1. In step by step manner, explain how the voltage-regulated channels produce an
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Question
1. In step by step manner, explain how the voltage-regulated channels produce an action potential.2. Explain how myelinated axon conducts action potentials, and why this conduction is faster than in an unmyelinated axon.
3. Suppose you are provided with an isolated nerve-muscle preparation in order to study synaptic transmission. In one of your experiments, you give that preparation a drug that blocks voltage-gated Ca++ channels: in another , you give tetanus toxin to the preparation. How will synaptic transmission be affected in each experiment? 1. In step by step manner, explain how the voltage-regulated channels produce an action potential.
2. Explain how myelinated axon conducts action potentials, and why this conduction is faster than in an unmyelinated axon.
3. Suppose you are provided with an isolated nerve-muscle preparation in order to study synaptic transmission. In one of your experiments, you give that preparation a drug that blocks voltage-gated Ca++ channels: in another , you give tetanus toxin to the preparation. How will synaptic transmission be affected in each experiment? 1. In step by step manner, explain how the voltage-regulated channels produce an action potential.
2. Explain how myelinated axon conducts action potentials, and why this conduction is faster than in an unmyelinated axon.
3. Suppose you are provided with an isolated nerve-muscle preparation in order to study synaptic transmission. In one of your experiments, you give that preparation a drug that blocks voltage-gated Ca++ channels: in another , you give tetanus toxin to the preparation. How will synaptic transmission be affected in each experiment? 1. In step by step manner, explain how the voltage-regulated channels produce an action potential.
2. Explain how myelinated axon conducts action potentials, and why this conduction is faster than in an unmyelinated axon.
3. Suppose you are provided with an isolated nerve-muscle preparation in order to study synaptic transmission. In one of your experiments, you give that preparation a drug that blocks voltage-gated Ca++ channels: in another , you give tetanus toxin to the preparation. How will synaptic transmission be affected in each experiment?
Explanation / Answer
1. ANS: Voltage regulated ion channels have the ability to produce an action potential. Take for example the sodium potassium pump. First there is a stimulus (depolarization) that gets the membrane potential up to its threshold. One the axon membranes are at threshold level the Na+ gates open and Na+ enter the axon through diffusion. This causes more depolarization of the membrane. The Na+ gates are voltage regulated and so more channels for Na+ open and there is a higher permeability. This causes a rapid reversal of membrane potential for the region until it finally goes from -70mv to 30 mv, at which point the Na+ channels close. The K+ channels open at this time and the K+ diffuses out of the cell during repolarization making the membrane potential more negative. These changes in membrane potential produce an action potential or a nerve impulse.
2. ANS: In an unmyelinated axon action potentials are conducted like a wave in sporting event. This is because the un myelinated axon has voltage gated sodium channels along the entire length of the membrane, while myelinates axons only have voltage gated sodium channels in nodal spaces. The nodal spaces are myelinated spaces. Because of this the action potential is much faster along myelinated axons.
3. ANS: The neurotransmitters are present in the storage vesicles of the nerve terminals These are the sac like structures that are formed from Me layer pica membrane lithe action potential reach the nerve terminals, the neurotransmitters the voltage gated calcium channels are activated The influx of calcium ions causes “exocytosis," through which the stored neurotransmitters are released from the synaptic vesicles The released neurotransmitters allow the synaptic transmission, That is the transmission of impulse from one neuron to the other neuron or effectors organ via the synapse.
If the voltage gated calcium channels are closed, exocytosis do not occur Thus, the neurotransmitter release and synaptic transmission do not occur Tetanus is a neurotoxin released by the Clostridium tetani It causes muscle spa, convulsions and lock jaw in the affected people This toxin acts by inhibiting the release of acetylcholine (ACI. neurotransmitter nom the presynaptc nerve terminal of the motor neurons, which prevents the muscle depolarization and contraction process The SNAREs are the targets of neurotoxins such as botulinurn toxin and tetanus. The primary function of SNARE proteins, allow the fusion of vesicles with their target membranes. Likewise they also facilitate the fusion of synaptic vesicles that store neurotransmitter with be presynaptic membranes in neurons Thus; inhibition of SNAREs inhibits the vesicle fusion and release of neurotransmitter.
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