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Neuro > CNS Physiology > Flashcards

CNS Physiology Flashcards

1
Q

What are the types of glia

A

Astrocytes
Oligodendrites
Microglia

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2
Q

Briefly describe the role of astrocytes

A 
Structural support
Provide nutrition to neurones
Remove neurotransmitters
Maintain ionic environment
Form BBB
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3
Q

Briefly describe how astrocytes provide energy for neurones

A

Neurones cant produce or store glycogen.
Glucose lactate shuttle:
When glucose is low e.g. reduced blood flow, or high activity metabolising glucose
Astrocytes produce lactate which can be transferred to neurones via MCT1 and MCT2

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4
Q

Briefly describe how astrocytes remove neurotransmitters

Give an example of a neurotransmitter

A

They have transporters for transmitters
Keeps extracellular conc low to terminate signal and enable more signals to be sent
Glutamate

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5
Q

Briefly describe how astrocytes maintain an ionic environment

A

They have a very low resting membrane potential
Remove potassium
(High levels of neuronal activity can lead to a rise in conc of potassium in brain ECF)

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6
Q

Briefly describe the role of oligodendrites

A

Myelinate axons in the CNS

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7
Q

Briefly describe the role of microglia

A

Phagocytosis to remove debris and foreign material.
They swell on sensing this material until they become active and phagocytic.
Also act as antigen presenting cells to T cells

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8
Q

Briefly describe the function of the BBB and some features of the brain capillaries which maintain this

A

Limits diffusion of substances from the blood to the brain ECF, maintaining the correct environment for neurones.
They have tight junctions, BM and the end of astrocyte processes.

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9
Q

What is the specialised immune system of the CNS called?

A

Immune privileged.

Inflammatory response is minimal (wouldn’t undergo rapid rejection of an allograft)

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10
Q

What are the 3 chemical classes of neurotransmitter in the brain?

A 
Amino acids (glutamate. glycine, GABA)
Biogenic amines (ACh, NA, dopamine, serotonin etc.)
Peptides (Substance P, somatostatin, CCK etc.)
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11
Q

Describe the main excitatory amino acids

A

Glutamate

Metabotropic- g coupled receptor
-linked to changes in IP3 and calcium or decreased cAMP

Ionotropic- integral ion channels
Kainate receptors- sodium/potassium
AMPA receptors- sodium/potassium
-mediate initial fast depolarisation
NMDA receptors- sodium/potassium and calcium
-normally blocked by magnesium, requires glutamate to bind to allow ion flow, glycine acts as co agonist

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12
Q

Briefly describe glutamate receptors role in memory

A

Activation of NMDA receptors can upregulate AMPA receptors.
Strong stimulation causes long term potentiation, strenghtening the synapse.
(calcium flow at NMDA receptors is important)

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13
Q

What is the consequence of too much calcium entering through NMDA receptors?
Give an example of when this may occur

A

Excitotoxicity- kills neurones

E.g. stroke

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14
Q

Briefly describe the main inhibitory amino acids

A

GABA in the brain
Glycine in the brainstem and spinal cord
Both have integral chloride channels
Both cause hyperpolarisation

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15
Q

Name the drugs that bind to GABA receptors and briefly describe their actions.

A

Barbiturates (problems with dependence, tolerance and overdose)
Benzodiazepines (used to treat insomnia, anxiety, epilepsy)
Sedative and anxiolytic- increase the inhibitory effect of GABA

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16
Q

What receptors does ACh act at in the brain?

What effect does it have?

A

Nicotinic
Muscarinic

Excitatory
Often present on presynaptic terminals to enhance release of other neurotransmitters

17
Q

Describe cholinergic pathways in the CNS

A

Neurones originate in basal forebrain (nucleus basalis) and brainstem.
They give diffuse projections to many parts of the cortex and hippocampus (via the septohippocampal pathway).
There are also local cholinergic inter neurones in the stratum corpus striatum.

18
Q

Degeneration of cholinergic neurones in the nucleus basalis is associated with what disease?

A

Alzheimer’s

19
Q

What is used to treat symptoms of Alzheimer’s?

A

Cholinesterase inhibitors

20
Q

What is the role of the cholinergic pathway in the CNS?

A

Arousal, learning, memory and motor control

21
Q

Briefly describe the dopaminergic pathways in the CNS

A

Mesocortical pathway- mood, arousal and reward
Mesolimbic pathway- mood, arousal and reward
Nigrostriatal pathway- motor control

22
Q

Briefly describe the conditions associated with dopamine dysfunction and their treatment

A

Parkinson’s disease- loss of dopaminergic neurones
-treated with levodopa
Schizophrenia- too much dopamine
-treated with antipsychotic drugs that act as antagonists at dopamine D2 receptors

23
Q

What is Carbidopa and what is it’s mechanism

A

Combined with levodopa.
Treatment of Parkinson’s disease.
Inhibits AADC, preventing conversion of LDOPA to dopamine.
It cannot cross the BBB.
So, more LDOPA crosses BBB and is converted to dopamine there

24
Q

What receptors does NA operate through?

A

G protein coupled alpha and beta adrenoreceptors (GPCRs)

25
Q

Where does NA come from in the CNS?

A

Locus coeruleus in the brain (inactive during sleep)

26
Q

What disorder may be associated with NA?

A

Depression may be a deficiency of NA

27
Q

Where is serotonin, 5-HT released from in the CNS?

A

Serotonergic neurones in the Raphe nuclei

28
Q

What disorders are associated serotonin? And how are they treated?

A

Depression and anxiety

SSRI (serotonin selective reuptake inhibitors)

29
Q

Briefly describe EPSP

A

Excitatory post synaptic potentials
Upon binding of a ligand to an ionotropic receptor, the influx of cations causes depolarisation in the postsynaptic terminal, this is an ESPS.
If an ESPS exceeds the threshold, an action potential is generated.

30
Q

Describe long term potentiation

referencing activity at glutaminergic synapses

A

AMPA and NMDA receptors present
AMPA activated by glutamate
AMPA causes initial depolarisation
NMDA activated by glutamate + cell depolarisation= Mg ion removal and Ca entry
This strong activation of the synapse releases a lot of glutamate, causing extra AMPA receptors to be added to the postsynaptic membrane. The synapse will then transmit AP more readily. This is called long term potentiation. It is regulated by long term depression.

31
Q

What is the function of serotonin

A

Involved in sleep, wakefulness and regulation of mood

Neuro (7 decks)

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