-muscle is an excitable tissue
-types:-1)skeletal,cardiac,smooth
cardiac-:
wall of heart
involuntary muscle
branching shows intercalated disc
self excitability
refractive period longer,doest get fatigue
skeletal:-
attached to bone
voluntary
no braching.
fatigueness
smooth:-
wall of hollow organs ,GIT,urinary bladder.
involuntary.
no branching.
self excitatory
refractive period moderatly longer.
motor unit :-single motor neuron innervating skeletal muscle is known as motor unit.
neuro muscular junction:it is the junction between motor of neuron and muscle fiber ,it is also called as myoneural junction.
Structure of NMJ:-
1)prejunctional membrane -axon terminal of motor neuron forms the pre junctional membrane,where it fix into the depressionin the sacrolemma called asterminal butter
-mylin is disappears at the junction
-contains vescles with neuro transmitter ACH
-contains mitochondria.
-synaptic cleft:-gap between pre and post junction membrane ,it is is about 20-30nm.,structuraly discontinues but functionaly it is continues.
acytyl choline esterase prensent in rim of junction fold
Events during transmission of impulse:-
-arrival of action potential at mitochondria at motor neuron.
-the prejunctional membrane becomes permeable to CA++
-Vesicles move toward prejunction membrane and they break and release neurotransmitter
-ACH travels to cleft and attaches to recepter in post junctional membrane.
-post junctional membrane permeable to sodium.
-there for sacrolemma depolarized action potential is developed
-spreads through sacrolemma through T-tubule cuases muscle contraction.
-end plate potential is developed.
-even at rest some amount of neurotransmitter are release and potential developed is called as miniature end plate potential(maintain rigidity of mucle)
-ACH cant remain at prolonged in cleft acetyl choline esterase enzyme breaks in to acetyl co-enzyme and choline
-acetylcoA+ choline----choline acetyl transferace
NMJ blockers;_
these are the substance which blocks the transmission of impulses from motor neuron to the skeletal muscle.
classification:-
1)prejunctional blockers:-inhibits release ACH eg:botulinum toxin
inhibit actin of ACH eg:tetanin toxin
2)post synaptic blockers :-competitive blockers eg:succinyl choline
Myasthemia gravis:-
NMJ disorder.
-auto immune disorder
-cuase-antibodies are produced against the recepter,it will destroy the recepter,
symptom :-
-depolirization will be weak cause weakness muscle
-fatigue
-extraoccular muscle is affected -drooping of eyelid
-masticatory deglutition muscles are affected.
-expression on face -facial muscles are affected.
-respiratory muscles affected
-enlargement of thymus due to production antibodies
treatment:-removal of thymus ,physostigmine/neostigmine-inhibit action of esterase.
muscle contraction:-(10 mark)
-muscle fibers -myo fibrils -myofilament-thick-myosin
-thin-actin,troponin,tropomyosin
sacromere:-
-structural and functional unit of mucle fiber
-its interval between two z lines
it consist of full A band and half I band on either side.
contraction :-
Z lines come nearer
-h zone disappear -m line
-width of A remains same
-width of I reduce
muscle protein :-
1myosin:-
2)actin-
3)troponin-I-inhibits action between myosin head and actin
- C-ca+ binding
-T -
4)tropomyosin filament cover active site of actin molecule
sacrotubular system:-
function-
T tubule transmits the impulse
L tubule release calcium attach the troponin c and there fore initiate muscle contraction.
Excitation contraction coupling:-
-muscles get excited and gets contracted and it is coupled by calcium ion
-from the motor neuron through NMJ impulse is conveyed in the the muscle ,which cause muscle is conveyed in the muscle ,which cause muscle contaction-which is a mechanical event
-maximum shortening of muscle-30%
6mm length muscle is contracted to 4mm
steps:-
1)arrival of action potential at NMJ.
2)release of ACH
3)action potential is conveyed to endplate to end plate and throughout the T tubule
4)release of calcium from L tubule system and it attaches the troponin C
5)tropomyosin slips and exposes active site in actin molecules.
6)myosin and actin complex formed.
7)actin molecule pulled toward center cause shorteneing
8)muscle contraction
relaxation :-calcium puped back to cisternae of Ltubule
-cross bridge breaks between actin and myosin
-dissociation of actin -myosin complex
-muscle complex
Energy source :-
1)ATP
2)creatinine phosphate ----ADP---ATP------creatinine
3Stored glycogen undergoes beta oxidation
Molecular basis of muscle contraction:-
1)cross bridge formation
-orientation of myosin filament head in one half of the thick filament fist opposite to other half
-there fore this filament can be pulled to the center from either side cuasing shortening of muscle .
-cross bridge between myosin head and actin molecules remains until one more molecule of atp fits in cleft of myosin head.
2)
Rigour mortis :-
stiffening of muscle (irreversible)after death.
-cuase exhaution of ATP therefore calcium cant come back to L tubule.
-the crossbridge between actin and myosin will not be broken since calcium still attached to to trponin C.
significance:-
-after 2h of death rigormortis occurs after 24 hrs decompositiojn occurs
-by looking at the condition we can determine the time of death.
types of muscle contraction:-
1)isotonic-tension remains same
-muscle sortens
eg:lifting of object.
