NEURO-MUCULAR JUNCTION ECC

NEURO-MUCULAR JUNCTION : 

NEURO-MUCULAR JUNCTION

PowerPoint Presentation: 

acetate + choline Na + - - + + end-plate potential (EPP) ~ -15 mV ~ -15mV + + + + + – – – – – ~ +40mV

Events at Neuromuscular junction: 

Events at Neuromuscular junction

DRUGS ACTING ON NMJ: 

DRUGS ACTING ON NMJ DRUGS THAT INCREASE ACTIVITY OF NMJ Drugs with Ach-like action Eg : Nicotine, Methacholine & Carbachol Drugs that inactivate acetylcholinesterases Eg : Physostigmine , Neostigmine , Di-isopropyl fluorophosphate (DIF)

PowerPoint Presentation: 

DRUGS THAT BLOCK NMJ A) By inhibiting Ach release Eg: Botulinum toxin B) By antagonizing Ach action 1. By competitive inhibition Eg: Curariform drugs 2. By persistent depolarisation Eg: Succinylcholine

MYASTHENIA GRAVIS: 

MYASTHENIA GRAVIS Antibodies against Ach receptors at postsynaptic membrane. Reduced Ach binding Muscle strength de creases with prolonged /repeated contractions

PowerPoint Presentation: 

Myasthenia Gravis Muscle weakness- eye lid drooping is early sign Proximal muscle weakness Weakness at the end of day Later stages respiratory muscle weakness- death

LAMBERT-EATON SYNDROME: 

LAMBERT-EATON SYNDROME Antibodies against Voltage-gated Ca 2+ channels at end-feet Reduced Ach release Muscle strength increases with prolonged/repeated contractions

NEUROMUSCULAR JUNCTION: 

NEUROMUSCULAR JUNCTION STRUCTURE NEUROMUSCULAR TRANSMISSION (EPP) GENERATION OF ACTION POTENTIAL DRUGS ACTING ON NMJ MYASTHENIA GRAVIS AND LAMBERT- EATON SYNDROME NMJ IN CARDIAC AND SMOOTH MUSCLES

PowerPoint Presentation: 

NEUROMUSCULAR JUNCTION IN CARDIAC & SMOOTH MUSCLES

Synapse en passant: 

Synapse en passant N eurotransmitter Acetylcholine NorEpinephrine

Excitation – Contraction Coupling: 

Excitation – Contraction Coupling The sequence of events that convert the action potential in muscle cell membrane to actual contraction is known as excitation – contraction coupling.

PowerPoint Presentation: 

Arrival of nerve impulse at axon terminal of motor neuron Ca ++ entry & Acetylcholine released Acetylcholine binds to receptors on motor end plate ( EPP ) Action potential created in sarcolemma It travels down T-tubules & activate DHP receptors Ca ++ channels on sarcoplasmic reticulum open & Ca ++ released Ca ++ binds to troponin C; tropomyosin-troponin complex shifts to expose binding sites Energy from ATP activates and “cocks” myosin cross bridges Cross bridges attach to binding sites on actin molecules Power stroke ; thin actin “slide” over thick myosin Binding of new ATP, breaking cross bridge; repeat steps 9-10 Cessation of nerve impulse and ACh release at motor neuron Acetylcholinesterase breaks down ACh Ca ++ actively transported back into sarcoplasmic reticulum Loss of Ca ++ from sarcoplasm allows tropomyosin-troponin to block active sites on actin Thin myofilaments actin “slide” back into resting position

PowerPoint Presentation: 

Functions of ATP in Skeletal Muscle Contraction Hydrolysis of ATP by myosin energizes the cross-bridges, providing energy for force generation. Binding of ATP to myosin dissociates cross-bridges bound to actin . Hydrolysis of ATP by the Ca ++ - ATPase in the sarcoplasmic reticulum provides energy for the active transport of Ca ++ back into the reticulum, lowering calcium levels, ending contraction, and allowing muscle to relax . Na + -K + pump uses ATP for restoring concentration of Na + and K + across muscle cell membrane after action potential.

Muscle Energetics: 

Muscle Energetics Stored ATP -3 sec Creatinine phosphate -5sec Glycogen – used anerobically - 1 min Glucose used aerobically with O 2 -hours