Lecture 12 - Muscle tissue-Skeletal, cardiac and smooth muscle Flashcards
Three main types of muscle
skeletal, cardiac and smooth muscle
Skeletal muscle structure
Long, cylindrical, multinucleate cells, obvious striations
One skeletal muscle fibre is one skeletal muscle cell
Skeletal muscle function
voluntary movement, locomotion, manipulation of the environment, facial expression, voluntary control (also for posture and standing)
Skeletal muscle location
in skeletal muscles attached to bones or occasionally to skin (allows movement of the skeleton)
Gross anatomy of the skeletal muscle
Epimysium - Connective tissue sheathing the muscle
Endomysium - Protecting individual muscle fibers
Perimysium - Sheaths bundles of muscle fibers
Fascicles - Bundles of muscle fibers
Hundreds of myofibrils typically in one muscle fibre which contain contractile units known as myofilaments that are required for muscle contraction
________ of myofibrils typically in ______ muscle fibre which contain ….
Hundreds of myofibrils typically in one muscle fibre which contain contractile units known as myofilaments that are required for muscle contraction
Sarcolemma
Cell membrane of the muscle fibre
Transverse tubule (T-tubule)
invagination of the sarcolemma into the cell
Sarcoplasmic reticulum
similar to endoplasmic reticulum. store and release calcium
NMJ
NMJ - motor neuron connected to skeletal muscle fibre at the NMJ
Each skeletal muscle fibre is connected to a motor neuron
Motor neuron - 1 per fibre
Muscle myofibril
Sarcomere = area between 2 Z lines
Sarcomeres are repeated thousands of times
From Z line into the sarcomere are the thin filaments and from the M line to the outside of the sarcomere are the thick filaments sticking out
Sarcomeres
repeating unit in skeletal muscle
area between 2 Z lines
Sarcomeres are repeated thousands of times
Myofilament structure
Actin = Contain binding sites for thick filament Tropomyosin = Protein strand that covers binding sites in relaxed state Troponin = Sits on tropomyosin and responds to signals for contraction, responds to calcium Myosin = Main protein of thick filament, elongated with distinctive head, head binds and “walks” along thin filament in order to create a contraction
Actin
Contain binding sites for thick filament
Tropomyosin
Protein strand that covers binding sites in relaxed state
Troponin
Sits on tropomyosin and responds to signals for contraction, responds to calcium
Myosin
Main protein of thick filament, elongated with distinctive head, head binds and “walks” along thin filament in order to create a contraction
Sarcomere zones
I band = only thin filaments, fairly lucid on electron micrograph
A band = stretches to either side of the M line, overlap of thick and thin filaments
H-zone = only contains thick filament
I band
I band = only thin filaments, fairly lucid on electron micrograph
A band
A band = stretches to either side of the M line, overlap of thick and thin filaments
H zone
H-zone = only contains thick filament
Muscle fibre action potential
Action potential comes down motor neuron
Binds to receptors on the plasma membrane of the muscle cell and initiates an action potential in the muscle fibre
Action potential signal flows down into the T tubule
Sarcomere contraction
Binding sites of actin to myosin are covered by tropomyosin
Binding of Ca2+ to troponin causes movement of tropomyosin, exposing binding sites
Myosin (thick filament) binds to actin (thin filament)
Myosin head changes shape and pulls thin filament to centre of sarcomere
ATP binds to myosin, and energy is utilized to detach myosin, reverting shape (ATP is hydrolysed to ADP and Pi)
Myosin head binds to another actin molecule further towards the Z-line
Note = ATP is not actually utilised by the initial pathway of muscle contractions but it is actually used to release the head of myosin and relax the muscle
Pull thin filament into the centre of the sarcomere with the power stroke
4 steps of cross bridge cycling
binding
power stroke
detachment
binding
binding of ATP to myosin
Resting myosin fibril with ADP and Pi bound to head
Action potential arrives at NMJ making free calcium available
Myosin head binds to actin
Power stroke: ADP released; myosin head changes position; filaments slide past one another
ATP binds to myosin causing it to release actin
ATP is split and myosin heads return to resting postion
What happens to sarcomere zones during contraction?
I band gets smaller
A band stays the same because the thick filament has not changed in length
H zone gets smaller
What happens to the distance between Z lines? Come closer together
Key point summary of the molecular basis of muscle contraction
The Ca2+ released from the sarcoplasmic reticulum when the muscle fibre is excited binds to the protein troponin
This binding enables the troponin protein complex to “pull tropomyosin aside” so that it no longer covers the active sites on actin
The heads of myosin molecules bind to the now-exposed active sites on actin
Swing movement of myosin head pulls thin filament inwards
Head is detached and shape reverted if bound to ATP
Clinical perspective - rigor mortis
Rigor mortis, begins about 3 hours after death and becomes maximal in about 12 hours. Within a few days, rigor mortis diminishes as muscle proteins break down.
Ca2+ leaks from sarcoplasmic reticulum into muscle fibres following death, exposing actin binding sites.
Myosin automatically binds and pulls thin filament (no ATP required)
New molecules of ATP needed for the unbinding of myosin and actin are not produced.
Thus, myosin remains attached to actin, and the contracted muscles do not relax.
Nemaline myopathy
Disease of skeletal muscle
1:50,000 births
Severity varies from neonatal lethal to low end of normal strength spectrum
Muscle weakness, swallowing dysfunction, impaired speech
Mutations in at least 10 different genes
-NEB (~50% of cases) – Nebulin – governs length of thin filament
-ACTA1 (15-25% of cases) – Actin isoform making up thin filament
Typically these mutations are in genes that make up the sarcomere proteins and in particular the thin filaments which connect into the Z line
Cardiac muscle
Continuous rhythmic activity
Develops early on in embryonic development
Inherent mechanisms of activation that can be modulated by external autonomic and hormonal stimuli
Need heart muscles to be beating all the time but we also need to be able to vary the rate of our heart beats in response to things like exercise therefore have various different factors that can influence the beating of the heart
Structurally intermediate to skeletal and smooth muscle
Description of cardiac muscle structure
branching, striated, generally uninucleate cells that interdigitate at specialised junctions (intercalated discs)
Branching shape and has striations made from the overlaps of the thin and thick filaments
Generally have one nucleus
Lots of capillaries in the cardiac muscle structure because it is quite an energy demanding structure
Function of cardiac muscle
as it contracts it propels blood into the circulation, involuntary control
Location of cardiac muscle
The walls of the heart
Intercalated discs
Cardiac muscle consists of individual heart muscle cells (cardiomyocytes) connected by intercalated discs to work as a single functional organ. They play vital roles in bonding cardiac muscle cells together and in transmitting signals between cells.
3 intercellular junctions that make up ICDs = desmosomes, fascia adherens, gap junctions (dont ggive a fuck - way to remember)
Desmosomes - anchor cells to each other via the cytoskeleton
Fascia - anchor actin filaments and transmit contractile forces (acts effectively as the Z line within our cardiac muscle cells, this junction is found uniquely in cardiac muscle) (physical propagation of contraction from one cell to another)
Communication or gap junctions - transmit contraction stimulus
Three intercellular junctions that make up an ICD
desmosomes, fascia adherens, gap junctions
Arrhythmogenic right ventricular cardiomyopathy – a disease of
desmosomes
Arrhythmogenic right ventricular cardiomyopathy
Prevalence of 1:5000
Cardiac muscles die and are replaced by fatty infiltration (can also get fibrosis)
Irregular heart beat - arrhythmia
Leads to heart attacks in otherwise healthy individuals
Genes for desmosome proteins explains prevalence
Fewer desmosomes, those that are present fragmented, different lengths
Problems caused by intracellular gap widening and disruption
Get ICDs widening and this itself causes widening of the gap junctions therefore cannot get signals moving between cells effectively which can lead to cell death and also the arythmogenic phenotype where the heart does not beat rhythmically
Cell death
Widening of gap junction may contribute to arrhythmogenicity.
Smooth muscle
Muscular component of visceral tissue e.g. blood vessels, gastrointestinal tract, uterus, bladder.
Under inherent autonomic and hormonal control i.e. involuntary.
Continuous contractions of slow force
Often whole muscle contracting in a wave-like fashion
Wave like fashion of contraction which allows us to propel substances through these various different tubes
Smooth muscle structure description
Spindle-shaped cells with central nuclei, no striations, cells arranged closely to form sheets
One nucleus per cell
Cells arranged closely to form sheets which makes sense because they have to work together to produce a wave like motion to move substance
Smooth muscle function
propels substances or objects (foodstuffs, urine, a baby) along internal passageways, involuntary control
Smooth muscle location
mostly in the walls of hollow organs
Smooth muscle contraction
Contractile filaments criss-cross the cell
Anchored to cell at focal densities in cytoplasm and focal adhesion densities on cell membrane
No striation pattern which means we do not have a clear arrangement of thick and thin filaments laying on top of each other instead we still have contractile filaments on our smooth muscle cells but they effectively criss cross the cell fairly randomly and they anchor to cells at focal densities in the cytoplasm and focal adhesion densities on the cell membrane
This arrangement allows for the smooth muscle cell when it contracts to take on a globular shape
Focal densities are functionally and structurally similar to Z line
Actin filaments link to both sides of dense bodies
Myosin filaments partially overlap actin like in skeletal muscle
Intermediate filaments provide cytoskeletal structure between densities (non contractile and they stretch between the focal densities which help to make up the cytoskeleton of our smooth muscle cells)
Works on the sliding filament theory as skeletal muscle. Thin actin molecules slide over thick myosin molecules and the smooth muscle cell takes on a globular shape.
Smooth muscle - cotnractile filaments are anchored to cell at
focal densities in cytoplasm and focal adhesion densities on cell membrane
Is there a striation pattern in smooth muscle
No striation pattern which means we do not have a clear arrangement of thick and thin filaments laying on top of each other instead we still have contractile filaments on our smooth muscle cells but they effectively criss cross the cell fairly randomly and they anchor to cells at focal densities in the cytoplasm and focal adhesion densities on the cell membrane
striation pattern in skeletal and cardic