2)isometric :-
tension increases
no lengthening or shortening of muscle
length of muscle remain same
-no work is done
eg:pushing the wall.
credits:therapist@physiotherapycls.com
-types:-1)skeletal,cardiac,smooth
cardiac-:
wall of heart
involuntary muscle
branching shows intercalated disc
self excitability
refractive period longer,doest get fatigue
skeletal:-
attached to bone
voluntary
no braching.
fatigueness
smooth:-
wall of hollow organs ,GIT,urinary bladder.
involuntary.
no branching.
self excitatory
refractive period moderatly longer.
motor unit :-single motor neuron innervating skeletal muscle is known as motor unit.
neuro muscular junction:it is the junction between motor of neuron and muscle fiber ,it is also called as myoneural junction.
Structure of NMJ:-
1)prejunctional membrane -axon terminal of motor neuron forms the pre junctional membrane,where it fix into the depressionin the sacrolemma called asterminal butter
-mylin is disappears at the junction
-contains vescles with neuro transmitter ACH
-contains mitochondria.
-synaptic cleft:-gap between pre and post junction membrane ,it is is about 20-30nm.,structuraly discontinues but functionaly it is continues.
acytyl choline esterase prensent in rim of junction fold
Events during transmission of impulse:-
-arrival of action potential at mitochondria at motor neuron.
-the prejunctional membrane becomes permeable to CA++
-Vesicles move toward prejunction membrane and they break and release neurotransmitter
-ACH travels to cleft and attaches to recepter in post junctional membrane.
-post junctional membrane permeable to sodium.
-there for sacrolemma depolarized action potential is developed
-spreads through sacrolemma through T-tubule cuases muscle contraction.
-end plate potential is developed.
-even at rest some amount of neurotransmitter are release and potential developed is called as miniature end plate potential(maintain rigidity of mucle)
-ACH cant remain at prolonged in cleft acetyl choline esterase enzyme breaks in to acetyl co-enzyme and choline
-acetylcoA+ choline----choline acetyl transferace
NMJ blockers;_
these are the substance which blocks the transmission of impulses from motor neuron to the skeletal muscle.
classification:-
1)prejunctional blockers:-inhibits release ACH eg:botulinum toxin
inhibit actin of ACH eg:tetanin toxin
2)post synaptic blockers :-competitive blockers eg:succinyl choline
Myasthemia gravis:-
NMJ disorder.
-auto immune disorder
-cuase-antibodies are produced against the recepter,it will destroy the recepter,
symptom :-
-depolirization will be weak cause weakness muscle
-fatigue
-extraoccular muscle is affected -drooping of eyelid
-masticatory deglutition muscles are affected.
-expression on face -facial muscles are affected.
-respiratory muscles affected
-enlargement of thymus due to production antibodies
treatment:-removal of thymus ,physostigmine/neostigmine-inhibit action of esterase.
muscle contraction:-(10 mark)
-muscle fibers -myo fibrils -myofilament-thick-myosin
-thin-actin,troponin,tropomyosin
sacromere:-
-its interval between two z lines
it consist of full A band and half I band on either side.
contraction :-
Z lines come nearer
-h zone disappear -m line
-width of A remains same
-width of I reduce
muscle protein :-
1myosin:-
2)actin-
3)troponin-I-inhibits action between myosin head and actin
- C-ca+ binding
-T -
4)tropomyosin filament cover active site of actin molecule
sacrotubular system:-
T tubule transmits the impulse
L tubule release calcium attach the troponin c and there fore initiate muscle contraction.
Excitation contraction coupling:-
-muscles get excited and gets contracted and it is coupled by calcium ion
-from the motor neuron through NMJ impulse is conveyed in the the muscle ,which cause muscle is conveyed in the muscle ,which cause muscle contaction-which is a mechanical event
-maximum shortening of muscle-30%
6mm length muscle is contracted to 4mm
steps:-
1)arrival of action potential at NMJ.
2)release of ACH
3)action potential is conveyed to endplate to end plate and throughout the T tubule
4)release of calcium from L tubule system and it attaches the troponin C
5)tropomyosin slips and exposes active site in actin molecules.
6)myosin and actin complex formed.
7)actin molecule pulled toward center cause shorteneing
8)muscle contraction
relaxation :-calcium puped back to cisternae of Ltubule
-cross bridge breaks between actin and myosin
-dissociation of actin -myosin complex
-muscle complex
Energy source :-
1)ATP
2)creatinine phosphate ----ADP---ATP------creatinine
3Stored glycogen undergoes beta oxidation
Molecular basis of muscle contraction:-
1)cross bridge formation
-orientation of myosin filament head in one half of the thick filament fist opposite to other half
-there fore this filament can be pulled to the center from either side cuasing shortening of muscle .
-cross bridge between myosin head and actin molecules remains until one more molecule of atp fits in cleft of myosin head.
2)
Rigour mortis :-
stiffening of muscle (irreversible)after death.
-cuase exhaution of ATP therefore calcium cant come back to L tubule.
-the crossbridge between actin and myosin will not be broken since calcium still attached to to trponin C.
significance:-
-after 2h of death rigormortis occurs after 24 hrs decompositiojn occurs
-by looking at the condition we can determine the time of death.
types of muscle contraction:-
1)isotonic-tension remains same
-muscle sortens
eg:lifting of object.
2)isometric :-
tension increases
no lengthening or shortening of muscle
length of muscle remain same
-no work is done
eg:pushing the wall.
credits:therapist@physiotherapycls.com
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