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Phys Lect 9
Question | Answer |
---|---|
Motor End Plate | the region of the muscle where the nerve synapses. It is a highly specialized region for chemical signal transmission. |
Motor Unit | Is a single muscle fiber and the motor nerve that innervates it. |
What is the relationship between motor nerves and muscle fibers? | Each muscle fiber is innervated by a motor nerve, but each motor nerve innervates several muscle fibers |
What is the neurotransmitter used at the neuromuscular junction | Acetylcholine (ACh). |
What type of receptors reside on the muscle fiber at the neuromuscular junction? | Nicotinic Receptors (Ionotropic receptors) |
What enzyme is responsible for degredation of ACh in the neuromuscular junction? | Acetylcholinesterase (AChE) |
What type of synapse is the Neuromuscular junction? | Chemical synapse |
Is the muscle AP generated at the motor end plate? | NO |
what is generated at the motor end plate once the motor nerve releases ACh and they bind to nicotinic receptors? | End Plate Potential (EPP). Large depolarization that then travels passively along the muscle membrane. IF large enough, they will activate voltage-gated Na+ channels. |
Can EPPs have different amplitudes? | YES, unlike APs, EPPs can have different amplitudes. **EX: When lifting heavier wgt, the motor nerve will fire APs faster which will create a larger EPP at the motor end plate leading to an AP/contraction in the muscle |
What determines the level of EPP amplitude? | The Level of neurotransmitter (ACh) released from the motor nerve. |
Why would a high frequency of APs in the motor nerve increase the amplitude of the EPP at the motor end plate? | A higher frequency of APs in the motor nerve will allow more Ca2+ into the terminal bouton and cause the release of more ACh into the neuromuscular junction. The increase in ACh will increase the amplitude of the EPP. |
What is the direct cause of an EPP at the motor end plate? | Opening of ACh nicotinic receptors. This generates the END PLATE CURRENT:(Na+ influx > K+ efflux) which leads to the EPP. |
What occurs at a negative Em? | No net positive Influx. which means there is more K+ efflux than Na+ influx |
What ions are Nicotinic ACh receptors permeable to? | Na+ and K+. At resting Em, the driving force for Na+ is much greater which allows a larger influx of Na+ than K+ efflux. |
How many molecules of ACh are required to open the Nicotinic ACh receptors? | 2 |
What terminates the End Plate Current | The degredation of ACh by AChEsterase. This leads to a decay of the EPP and stops APs in the muscle fiber. **The Choline molecule is re-captured by the PREsynaptic motor neuron. |
What is the result of AChEsterase Inhibition? | ACh stays bound to the nicotinic ACh receptors, generating a continuous EPC -> EPP -> AP (muscle contraction). |
How is ACh regenerated in the presynaptic motor neuron at the neuromuscular junction? | Na+ - choline Symporter causes the re-uptake of choline into the motor nerve. Choline Acytltransferase: Choline + Acytl CoA = ACh |
Neuromuscular transmission modification: Increased muscle AP | 1.AChE Blockers. |
Neuromuscular transmission modification: Decreased muscle AP | 1.Na+ voltag-gated channel blockers in the motor nerve. 2.Ca2+ voltage-gated channel blockers in the terminal bouton. 3.Nicotinic ACh receptor blockers. 4.Na+ voltage-gated channel blockers in the muscle fiber. |
Myasthenia-Gravis | Autoimmune disease. Antibodies attack nicotinic ACh receptors which will lead to muscle weakness due to no EPP and AP. **Treatment: AChE blockers allowing ACh to hang around longer in the neuromuscular junction. |
Lambert-Eaton Syndrome | Autoimmune. Antibodies against presynaptic motor nerve Ca2+ channels. |
Why do AChE blockers not work with Cobra Venom? | the venom blocks all nicotinic ACh receptors which means the ACh in the neuromuscular synapse is ineffective no matter its concentration. |
Why does muscle weakness progress throughout the day with Myasthenia-Gravis? | Due to depletion of ACh. W/ decreased #/sensativity of nicotinic ACh receptors, more ACh is needed for each muscle contraction. Eventually the ACh stores in the motor nerve become depleted and the muscle can no longer contract (No ACh -> No EPP -> No AP) |