Histology Flashcards
How many nerves is each fibre of skeletal muscle innervated by?
1,however one neuron innervates multiple muscle fibres (motor unit)
What structures helps with proprioception (length and tension)
Muscle spindles and golgi tendon organs
What does the basal ganglia help with?
Maintaining tone and posture
What are primary muscle diseases called?
Myopathies
Why does muscle have to be fresh-frozen not fixed with aldehyde?
So enzymes are active (need to thaw so reactions occur again and can see the products of reaction via dyes) - oxidative enzyme activity
What are the 2 broad types of muscle fibres?
Slow twitch (type 1, oxidative, fatigue resistant - stain red)
Fast twitch (fatigue rapidly. 2 A = glycolytic and oxidative 2B = relies on glycolysis - stain white)
Motor unit
A lower motor neuron and the fibres it innervates. All fibres innervated by this neuron will be either fast or slow twitch.
Size of motor unit varies between muscles - smaller units when more dexterity and co-ordination is needed. eg many small motor units in hand.
Denervation and Reinnervation
Loss of innervation causes fibre atrophy.
Adjacent motor units will attend to reinnervate the fibres by collateral sprouting.
This creates larger motor unit and fibres may switch to become other type of fibre (eg fast becomes slow twitch fibre)
Basic unit of contraction is called a
Sarcomere
Sarcomere consists of
Thick (myosin) and thin (actin) filaments.
Actin attached to z disc (edges of sarcomere), myosin in middle of sarcomere in A-band, darker. Where only actin is lighter in I-band.
Several proteins at the z-line (a-actinin, titin, nebulin, desmin)
Sliding filament theory
Energy required from hydrolysis ATP to ADP for movement of myosin head
Power stroked releases ADP.
Shortening due to filaments sliding, not actin or myosin changing length.
Initiated by increased cytosolic Ca2+
How can you test for muscle damage?
When muscle fibres damaged, creatine kinase is released. Increased levels of CK = damage
What does creatine kinase (CK) help do?
Replenish creatine phosphate, a short term energy store.
Where do you get all your mitochondrial DNA from?
Mother
What is heteroplasmy?
Different organs and cells contain different amounts of the mutated DNA in their mitochondria.
Genetic dysfunction of mitochondria
Complex 4 produces brown staining which obscures the complex 2 staining.
Diagnostic marker of mitochondrial pathology.
Mechanism to deal with strain on cell membrane in sarcomere
extracellular protein joins to intracellular membrane l(inked to sarcoglycans), inside of membrane protein called dystophin joins it all to actin.
Dystrophin
Links actin to transmembrane complex for stability.
Is x-linked as gene for it is on Xp21.
Mutations can cause the protein not to be formed or to be too short.
Women can carry disease. Few women, may manifest disease due to lyonization.
Neuromuscular transmission
Nerve impulse down axon, causes pre-synaptic vesicle containing ACh to be released into cleft.
ACh bind to receptor.
Cation entry results in depolarisation, endplate potential.
An action potential travels across muscle cell membrane into T-tubule system.
Calcium released from sarcoplasmic reticulum leading to activation of contraction.
Disorders of neuromuscular transmission
Not enough ACh receptors due to anti-AChR antibodies, causes variable weakness, fast to fatigue = Myasthenia gravis.
Acetyl cholinesterase inhibitors can improve muscle function
Myelinated sheath
Schwann cells responsible for myelin sheath (insulator) in PNS.
One cell responsible for one segment of myelin.
Nodes of Ranvier lie between myelin segments, where depolarisation of membrane occurs. Conduction much faster as skips over the insulating myelin sheath.
Myelination allows saltatory conduction.
Types of peripheral neuropathies
Neuronopathies = damage to motor or sensory neurons
Axonopathies = damage to axons
Demyelination = selective damage to myelin sheaths
Axonal degeneration / regeneration
Injury to axon, globules of myelin and axon debris form, initially within Schwann cell.
Axonal sprouts form from proximal part of damaged axon and grow along columns of proliferating Schwann cells.
Regenerated axons can remyelinate.
Demyelination
Injury to Schwann cell in PNS. Remyelination results in thinner sheath. Slower conduction.
