** in order to activate it and produce **glycine** at another synapse which will **inhibit** the hamstring muscle causing it to relax in order to not produce the opposing force.
68
Explain how glutamate can cause excitotoxicity through NMDA receptors.
NMDA receptors activate and cause an influx of Ca2+. Too much Ca2+ can be damaging to the cell and cause it to **die**. As the cell dies it will release a substantial amount of **potassium** which will circulate freely in the ECF now causing an increased concentration. This causes an increase in K+ in ECF and will cause easier depolarisation of adjacent neurons. This depolarisation will activate NMDA receptors in other places and more cells will die. This leads to a spread of excitotoxicity.
69
Explain how NMDA receptors are activated.
NMDA receptors are not solely activated by glutamate. Glutamate will bind to the NMDA receptors but **magnesium** will be stuck in the pore of the ion channel. Prolonged depolarisation of the cell and AMPA receptors will eventually remove the magnesium from the NMDA pore in order to let Na+ and Ca2+ to move into the cell.
70
Briefly explain the CNS immune response.
It does not undergo any rapid rejection of a foreign object as that would be harmful for the brain. No **inflammatory** response happens because the brain would not be able to tolerate an increased volume. The microglia can act as **antigen presenting cells** and present antigen to **T-cells** which can enter the CNS. The CNS **inhibits** the initiation of the pro-inflammatory T-cell response.

Clinical Neuroscience (22 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions