Brainscape's Knowledge GenomeTM

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


See full index

Neurology (BRS) > Cells of NS and neuromuscular junction > Flashcards

Cells of NS and neuromuscular junction Flashcards

1
Q

Functions of neurons

A
  1. Excitability
  2. Conductivity
  3. Secretion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Key features of neurons

A
  • Excitable cells responsibly for electric transmission
  • Heterogenous morphology
  • Non-dividing cell
  • Share common features
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Cell body of neuron

A

Aka soma/perikaryon
- Contains nucleus, ribosomes and neurofilaments for structure and transport

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

Dendrites

A

Unmyelinated processes responsible for transmission of signals towards cell body

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

Axon

A

Elongated, usually myelinated process responsible for transmission of signals away from the cell body
- Branches off into collaterals
- Axon terminal interacts with next neuron at synapse

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

Where does the axon originate from?

A

Soma at axon hillock

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

Unipolar

A

1 axonal projection from soma

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

Pseudounipolar

A

1 axonal projection from soma which bifurcates

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

Bipolar

A

2 axonal projections from soma

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

Multipolar

A

ultiple axonal projections from soma

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

Example of bipolar neurons

A

Olfactory, retinal neurons

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

Types of neuron morphology

A
  1. Pyramidal
  2. Purkinje
  3. Golgi
    [Last 2 seen in GABA neurons in cerebellum]
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

5 types of cells in the CNS

A

Neuron
Oligodendrocyte
Astrocyte
Microglia
Ependyma

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

Oligodendrocyte

A

Glial cell producing myelin for multiple axons

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

Astrocyte

A

Most abundant type of cell in CNS
- Forms blood brain barrier (Structural)
- Production of neurotrophic factors (Cell repair)
- Reuptake of neurotransmitters (Homeostasis)

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

Microglia

A

Neuronal macrophages
- Tend to need to be activated
- Less static than astrocytes

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

Ependyma

A

Epithelial cells lining the ventricles and central canals, synthesis of CSF [ciliated columnar epithelium]

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

Cells of the PNS

A

Astrocytes
Microglia
Ependymal cells
Schwann cells (forms myelin sheath but one axon per cell)

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

4 key physiological ions involved in RMP

A

Potassium, sodium, chloride, calcium

20
Q

What are the relative ion concentrations like across the membrane?

A
  • Extracellular → Ca2+, Na+, Cl- (high)
  • Intracellular → K+ (high)
21
Q

What is RMP maintained by?

A
  1. Differential permeability of cell membrane to positively charged ions Na+ and K+
  2. Negatively charged intracellular proteins which the membrane is impermeable to
  3. Na⁺-K⁺ ATPase
    ↳ 3 Na⁺ moved out of the cell for every 2 K⁺ moved into the cell, which maintains RMP at equilibrium
22
Q

What is the RMP like for neuronal cells?

A
  • Negative charge inside compared to out
    Between -40 and -90mV
23
Q

At RMP, what is the status of the VGSCs and VGKCs?

A

Closed

24
Q

Sequence of events causing an action potential

A
25
Q

How is the Na+ and K+ imbalance caused by the AP rectified?

A

⭐ Na+-K+-ATPase
[3 Na+ out, 2 K+ in]

  1. Resting configuration - Na+ (from the inside of the cell) enters vestibule and is phosphorylated → ions are pumped through protein
  2. Active configuration - Na+ removed from cell → K+ enters the vestibule
  3. Pump returns to resting configuration → K+ is transported back into cell
26
Q

How does the AP normally spread along an unmyelinated axon?

A

Cable transmission

27
Q

What is saltatory conduction?

A

AP jumps between nodes

28
Q

Myelin

A

Prevents AP spreading due to high resistance and low capacitance

29
Q

Nodes of Ranvier

A

Small gaps of myelin intermittently along axon that can conduct AP (high conc of VGKCs and VGSCs)

30
Q

What are the steps to neurotransmission?

A
  1. Propagation of AP> Na+ influx → membrane depolarisation → AP moves along neurone> VGKC opening → K+ efflux → repolarisation
  2. NT release from vesicles> AP opens VG-Ca 2+ channels at presynaptic terminal> Ca 2+ influx → vesicle exocytosis
  3. Activation of post-synaptic receptors> NT binds to receptors on post-synaptic membrane> Receptors modulate post-synaptic activity
  4. NT reuptake> NT dissociated from receptor> Metabolised by enzymes in synaptic cleft> Recycled by transporter proteins
31
Q

Autocrine neurotransmission

A

NT binds to auto-receptors on presynaptic neuron

32
Q

Paracrine transmission

A

NT binds to post-synaptic neuron

33
Q

Types of synaptic organisation

A
  • Axodendritic → presynaptic terminal and neuronal dendrite
  • Axosomatic → presynaptic terminal to neuronal soma
  • Axoaxonic → presynaptic terminal to neuronal axon
34
Q

Key features of NMJ

A
  • Specialised synapse → axon terminal to muscle membrane
  • Unidirectional chemical communication between peripheral nerve and muscle
  • Paracrine
35
Q

Neurotransmission across NMJ

A
  1. Depolarisation from Na+ influx → Ca2+ influx into presynaptic terminal
  2. Exocytosis of vesicles containing ACh → release of ACh into synapse
  3. ACh binds to nicotinic ACh receptors (nAChR) on skeletal muscle → change in end-plate potential EPP
  4. Miniature EPP → quantal ACh release
36
Q

Describe the excitation-contraction coupling at the NMJ

A
  1. Graded depolarisation (when beyond threshold potential) of the sarcolemma triggers an AP
  2. AP in t-tubules triggers conformational change in VG-DHP receptors → opening of RyR Ca²⁺ channels on sarcoplasmic reticulum
  3. Ca²⁺ movement into cytoplasm → actin-myosin binding → muscle contraction
37
Q

Sarcoplasmic reticulum

A

Location: surrounds myofibrils (contractile units of muscle)
Function: Ca2+ storage → Ca 2+ release following sarcolemma depolarisation

Effect: Ca 2+ → myofibril contraction → muscle contraction

38
Q

Disorders of the NMJ [3]

A

→ Botulism
→ Myasthenia Gravis
→ Lamber-Eaton myasthenic syndrome [LEMS]

39
Q

What is botulism?

A

When botulinum toxins BTx irreversibly disrupt exocytosis of ACh containing vesicles from the presynaptic terminal

40
Q

What are the effects of botulism?

A

→ Muscle paralysis [keeps muscles contracted] due to presynaptic blockade
→ Mainly ocular effects seen

41
Q

What is Myasthenia Gravis?

A

Autoimmune disorder where antibodies are directed against neuromuscular nACh receptors

42
Q

Effects of MG

A

→ Muscle weakness and fatiguability (becoming more pronounced with repetitive use)
→ Ptosis (eyelid drooping)

43
Q

What is LEMS?

A

Autoimmune disorder where antibodies are directed against presynaptic VGCCS

44
Q

Effects of LEMS

A

→ Reduced ACh reease from presynaptic terminal
→ Muscle weakness, autonomic dysfunction

45
Q

How do you differentiate between botulism, MG and LEMS?

A
  1. Botulism and MG → ocular effects
  2. MG and LEMS → whole body
  3. Botulims → autonomic side effects e.g. reduction in heart rate and gastrointestinal effects
  4. Small cell lung cancer has a correlation with LEMS
  5. Further testing to identify antibodies present

Neurology (BRS) (12 decks)

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