Neuromuscular juncti
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| motor unit | the whole assembly of muscle fibers which are innverated by one single motor nerve
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| neuromuscular junction | -end plate
-a specialized synaptic region when a motor axon contact a single muscle fiber
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| Bouton | the ending of axon where it finally contact the muscle cell
- contain synaptic vesicle
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| postfunctional folds | located in the muscle plasma membrane in postsynaptic region
-greatly increase surface area
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| Synaptic cleft | fill with meshwork of protein and proteoglycan, part of EMC
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| what kind of molecules exist in synaptic basal lamina and their function | Collagen, laminin, agrin: mediate adhesion of neuromuscular junction, important for synapse development and regeneration
-High concentration of AChE to terminate synaptic trnasmission
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| Acetylcholinesterase | -found in synaptic basal lamina
-hydrolyze ACh to choline and acetate
-terminate synaptic transmission
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| Where is synaptic vesicles are made and how did it translocate to bouton region of axon? | synthesize in cell body of motor neuron in spinal cord
-translocated to nerve terminal through microtubule-mediated process
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| What molecules are in synaptic vesicles? | ACh
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| synthesis of ACh | -synthesis in nerve terminal
-Choline + acetyl coenzyme A through action of Choline acetyltransferase
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| How does ACh pack into synaptic vesicle | Through Ach-H exchanger which is driven by vesiclular proton electrochemical gradient (low pH and +ve voltage)
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| How does vesicular proton electrochemical gradient is generated? | through Vaculoar-H+ pump fuel by ATP
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| Where do we find AChR? | high density at the crest of Postjuncitonal folds
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| Nerve simulation at postsynaptic region can generate which 2 types of response | 1) Graded electrical response
2) action potential if reach threashold
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| D-Tubocurarine | chemical use to block AChR
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| the delay in transient depolarization of the muscle membrane after stimulation is due to? | 1) time required to release ACh
2) diffusion of ACh across synapse
3) Activation of postsynaptic receptor (AChR)
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| how does distance affect amplitude and delay in peak Vm | increase distance will decrease amplitude of potential change and increase the delay to reach peak Vm
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| What contribute to the end-plate potential? | The depolarizing end-plate current which cause by binding of ACh to AChR and open the iontropic nicotinic receptor
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| What ions are permeable to AChR? | Cation, Na+, K+
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| What direction does Na+ and K+ move after the opening of AChR channel | Na+ influx into cell
K+ efflux out of cell
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| is AChR channel a selective or non-selective channel | Non-selective cation channel
permeabile to all cation but not to anion
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| What is the threshold for postsynaptic cell to generation Action potential? | -50mV
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| Does receptor-gated channels for serotonin and glutamate generate excitatory or inhibitory postsynatptic potential? | Excitatory postsynaptic potential as it is a cation selective and cause depolarization
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| Does receptor-gated channels for glycine and GABA generate excitatory or inhibitory postsynatptic potential? | Inhibitory postsynaptic potential as it is an anion selective and result in hyperpolarization
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| How does neuromuscular joint keep its ability to maintain high rate of transmission? | 1) there are large inventory of ready synaptic vesicle in nerve terminal
2) its ability to synthesize new ACh and pack them into vesicle
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| Miniature End-plate potential (MEPP) | its the spontaneous Vm fluctuation similar to EPP
the resting muscle fiber also have small depolarization due to random release of synaptic vesicle even in absence of stimulation
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| What does it mean by ACh release is quantized? | each synaptic vesicle release certain amount of ACh and the sum of all vesicle released will determine EPP
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| how does Mg2+ and Ca2+ concentration affect amplitude of EPP | amplitude of EPP decrease if there is
1) increase in Mg2+ concentration which will partially block presynatic calcium channel
2) decrease in calcium entry into presynaptic terminal
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| Curare | the antagonist of AChR, will block the receptor and inhibit small depolarization (MEPP)
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| NeoStigmine | inhibitor of AChE, will increase size and duration of MEPP
