Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Neuro > Neurotransmitters > Flashcards

Neurotransmitters Flashcards

1
Q

What are the three most abundant lipids found in myelin sheath?

A

Cholesterol, plasmalogen, galactosylcerebroside

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

Can myelin be synthesized without cholesterol?

A

No. Cholesterol makes up more than 40% of myelin’s lipids and is the rate-limiting step for myelin formation. (Myelin is 70% lipids : 30% protein)

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

Plasmalogen functions

A

Antioxidants, main phospholipid in myelin

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

Galactosylcerebroside functions

A

Extremely hydrophobic, acts as extracellular glue in myelin

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

What are the two main protein components of myelin?

A
  1. Proteolipid (PLP) in CNS or Protein zero (P0) in PNS
  2. Myelin basic protein (MBP)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Proteolipid (PLP) in CNS or Protein zero (P0) in PNS

A

Extracellular leaflet. Very hydrophobic protein that aids in myelin compaction

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

Myelin basic protein (MBP)

A

Helps to stabilize myelin from inside by binding to negative charges on both sides of it

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

Gangliosides in peripheral nerves

A

Primarily localized in outer leaflets of plasma membranes and involved in
1. cell-cell recognition
2. Adhesion
3. Signal transduction

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

Antibodies to ganglioside causes

A

Guillain-Barré syndrome

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

What are 4 causes of decreased reflexes?

A
  1. ALS: amyotrophic lateral sclerosis
  2. GBS: guillain barre
  3. CIDP: chronic inflammatory demyelinating polyneuropathy
  4. Hypothyroidism
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Name 4 main nutrients that are allowed transport across BBB

A
  1. GLUT1, GLUT3 transporters allow the brain to use Glucose as fuel.
  2. Monocarboxylic transporters e.g. lactate, pyruvate, acetate, ketone bodies
  3. Large neutral amino acids (LAT1) allow LNAAs e.g. Phe, Tyr, Trp, Leu, Ile, Val, Met, His
  4. Cationic amino acid transporter e.g. Lys, Arg, Ornithine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Why are small neutral amino acids sometimes transported out via the Alanine-preferring-system carrier?

A

They are used as neurotransmitters in the brain. Letting large amounts of them in will disrupt neural firing.

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

GLUT1 def syndrome

A

GLUT1 is used as glucose transporters in endothelial cells lining the BBB. Deficiency causes neonatal seizures within the first month of life, developmental delay, and complex motor disorder due to insufficient energy to the brain. Treatment is ketogenic diet

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

What is the hierarchy of nutrients the brain will use for energy?

A
  1. Glucose
  2. Ketone bodies during starvation, diabetes, or breastfed neonate
  3. Lactate during vigorous exercise
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

EATT

A

Excitatory amino acid transporters that take up Glutamate into astrocytes to turn them into glutamine before returning them to neurons.

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

Astrocytes will send … to neurons after using up glucose.

A

Lactate

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

Which enzyme’s activity in the glycolytic pathway is higher in neurons?

A

Pyruvate dehydrogenase: PDH, active TCA and Ox-Phos

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

How are small molecule neurotransmitters synthesized?

A

Enzymes are synthesized at the cell body, and the precursors are recycled near the presynaptic terminal from the synaptic cleft.

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

How are neuropeptides synthesized?

A

Propeptides and enzymes within vesicles are sent from the cell body. Enzymatic cleavage to transform them into smaller active peptide neurotransmitter is done nearer to the presynaptic terminal.

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

How is glutamate synthesized?

A
  1. Alpha-ketoglutarate (reduction via enz. GDH or transamination via GABA transaminase)
  2. ย่อยจาก glutamine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Excitotoxicity

A

Glutamate is unique in that when they act on neuronal
cell bodies they can produce so much calcium influx that neutrons die. Glutamate excitotoxicity occur when cellular energy reserve depleted e.g. failure of energy-dependent reuptake pumps in ischemic stroke. Excess glutamate in synaptic cleft & overstimulation of postsynaptic glutamate receptor lead to influx of lethal amount of Ca2+ into neurons.

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

GABA synthesis

A

Decarboxylation of glutamate using GAD (found exclusively in GABAergic neurons). GABA shunt describes the process of recycling GABA

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

GABA inactivation

A

Reuptake via GABA transporter (GAT)

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

Benzodiazepine

A

Sedative effect by increasing affinity of GABA to its receptor. Similar effect to alcohol.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Which neurotransmitters synthesis requires vitamin B12?

A

vitamin B12 requirement for choline synthesis may contribute to the neurologic symptoms of vitamin B12 deficiency.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Ach inactivation

A

Acetylcholine esterase (ACE)

27
Q

Hemicholinium

A

Choline, Ach substrate, is actively transported into presynaptic nerve terminal by Na- choline transporter (CHT), which can be blocked by the drug hemicholinium.

28
Q

Vesamicol

A

Blocks VAT from transporting Ach into vesicles

29
Q

Nicotinic receptors are …

A

Ionotropic

30
Q

Muscarinic receptors are…

A

Metabotropic

31
Q

What is the special feature of generalized muscle weakness in NMJ patients?

