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Calcium (Ca2+) channels open on the synaptic end bulb in response to depolarization (from the action potential), inducing exocytosis of synaptosomes containing neurotransmitter, resulting in neurotransmitter being released into the synaptic cleft...further propagating the signal to the next neuron or set of neurons.

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Q: What type of ion channel opens on the synaptic end bulb in response to depolarisation?
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What is the most important ion channel for cells to coordinate activities during synaptic transmission?

The K+ leak channel is the most important. It opens at around -70mV.


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Which statement correctly describes what causes the second voltage-gated Na plus channel to open?

After the first channel opens, the movement of many types of ions (both inside and outside the cell) alters the distribution of charges near the second channel, causing it to open.


Which ion channel opens in response to a change in membrane potential and participates in the generation and conduction of action potentials?

Sodium channels. A neuron's membrane potential may depolarize for many reasons (neurotransmitters, mechanical deflection, electrical synapse, etc). When that membrane depolarizes to the point of its threshold of activation, then voltage gated channels open up an allow an influx of sodium into the cell. This rapidly depolarizes the cell's membrane, causing that upward peak or rising phase to occur.


What happens to your acetylcholine when you stumble?

from answers.com When a nerve impulse reaches an axon ending, voltage-gated calcium channels in the axonal membrane open and calcium, which is extremely low inside the cell, enters the nerve ending. The increase in calcium-ion concentration causes hundreds of synaptic vesicles to fuse with the cell membrane and expel acetylcholine into the synaptic cleft (exocytosis). The acetylcholine released at a neuromuscular junction binds reversibly to acetylcholine receptors in the muscle end-plate membrane, a postsynaptic membrane that is separated from the nerve ending by a very short distance. The receptor is a cation channel which opens when two acetylcholine molecules are bound, allowing a sodium current to enter the muscle cell and depolarize the membrane. The resulting impulse indirectly causes the muscle to contract.

Related questions

What is the most important ion channel for cells to coordinate activities during synaptic transmission?

The K+ leak channel is the most important. It opens at around -70mV.


What happens after nerve signal reaches a synaptic knob?

In general, action potentials that reach the synaptic knobs cause a neurotransmitter to be released into the synaptic cleft. The arrival of the action potential opens voltage-sensitive calcium channels in the presynaptic membrane.


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Type of membrane channel that opens when distorted?

Mechanically-gated


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When a sodium channel opens and sodium rushes into a myocyte the cell membrane becomes?

The cell becomes depolarized


What are the roles of membrane carriers in synaptic function?

Chemical synapses comprise of 3 main parts: the presynaptic neuron (in all it's vessicles and glory), the synaptic cleft, and the post synaptic neuron. From basic neurobiology, we know that the presynaptic neuron fires, and the post synaptic neuron takes it like a bitch.The main function of a synapse is to cause changes in the membrane potential of the post synaptic neuron. But what is the mechanism behind it? It largely has to do with membrane carriers. Before a synapse can fire, it has to be depolarised enough to reach threshold, so that a large proportion of ion gate channels open, ions swoop in, change the action potential and trigger the secretion of neurotransmitters. But let's start from the beginning. Membrane carriers (ion channels) that sit in between the lipid bilayer of the neuronal cell membrane allow and control the ebb and flow of certain cations, anions and proteins. Some ion channels are gated, opening and closing in response to a change in voltage (voltage-gated channels) or in response to certain neurotransmitters (ligand-gated channels). The relative internal environment inside a neuron is slightly more negatively charged than its external environment. At rest, this difference of charge, or action potential, sits at about - (50 - 80) mV. At this stage, the diffusion into and out of the cell by K+ is at equilbrium. However, the cell's membrane is not perfectly impermeable to Na+, so Na+ slowly diffuses in. If this were uncontrolled, the internal environemnt would depolarize until it reached zero, and the neuron would be unable to fire. The sodium-potassium pump actively pumps out Na+ and pumps in K+, so the equilibrium is maintained. However, if the influx of Na+ exceeds that of the capacity of the sodium-potassium pump to expel the Na+, then the inside of the cell slowly depolarises. Once the internal environment of the cell reaches -40mV, then threshold is reached. At this point, voltage-gated Na+ channels open, and a rapid influx of Na+ changes the action potential of the cell to around +40 mV. The Na+ channels close in response to the change in action potential. K+ channels open tot he same change in action potential, increasing the cell membrane's permeabilty to K+. This repolarises, and hyperpolarises the cell. At this more, all the gated channels close, and the cell returns to it's resting potential. This action potential travels down the interior of the presynaptic axon, until it reaches the presynaptic terminal. In response to the sudden depolarisation, voltage-gated calcium channels open and Ca2+ enter the axon terminal. The Ca2+ causes synaptic vessels (filled with neurotransmitter goodness) to fuse with the pre-synaptic membrane, and burst, releasing it's gooey-goodness into the synaptic cleft. The post synaptic membrane have receptor sites specifically designed for particularly neurotransmitters. Depending on the neurotransmitter released, the receptor-neurotransmitter complex either indirectly or directly opens certain ligan-gated ion channels in the post synaptic membrane. For example, Ach is a neurotransmitter that can have either excitatory and inhibitory effects depending on the synapse. At an excitatory synapse, Ach will cause ligand-gated channels to open for Na+ and K+ ions. This causes depolarisation in the postsynaptic cell, and if the depolarisation is sufficient to reach threshold, the whole process is repeated in that neuron. At an inhibitory synapse, Ach will cause ligand-gated channels to open up for Cl-. This causes a hyperpolarisation in the cell, and takes it further away from firing threshold. The remaining neurotransmitter left in the synaptic cleft is either reuptaken by the presynaptic terminal via pinoctosis, or it is broken down by enzymes. This ensures that the transmissionis brief.


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Toy story started channel tunnel opens super Mario was introduced simpsons were introduced


Why do glucose need insulin to enter cells?

Most cell membranes are NOT permeable to sugar unless insulin opens a channel.


What chemical acts like a key to a cell?

hormones such as insulin opens up channel proteins which are like doors to a cell. Channel proteins allow larger molecules, such as sugar, to enter the cell.


Who do your nerves work?

This is a very complex question. Essentially nerves transmit signals by maintaining a resting potential of -70mV across the cell membrane by keeping large molecular anions (negatively charged molecules) in the cell and actively transporting sodium (Na2+) out of the neurone (the nerve cell). When the neurone is stimulated by some neurotransmitter such as acetylcholine the receptor opens up Na2+ gateways in the membrane allowing Na2+ ions to enter the neuron partially de-polarising the neurone. If enough of these receptors are activated and gateways opened then depolarisation reaches a threshold level. At this point voltage gated ion channel in the membrane open allowing Na2+ ions to rush in depolarising the call to around +30mV at which point voltage gated K+ ion channels open allowing these to rush out repolarising the cell. The cell then enters a brief refractory period where it will nolonger depolarise, this acts as a means to control signalling. The depolarisation occurs in a wave down the axon of the neurone. As the action potential reaches the synaptic knob of the axon voltage gated ion channels allow Ca2+ to enter. This causes exocytosis of neurotranmitters contained in vesicles into the synaptic cleft. These neurotransmitteres then attach to receptors the postsynaptic membrane and depending on whether the neurotransmitter is excitory such as acetylcholine or inhibitory like dopamine will allow sodium ions to enter depolaizing the call if excitory. Inhibitory neurotransmitters hyperpolaise the cell and prevent the neurone 'fireing'