Neurones and Glia Flashcards

1
Q

What are 4 functions of Glia?

A

Support neurones
Nourish neurones
Insulate neurones
Remove “waste”

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2
Q

Describe the 5 roles of astrocytes. (8)

A

Structural support
Help to form the BBB
Provide nutrition for neurones through storing glucose as glycogen and making 2 lactate, transferred to neurones through the glucose-lactate shuttle.
Uptake of neurotransmitters so the extracellular concentration is low to allow repolarisation of the post-synaptic dendrite.
Maintain low extracellular K+ through Na+/K+ ATPase, NKCC2 and passive K+ and Cl- channels.

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3
Q

Describe the functions of oligodendrocytes. (2)

A

Myelination of axons within the CNS. Myelinate portions of many axons.

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4
Q

Describe microglia (3)

A

Mesoderm derived (not ectoderm), activated by foreign material and differentiate into phagocytes. Main defence system of the brain.

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5
Q

Describe the immune privilege of the brain. (2)

A

Because the skull prevents the normal inflammatory response, T cells that are activated by microglia (acting as APCs) have their pro-inflammatory responses blocked.

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6
Q

Describe the process of neurotransmission. (8)

A

Depolarisation of the presynaptic terminal - VOCC open and calcium floods in - vesicles fuse with presynaptic membrane and release neurotransmitter - diffusion across cleft - binds to receptor on postsynaptic membrane - response here depends on nature of receptor (ligand gated or GOCR) and the neurotransmitter (inhibitory or excitatory).

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7
Q

List 3 amino acid neurotransmitters. (3)

A

Glutamate, glycine and GABA

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8
Q

List 3 biogenic amines that act as neurotransmitters. (3)

A

Dopamine, seratonin and noradrenaline.

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9
Q

Describe the classifications of glutamate receptors and their mechanisms of action. (7)

A

Ionotropic - AMPA (Na+/K+ channels), NMDA (Na+/K+/Ca2+ channels), Kainate (Na+/K+ channels)
Metabotropic - mGluR 1-7 - GPCRs that increase AMPA expression.

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10
Q

Describe how glutamate acts as an excitatory neurotransmitter. (7)

A

Glutamate acts on AMPA receptors, which cause cellular depolarisation, and NMDA receptors, which will only open to Ca2+ if the cell is depolarised, but cause the excitatory postsynaptic potential, which temporalily increases the resting membrane potential, making action potentials more likely.

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11
Q

Describe the different points of action for glycine and GABA. (2)

A

Glycine is inhibitory in the brain and spinal cord, GABA, is inhibitory in the brain only.

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12
Q

Describe how glycine and GABA act as inhibitory neurotransmitters. (5)

A

GABAa and glycine receptors have integral Cl- channels which cause hyperpolarisation of the membrane causing an inhibitory postsynaptic potential which lowers the rest in membrane potential and results in decreased action potential firing.

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13
Q

Describe the mechanism of action of barbiturates. (2)

Describe why they are not commonly used anymore. (2)

A

Bind to GABAa receptors and enhance the response to GABA so less action potentials fire. They have been used (in the past) as anti-convulsants, but have very strong addictive traits and withdrawal.

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14
Q

Give an example of the interplay between excitatory and inhibitory synapses. (8)

A

The L3 knee jerk reflex.
Sensory fibres detect stimulation of the patellar tendon and send impulses to L3.
A glutamatergic excitatory synapse prompts the motor fibres of the quads to contract.
A glycinergic inhibitory synapse (between an intermediate neurone and the motor neurone) prompts the motor fibres of the hamstrings to relax.
This makes the leg straighten.

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15
Q

Describe which synapses in the body Acetyl Choline is the neurotransmitter. (6)

A

In the PNS it is active in all neuromuscular junctions, all ANS ganglionic synapses, and parasympathetic post-ganglionic synapses.
Also has actions in the CNS acting at nicotininc and muscarinic receptors in the brain.
Receptors for ACh are often present on the presynaptic membrane of glutamatergic synapses to enhance glutamate release.

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16
Q

Describe why cholineesterase inhibitors can be a useful treatment in Alzheimer’s Disease. (2)

A

Degeneration of cholinergic neurones in the basal nucleus is associated with Alzheimer’s, so cholineesterase inhibitors can be useful to alleviate symptoms.

17
Q

Describe the dompamergic pathways in the brain and their functions. (4)

A

Mesocortical and mesolimbic - mood, arousal and reward
Nigrostriatal - motor
Tubero-hypophyseal - prolactin release.

18
Q

Describe the disease associated with the loss of dopamine pathways in the brain. Describe the treatment of this disease. (5)

A

Parkinson’s Disease is associated with the loss of nigrostriatal pathways in the brain, so motor control is reduced. It is treated with levodopa (or L-DOPA) which can cross the BBB unlike dopamine itself. It is metabolised to dopamine within the brain by DOPA decarboxylase.

19
Q

Describe the disease associated with too much dopamine in the brain, give one endogenous cause of these symptoms without the disease process and describe the treatments for the disease. (3)

A

Schizophrenia is associated with the release of too much dopamine in the brain, so can be treated with D2 receptor antagonists.
Amphetamines release dopamine and noradrenaline, meaning their use can prompt schizophrenic-like symptoms.

20
Q

Describe the actions of noradrenaline in the PNS. (2)

A

Noradrenaline acts in the PNS through GPCRs alpha and beta adrenoceptors. It is the post-ganglionic synapse neurotransmitter in the sympathetic NS.

21
Q

Describe the distribution and functions of noradrenaline in the brain. (4)

A

Fibres distributes widely through the hypothalamus, amygdala, cerebrum and cerebellum.
It is produced by the locus coeruleus (located in the pons) and contributes to wakefulness and mood.

22
Q

Describe the distribution and function of seratonin in the brain. (4)

A

Fibres distributes widely through the hypothalamus, amygdala, cerebrum and cerebellum.
It is produced by the Raphe nucleus in the brainstem, and contributes to wakefulness and mood.