A

Muscle weakness begins in smaller muscles, thus the first symptom is often droopy eyelids (ptosis).

32
Q

Alpha neurotoxin e.g. cobra, banded krait

A

They bind to nAChR, preventing Ach from binding to it.

33
Q

Curare

A

Blocks NMJ, causing gradual total paralysis including respiratory.

34
Q

Non-depolarizing neuromuscular blocking agents (NMBAs)

A

-curium, -curonium (same mechanism as curare)
prevents Ach from binding to nAchR

35
Q

depolarizing neuromuscular blocking agents (NMBAs) e.g. succinylcholine

A

Causes continuous depolarization, until the gates are maintained in inactivation state.
This is called the DEPOLARIZATION BLOCK.

36
Q

What is the clinical difference in depolarizing neuromuscular blocking agents (NMBAs) and non-depolarizing neuromuscular blocking agents (NMBAs)?

A

depolarizing neuromuscular blocking agents (NMBAs) will also have muscle fasciculations

37
Q

What is the classical presentation of MG?

A

Decremental response on repetitive nerve stimulus (RNS).

38
Q

Common underlying causes behind MG

A

Thymoma, thyroid diseases produce AchR Ab which bind to and cause nAchR dysfunction.

39
Q

How can we test for MG without tools?

A

Asking the patient to look up continuously will cause the patient’s eyelids to droop further.

40
Q

Pyridostigmine

A

Acetylcholinesterase inhibitor

41
Q

Ice pack test

A

Diagnostic test for MG

42
Q

Abdominal pain, profound sweating, diarrhea, excessive salivation, lacrimation, urinary incontinence and generalized weakness. Further examination will also show …

A

Bradycardia, bilateral miosis, hyperactive bowel sound, and muscle fasciculation.
The patient likely has an excess of Ach inhibitor or ingested insecticide.

43
Q

Organophosphate

A

Binds to and inactivates AchE
Symptoms: SLUDGE - M (muscarinic effect of nAchR)
Salivation
Lacrimation
Urinary incontinance
Diarrhea
Gastric pain
Emesis
Miosis
Nicotinic effect: muscle fasciculation and weakness

44
Q

Nerve gas Sarin

A

organophosphorus compounds

45
Q

Alzheimer’s disease

A

Basal forebrain and brainstem cholinergic system atrophy. Symptomatic relief can be given using AchE inhibitors e.g. Rivastigmine, Donepezil, Galantamine. The effect is not sustained.

46
Q

catecholamines

A

Dopamine, NorE, E

47
Q

Catecholamine precursor

A

Tyrosine, can be synthesized from Phe in the liver

48
Q

What vitamin is needed to synthesize Dopamine?

A

Vitamin B6

49
Q

What vitamin is needed to turn NorE into E?

A

SAM B12, folate

50
Q

Inactivation of Catecholamine

A

MAO (monoamine oxidase) more abundant in neuron
COMT (Catechol-O-methyltransferase) more abundant outside of NS

51
Q

What is the endproduct of dopamine?

A

Homovanillic acid (HVA)

52
Q

What is the endproduct of NE?

A

Vanillylmadelic acid (VMA)

53
Q

Serotonin (5-HT) precursor

A

Tryptophan via LNAT

54
Q

Serotonin inactivation

A

MAO

55
Q

Dopaminergic projections

A
  1. Nigrostriatal pathway
  2. Mesolimbic & mesocortical pathway
  3. Tuberoinfundibular pathway
56
Q

Nigrostriatal pathway

A

Initiates & maintains Motor behaviors: from substantia nigra to caudate and putamen

57
Q

Mesolimbic and mesocortical pathway

A

From ventral tegmentum to amygdala, hippocampus, nucleus accumbens, septal area, and frontal cortex.
Initiates & maintains Goal-directed and reward-mediated behaviors

58
Q

D1 receptor

A

Increased cAMP, stimulation of postsynaptic cell
D2 cell is the opposite effect

59
Q

Carbidopa, Benserazide

A

Prevents levodopa from being synthesized into dopamine outside of the brain. Cannot follow into the brain.

60
Q

How do anticholinergics (muscarinic receptor antagonists) relieve parkinsonism?

A

Dopamine is normally inhibitory towards Ach release, which results in smooth motor behavior. Anticholinergics helped relieve symptoms by preventing this excess of Ach from binding to mAchR.

61
Q

Schizophrenia cause

A

Excessive dopamine in mesolimbic pathway. This causes hallucinations, delusions, and disorganized thought.

62
Q

Antipsychotic drug mechanism

A

D2 antagonist in mesolimbic pathway.
This has the adverse effect of “Drug-induced parkinsonism”, which is why anticholinergics is often given in tandem to reduce these side effects.

63
Q

Noradrenergic projections

A

Locus ceruleus:
Attention, Arousal, Vigilence
Pain modulation

64
Q

Cheese reaction

A

Tyramine is normally degraded by MAO. Patients on MAO inhibitors, e.g. selegiline, rasagiline, cannot eat cheese because they will cause catecholamines to leak into the circulation and cause extensive symp activation and potential death.

Neuro (18 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions