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Excitable Cells > Neuropathologies > Flashcards

Neuropathologies Flashcards

1
Q

What is a synaptopathy?

A

brain disorders that have arisen from synaptic function

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2
Q

How does a synapse work?

A
  1. Action potential arrives
  2. Opening of voltage-gated calcium channels
  3. Vesicle fusion
  4. Neurotransmitter release
  5. Postsynaptic events
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3
Q

What are the different synaptopathy mechanisms?

A

a) Alterations in neurotransmitter synthesis or release
b) Alterations in pre-synaptic vesicle machinery
c) Alterations in signalling, expression and function of postsynaptic neurotransmitter receptors

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4
Q

What forms synapses with other neurones?

A

Dendritic spines

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5
Q

What can long term potentiation and depression lead to in terms of dendritic spines?

A
  • Long term potentiation (LTP) can lead to increased spine size
  • Long term depression (LTD) can lead to decreased spine size
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6
Q

What does spine size correlate with and what is it linked to??

A

Spine size correlates with postsynaptic density, number of glutamate receptors and synaptic strength, and is linked to synaptic plasticity, learning and memory

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7
Q

What dendritic spine morphological changes do you see with cocaine addiction and Alzheimer’s disease?

A
  • Cocaine addiction: bigger, mature spines

- Alzheimer’s disease/ mental retardation: thinner, immature spines

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8
Q

What do synaptopathies result from?

A
  • Genetics
  • Drug use
  • Ageing
  • Viral infections
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9
Q

What do synoptapathies lead to?

A
  • Abnormal density and morphology of dendritic spines
  • Aberrant synaptic signalling and plasticity
  • Synapse loss
  • Neuronal death
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10
Q

What is epilepsy characterised by and what increases the susceptibility of getting it?

A
  • Cause unknown
  • Affects around 50 million people worldwide
  • Characterised by the occurrence of epileptic seizures which are uncontrolled and excessive synchronised electrical activity of central neurons
  • Cause unknown but infection, stroke and traumatic brain injury increase the susceptibility of developing epilepsy
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11
Q

What is the hypothesis about epilepsy?

A
  • Thought to be caused by an imbalance of excitatory and inhibitory circuits
  • Glutamatergic neurotransmission is enhanced, while GABA release is decreased
  • So overall increase in excitatory neurotransmission
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12
Q

What are current treatments for Epilepsy?

A
  • Current treatment includes anti-convulsant and anti-epileptics
  • Levetiracetam reduces neurotransmitter release at glutamatergic synapses
  • Valproate increases amount of inhibitory GABA
  • Phenytoin prolongs inactivation of Na+ channels
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13
Q

In inherited epilepsy what can many of the genetic causes be traced to?

A

A mutation in an ion channel such as the GABAA receptor, voltage-gated potassium channels, voltage-gated sodium channels, chloride channels and neuronal nicotinic acetylcholine receptors

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14
Q

What are ion channels?

A

proteins that span across the cell membrane allowing passage of ions from one side of the membrane to the other

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15
Q

What do voltage gated channels and ligand gated channels open in response to?

A
  • Voltage gated channels: opens in response to change in the membrane potential
  • Ligand-gated channels: opens in response to a specific extracellular neurotransmitter
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16
Q

What do ions play critical roles in?

A

Controlling neuronal excitability

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17
Q

What are channelopathies and what can they lead to?

A
  • Channelopathies are a group of disorders resulting from the dysfunction of ion channels; usually from genetic or autoimmune origin
  • Channelopathies can lead to different types of epilepsy, migraine, ataxia an paralysis
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18
Q

What can abnormal K+ and Ca2+ channels in the brain lead to?

A

Abnormal K+ and Ca2+ channels in the brain -> repolarisation defects -> convulsions (epilepsy)

19
Q

What are GRIN2B mutations and what do they lead to?

A
  • Mutations in GRIN2B, the gene encoding NR2B, the beta-2 subunit of the NMDA receptor, which is a ligand-gated ion channel that binds to glutamate
  • Gain of function -> hyperexcitability -> seizures
  • Loss of function -> hypo excitability -> learning difficulties and neurodevelopmental problems (as there are not enough connections in the brain)
20
Q

What is Myotonia congenita?

A
  • The goats’ muscles are sometimes unable to relax after they’ve contracted, causing the goats to keel over
  • This is caused by a mutation in the skeletal muscle chloride channel, CLCN1 and can be triggered when the animals are startled or excited
21
Q

What is malignant hyperthermia and what does it cause?

A
  • Malignant hyperthermia is a condition that occurs in attacks, in response to specific triggers
  • It involves a state of hyperactivity in muscle cells due to excessive release of calcium from the sarcoplasmic reticulum. This causes the muscles to contract and become rigid and cause a high fever. It can also cause a very fast heart rate
  • If untreated it can cause rhabdomyolysis (muscle breakdown) and very high blood potassium levels which can be fatal.
22
Q

How do most people live with malignant hyperthermia, what are some of the triggers and what is it most commonly caused by?

