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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
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2
Q

Key features of neurons

A
  • Excitable cells responsibly for electric transmission
  • Heterogenous morphology
  • Non-dividing cell
  • Share common features
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3
Q

Cell body of neuron

A

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

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4
Q

Dendrites

A

Unmyelinated processes responsible for transmission of signals towards cell body

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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

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6
Q

Where does the axon originate from?

A

Soma at axon hillock

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7
Q

Unipolar

A

1 axonal projection from soma

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8
Q

Pseudounipolar

A

1 axonal projection from soma which bifurcates

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9
Q

Bipolar

A

2 axonal projections from soma

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10
Q

Multipolar

A

ultiple axonal projections from soma

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11
Q

Example of bipolar neurons

A

Olfactory, retinal neurons

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12
Q

Types of neuron morphology

A
  1. Pyramidal
  2. Purkinje
  3. Golgi
    [Last 2 seen in GABA neurons in cerebellum]
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13
Q

5 types of cells in the CNS

A

Neuron
Oligodendrocyte
Astrocyte
Microglia
Ependyma

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14
Q

Oligodendrocyte

A

Glial cell producing myelin for multiple axons

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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)

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16
Q

Microglia

A

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

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17
Q

Ependyma

A

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

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18
Q

Cells of the PNS

A

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

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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?

24
Q

Sequence of events causing an action potential

25
How is the Na+ and K+ imbalance caused by the AP rectified?
⭐ 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
How does the AP normally spread along an unmyelinated axon?
Cable transmission
27
What is **saltatory conduction**?
AP jumps between nodes
28
Myelin
Prevents AP spreading due to high resistance and low capacitance
29
Nodes of Ranvier
Small gaps of myelin intermittently along axon that can conduct AP (high conc of VGKCs and VGSCs)
30
What are the steps to neurotransmission?
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
Autocrine neurotransmission
NT binds to auto-receptors on presynaptic neuron
32
Paracrine transmission
NT binds to post-synaptic neuron
33
Types of synaptic organisation
- **Axodendritic** → presynaptic terminal and neuronal dendrite - **Axosomatic** → presynaptic terminal to neuronal soma - **Axoaxonic** → presynaptic terminal to neuronal axon
34
Key features of NMJ
- Specialised synapse → axon terminal to muscle membrane - Unidirectional chemical communication between peripheral nerve and muscle - Paracrine
35
Neurotransmission across NMJ
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
Describe the excitation-contraction coupling at the NMJ
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
Sarcoplasmic reticulum
**Location**: surrounds myofibrils (contractile units of muscle) **Function**: Ca2+ storage → Ca 2+ release following sarcolemma depolarisation **Effect**: Ca 2+ → myofibril contraction → muscle contraction
38
Disorders of the NMJ [3]
→ Botulism → Myasthenia Gravis → Lamber-Eaton myasthenic syndrome [LEMS]
39
What is botulism?
When botulinum toxins BTx **irreversibly** disrupt exocytosis of ACh containing vesicles from the presynaptic terminal
40
What are the effects of botulism?
→ Muscle paralysis [keeps muscles contracted] due to presynaptic blockade → Mainly ocular effects seen
41
What is Myasthenia Gravis?
Autoimmune disorder where antibodies are directed against neuromuscular nACh receptors
42
Effects of MG
→ Muscle weakness and fatiguability (becoming more pronounced with repetitive use) → Ptosis (eyelid drooping)
43
What is LEMS?
Autoimmune disorder where antibodies are directed against presynaptic VGCCS
44
Effects of LEMS
→ Reduced ACh reease from presynaptic terminal → Muscle weakness, autonomic dysfunction
45
How do you differentiate between botulism, MG and LEMS?
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)

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