Cells Of The Nervous System And Neuromuscular Junction

Question 1

What are neurons

Answer 1

Excitable cells of cns
Heterogenous morphology
Non dividing cells but there is evidence that neurones may divide in brain which is important for growth

Question 2

Abundant cell type in the CNS

Answer 2

Astrocyte
Are structural cells which contribute to blood brain barrier,synapses formation,neuronal maturation and plasticity ,cell repair

Question 3

Oligodendrocytes and schwann cells

Answer 3

Myelin producing cells
Oligodendrocytes work in the CNS and can myelinate a number of axons whereas shwann cells work in the PNS and only myelinate a single axon

Question 4

Microglial cells

Answer 4

Macrophage like cells of CNS that perform immune functions
Usually quiescent but can be activated

Question 5

Ependymal cell

Answer 5

Epithelial cells that regulate production of cerebrospinal fluid

Question 6

Resting membrane potential

Answer 6

Around -70mV

Question 7

What are the 4 major physiological ions and what are their concs out and in of cell?

Answer 7

Potassium (K+)- low extracellular

sodium (Na+)- high extracellular

chloride (Cl-)- high extracellular

calcium (Ca2+)- high conc grad for it (high extracellular and low intracellular)

Question 8

Neuronal action potentials

Answer 8

Voltage gated Na+ channels and voltage gated K+ channels are closed
When three is excitement membrane is depolarized and VGSCs open causing Na+ influx into cell

Question 9

Explain how the ions are involved in the restoration of the resting membrane potential?

Answer 9

Voltage gated potassium ion channels (VGKCs) opens at slower rate, leading to efflux of K+ from cell which repolarises the membrane

Question 10

How is imbalance of sodium and potassium ions restored

Answer 10

Thrhough Na+/k+ATPase pumps

1) In pump’s resting configuration → Na+ enters vestibule and upon phosphorylation they are transported through the protein → Na+ being actively pumped out of cell

2) In pump’s active configuration → Na+ removed from cell and K+ enters the vestibule
3Na+ pumped out and 2K+ enter cells

Question 11

Nodes of ranvier

Answer 11

Small gaps of myelin along axon

Question 12

Saltatory conduction

Answer 12

AP Juno’s between nodes to get to presynaptic terminal quicker
AP spread by cable transmission

Question 13

Myelin function

Answer 13

Prevents action potential from spreading as it has high resistance and low capacitance

Question 14

What 3 ways are synapses organized in

Answer 14

Axodendritic synoase-connection. Etween presynaltuc terminal and neuronal dendrite
Axosomatic-between presynaptic terminal and neuronal soma
Axoaxonic synapse-connection between presynaptic terminal to neuronal axon

Question 15

What happens when action potential reaches synapse

Answer 15

AP opens Ca2+ channels at presynaptic terminal
Ca2+ influx causes exocytosis of vesicles
Neurotransmitter released into synaptic cleft
Neurotransmitter binds to receptors on post synaptic membrane

Question 16

What enzyme breaks down NT

Answer 16

Cholinesterase

Question 17

How does an action potential travel across neuromuscular junction

Answer 17

Action potential propagated along axon (Na+ and K+) → Ca2+ entry at presynaptic terminal

Ca2+ entry → ACh release into synapse

ACh binds to nicotinic ACh receptors (nAChR) on skeletal muscle → change in end-plate potential (EPP)

AP travels through T-tubules that are continuous with sarcolemma & closely connected to sarcoplasmic reticulum

Question 18

Sarcoplasmic reticulum

Answer 18

Ca2+ storage → Ca2+ release following sarcolemma depolarisation

Ca2+ → myofibril contraction & muscle contraction

Question 19

What is Myasthenia Gravis (explain its pathophysiology) and what symptoms does it cause?

Answer 19

Autoimmune disorder: antibodies directed against ACh receptor

Causes fatigable weakness (becomes more pronounced with repetitive use)

Pronounced/severe facial weakness

The hallmark finding of myasthenia gravis is fatigable, painless muscle weakness that improved with rest

Primary treatment involves acetylcholinesterase inhibitors to increase ach at nmj

Question 20

• What is Lambert-Eaton myastenic syndrome (LEMS) (explain its pathophysiology) and what symptoms does it cause?

Answer 20

Autoimmune disorder: antibodies directed against Voltage-gated Calcium channels (VGCCs)

generalised fatigue and weakness which improves with activity

Question 21

What is Botulism (explain its pathophysiology) and what symptoms does it cause?

Answer 21

Botulinum toxin (BTx): irreversibly disrupts stimulation-induced ACh release from presynaptic nerve terminal

Difficulty swallowing.
Muscle weakness.
Double vision.
Drooping eyelids.
Blurry vision.
Slurred speech.
Difficulty breathing.

Question 22

What are the four different neuron morphologies

Answer 22

Unipolar-cell body with single axonal projection
Pseudounipolar-single body with single axonal projection that bifurcates into two different branches
Bipolar-single body with two projections one is the axon and the other is dendrite
Multipolar neurons-numerous projections from cell body 1 is axon rest are dendrites

Question 23

Astrocytes role

Answer 23

Provide structural support
Regulate Extracellular environment by controlling ion concentration
Promote synapse formation and contribute to blood brain barrier

Question 24

Glial cells

Answer 24

Support and protect neurones
Provide insulation and nutrients