Skeletal muscle Flashcards
Structure
Large cells that extend the length of the muscle, with multiple nuclei.
Do not contain gap junctions like SM and CM.
Actin is connected to Z lines (like in CM)
Contraction mediated by troponin/tropomyosin complex.
Skeletal muscle contraction mechanism
an increase in IC Ca causes sliding of the actin and myosin filaments along the sacromere.
Contraction dependent upon Ca binding to troponin C. This causes troponin to conformationally change, moving tropomyosin further up the actin. This reveals the actin the tropomyosin was bound to, which is then bound to by myosin.
The force of the contraction is dependent on the frequency of AP stimulation.
Skeletal muscle innervation and motor units
somatic, para, and symp
Somatic acts on nAChRs, para acts on mAChRs, symp acts on a-ARs
A motor unit is a single myelinated axon that branches close to its target. It innervates several muscle fibres at the NMJ. All these fibres contract as one unit.
Neuromuscular blockers
Non-depolarising (e.g., atracurium, vecuronium), or depolarising (e.g., suxamethonium, decamethonium)
Non-depolarising are competitive nAChR antagonists. Can be reversed by AChEIs.
Depolarising are nAChR agonsits that causes inactivation of the nAChRs due to their long duration of action (much longer than endogenous ACh), leading to desensitisation. Will be initial twitches, but then will be neuromuscular blockade
Botox
Destroys SNARE protein, which is inolved in vesicular docking - necessary in ACh release.
Causes long term neuromuscular blockade. May be used for cervical dystonia (head/neck spasms), blepharospasm (eye spasms), or severe excessive sweating.
Myasthenia gravis pathology and treatments
Most common form is where autoimmune antibodies are produced for the nAChRs found at the NMJ, leading to muscle weakness and atrophy.
To treat, AChEI are used, e.g., neostigmine, pyridostigmine.
Short acting AChEIs are used to diagnose - will see instant increase in muscle strength (e.g., edrophonium)