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| mechanism of termination of neurotransmitter action | 1) enzymatic destruction of ACh by AChE
2) re-uptake of neurotransmitter by specific high affinity transport system
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| Where are the re-uptake transport system locate? | presynaptic plasma membrane and surround by glial cell
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| for the transporter family specific for catechdamines, serotonin, GABA, glycine and choline, which ion do they use to couple the transportation? | NA+ and Cl-
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| for the transporter family specific for excitatory amino acid glutamate and asparatate, which ion do they use to couple the transportation? | Na+ and H+ , exchange for K+
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| describe three form of AChE | 1) G form (globular): monomer, dimer, tetramer, soluble or membrane bound through GPI linkage
2) A form (asymmetric): 1-3 tetramer of globular enzyme, couple through disulfide bond or collagen-like structural protein
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| what is the most common form of AChe found in neuromuscular joint? | the asymmetric form with 12 catalytic subunit attach to collagen-like tails
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| mechanism of ACh hydrolysis | step 1: hydrolysis of choline from ACh by AChE and form intermediate group in which acetate group is covalently bound with serine group on enzyme
step 2: hydrolysis and release choline and free the enzyme
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| What happen to the extracellular choline after AChE hydrolysis | it will be uptake by high affinity Na+ coupled uptake system and reuse to synthesize new ACh
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| Tetrodotoxin & Saxitoxin | -block the depolarizing phase of AP at nerve terminal
-type of guanidinium neurotoxin
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| Dendrotoxin | -Mamba snake toxin
-inhibit repolarization due to blockage of some isoform of Voltage gated K+ channel
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| What is the effect of Dendrotoxin on Action potential at terminal? | the toxin facilitate the release of ACh and inhibit repolarization, therefore increase duration of AP and facilitate the entry of extra Calcium to nerve terminal
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| Describe the bimodal distribution of myasthenia gravis | 1) 20s, usually women with thymus hyperplasia
2) 60s, men with coexisting thymus gland cancer
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| Cause of myasthenia gravis | an acquired autoimmune disroder which antibodies directed against the receptor and result in skeletal muscle weakness.
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| What are the symptoms of myasthenia gravie | fatigue and weakness of skeletal muscle (extraocular muscle only or all skeletal muscle).
Symptom usually worse at the end of day or after exertion. May result in paralysis of repiratory muscle
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| Treatment plan for myasthenia gravie | 1) enhance cholinergic transmission
2) Thymectomy
3)Immunosuppression
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| Pyridostigmine | AChE inhibitor which can be use to enhance cholinergic tranmission but dosage need to be carefully monitored
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| What is consequence of overdosage with pyridostigmine? | 1) overstimulation of postsynaptic receptor
2) prolonged depolarization
3) inactivation of neighboring Na+ channel
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| Corticosteroid | immunosuppressant use to treat Myasthenia gravie
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| Plasmapheresis | remove of anitbodies from the patient's serum,a treatment for myasthenia gravie
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| mechanism of antibodies in Myasthenia gravie | the Anti-AChR antibodies bind one or more subunit of AChR, they bind and activate complement and accelerate destruction of receptor, therefore decrease the surface density of AChR in junctional fold
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| Which AChR subunit does anitbodies usually bind to? | Alpha-AChR: MIR (Main immunogenic region)
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| cause of Lambert-eaton syndrome? | Antibodies that attach Presynaptic Ca2+ channel
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| how to distinguish Lambert-Eaton Syndrome from Myasthenia | 1) Lambert-Eaton Syndrome usually attack limb muscle , not ocular / bulbar muscle
2) repetitive stimulation of particular muscle can increase contractile strength and enhance amplitude of postsynaptic action potential
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| What happen to patient with myasthenia and has a muscle continuously stimulated? | The repetitive stimulation will decrease strength and lead ot progressive lessening of A.P.
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| Congenital myasthenic syndrome | inherited disorder, present at birth, affect meuromusclar disorder
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| list few symptom and sign of congenital myasthenic syndrome | 1) AChE deficiency, abnormal presynaptic release of ACh, defective AChR funciton
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| What is the point mutation on AChR and its effect | Thr ==> Pro at AChR subunit which affect the formation of channel pore. This cause excessive depolarization and pathological consequences at muscle and plate
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