A
  • Most people are able to lead a normal life if they avoid the triggers
  • One of the most common triggers is general anaesthesia but some people can also experience an attack if they become very hot due to exercise.
  • Malignant hyperthermia is most commonly caused by a mutation in the ryanodine receptor (a sarcoplasmic reticulum calcium channel)
23
Q

What are some pathological changes to astrocytes that take place after traumatic brain injury or a stroke?

A

Astrological reactivity: hypertrophy and proliferation (bigger and more of them) – neuroprotection

24
Q

What are some pathological changes that take place to astrocytes with Alzheimer’s disease, Huntington’s disease, schizophrenia and major depressive disorders?

A

Astrodegeneration: atrophy and functional aethenia – neurotoxicity

25
Q

What are the three functional states of microglia?

A
  1. Nurturer
  2. Sentinel
  3. Warrior
26
Q

What are Microglia in their nurturer state?

A
  • Highly ramified and evenly spaced
  • Maintain milleu homeostasis
  • Synaptic remodelling and migration
  • Removal of apoptotic neurones
27
Q

What are features of microglia in their sentient state

A
  • Abundant processes and in motion

- Surveillance and sensing

28
Q

What are features of microglia in their warrior state?

A
  • Stocky and less ramified; they accumulate

- Defence against infectious pathogens and injurious self-proteins

29
Q

What are effectors of microglia function associated with and how does this work?

A
  • Disease stimulus
     Tau (dementia)
     HTT (Huntington’s)
  • Proteins disrupts microglial housekeeping functions
  • Exaggerated proinflammatory response, Neurotoxicity, Neurodegeneration
30
Q

What is multiple sclerosis caused by?

A

A loss of myelin

31
Q

What does a loss of myelin in the brain and spinal cord lead to?

A

impairment of axonal conductance and nerve damage

32
Q

What are some symptoms of multiple sclerosis?

A
  • Limb
  • Numbness/weakness
  • Electric-shock sensations
  • Tremor
  • Vision problems
  • Fatigue, dizziness
  • There is no cure, but treatment can help manage symptoms
33
Q

In encephalitis and MS how is inflammation caused?

A
  • Demyelinating disease or encephalitis
  • Leukocyte invasion of CNS parenchyma
  • Cytokine production by lymphocytes and myeloid cells
  • Tissue damage
34
Q

How is inflammation triggered in neurodegenerative processes such as AD and PD?

A

triggered by CNS-resident cells

  • Homeostatic imbalance/ toxin protein aggregates
  • Activation of stromal cells and microglia
  • Cytokine
35
Q

What are neuroinflammation events?

A
  1. Increased production of cytokines and reactive oxygen species (ROS)
  2. Molecular rearrangement of postsynaptic glutamate receptors
  3. Impairment of hippocampal LTP
  4. Axonal and dendritic loss
36
Q

How are the endothelial cells that line the capillaries joined together in the brain?

A

joined together by tight junctions which restrict the movement of solutes and the migration of cells and pathogens into the brain.

37
Q

What are endothelial cells surrounded by in the brain and what is needed in order to move substances across the blood-brain barrier?

A

The endothelial cells are surrounded by pericytes and the astrocytic ‘feet’. These are projections of astrocytes that are associated with the capillaries. In order to move substances across the blood-brain barrier, active transport is needed

38
Q

Why is the blood brain barrier beneficial?

A

it protects the brain from infections that are happening in the periphery

39
Q

What is a problem with the blood bran barrier?

A

it excludes many drugs from the brain which can make it difficult to target brain disorders

40
Q

What is the main function of the blood brain barrier?

A

to separate the circulating blood and brain compartments and regulate blood-to-brain and brain-to-blood transport of solutes

41
Q

What does the delivery of blood through the blood brain barrier require?

A

 Healthy blood vessels
 Normal formation of blood vessels
 Adequate blood flow
 Recruitment of active transport systems (e.g. CMT or RMT)

42
Q

What does the breakdown of the blood brain barrier promote and why?

A

• Blood brain barrier breakdown promotes neurodegeneration

  • Increased vascular permeability
  • Toxic blood-derived molecules, cells and microbial agents enter brain
  • Inflammatory and immune responses
  • Neuronal injury, synaptic dysfunction, loss of neurons, loss of brain connectivity, neurodegeneration
43
Q

Why is delivery of drug to the brain impaired when the blood brain barrier breaks down?

A
  • Impaired solute transport
  • Diminished ISF (interstitial fluid) regional flow
  • Decreased function of active transport systems
  • Drugs can get trapped in enlarged perivascular spaces

Excitable Cells (22 decks)

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