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Q: What is the presynaptic neuron release neurotransmitters in response to an influx of sodium ions?
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Why increasing extracellular potassium ion reduces the net diffusion of potassium ion out of neuron through the potassium leak channel?

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Related questions

What is the presynaptic neuron release neurotransmitters in response to an influx of?

Sodium ions


Presynaptic neurons release neurotransmitters by?

An action potential travels down the neuron and reaches the presynaptic knob. This causes the Calcium ion channels to open and allow an influx of calcium into the knob. The increased concentration of calcium causes the secretory vesicles within the knob to bind to the outer membrane and release their neurotransmitter (e.g. ACh) into the synaptic cleft.


How does neurotransmitters initiate depolarization?

Let's picture a presynaptic neuron, a synaptic cleft, and a postsynaptic neuron. An action potential reaches the terminal of a presynaptic neurone and triggers an opening of Ca ions enters into the depolarized terminal. This influx of Ca ions causes the presynaptic vesicles to fuse with the presynaptic membrane. This releases the neurotransmitters into the synaptic cleft. The neurotransmitters diffuse through the synaptic cleft and bind to specific postsynaptic membrane receptors. This binding changes the receptors into a ion channel that allows cations like Na to enter into the postsynaptic neuron. As Na enters the postsynaptic membrane, it begins to depolarize and an action potential is generated.


What is the name of the cell that releases the neurotransmitters?

Exocytosis. As a result of the influx of Calcium ions, the synaptic vesicles transport the neurotransmitter Ach (Acetylcholine) to the presynaptic membrane, the vesicles fuse to the membrane, and the neurotransmiffer, Ach, diffuses. Once the neurotransmitters cross the synaptic cleft, they bind to the receptors on the post synaptic membrane. Hope it helps a bit.


What happens when presynaptic cell's produce action potentials?

When presynaptic cells produce action potentials, it triggers the opening of voltage-gated calcium channels in the presynaptic membrane. This influx of calcium ions into the presynaptic cell triggers the release of neurotransmitter molecules from small, membrane-bound vesicles. The released neurotransmitters then diffuse across the synapse and bind to receptors on the postsynaptic cell, generating a response in the postsynaptic cell.


What do the bubbles of chemical crossing the synapse do?

Chemicals called neurotransmitters move across the synaptic gap by diffusion and carry a neural signal across to the receiving neuron. But the 'bubbles' (vesicles) which contained the neurotransmitter chemicals do NOT themselves cross the synaptic gap, they just release the neurotransmitters into the synaptic gap. (The neurotransmitters move across the synapse, the vesicles do not.)The vesicles release their contents of neurotransmitters into the synaptic gap by a process called exocytosis, in which the neural impulse which reaches the terminal button of the presynaptic neuron causes voltage-gated calcium ion pores to open, allowing an influx of calcium ions, which leads to the fusing of the vesicles to the cell membrane, which amounts to the vesicles 'turning themselves inside out' as the membrane of the vesicle merges with the cell membrane, which expels the neurotransmitters into the synaptic gap.The neurotransmitters flow across the synapse to bind with the postsynaptic neuron, potentially triggering neuron excitation (firing) or inhibition (preventing firing).


What is the sequence of events in the process of synaptic transmission?

Neurons communicate with each other by sending electrical signals across a synapse. In a three neuron loop the series of events that happen in synaptic transmission are as follows: Neuron 1 sends an electrical signal (action potential) down its axon towards the synapse. The action potential causes the release of neurotransmitters (chemicals) from the terminal button of Neuron 1 into the synaptic cleft. The neurotransmitters bind to the receptors of Neuron 2. This binding triggers a new action potential in Neuron 2 which travels down its axon. The action potential causes the release of neurotransmitters (chemicals) from the terminal button of Neuron 2 into the synaptic cleft. The neurotransmitters bind to the receptors of Neuron 3. This binding triggers a new action potential in Neuron 3 which travels down its axon. The action potential causes the release of neurotransmitters (chemicals) from the terminal button of Neuron 3 into the synaptic cleft. The neurotransmitters bind to the receptors of Neuron 1 closing the loop.This series of events is repeated continuously allowing for the communication between neurons in a three neuron loop.


Binding of the neurotransmitters with muscle membrane receptors causes the membrane to become permeable to sodium resulting in the influx of sodium ions an what of the membrane?

depolarization


What is the presynaptic knob ca2?

Your question isn't very clear.... Presynaptic knob is the neurone before the synapse. Postsynaptic knob is the neurone after the synapse. Calcium ions diffuse into the presynaptic knob down their concentration gradient when an impulse arrives at the presynaptic knob. This causes the vesicles to move towards the presynaptic membrane and fuse with it. This releases the neurotransmitter (e.g. Ach). The Ach diffuses down their concentration gradient in the synaptic cleft then binds with receptors on the post synaptic membrane. This binding causes the Na+ ion channels to open, and the influx of Na+ ions causes depolarisation, and a new action potential in the postsynaptic knob. Then the acetate and choline diffuses back into the presynaptic membrane and is recombined using ATP.


When hinding of the neurotransmitters with muscle membrane receptors causes the membrane to become permeable to sodium resulting in the influx of sodium ions and what membrane?

action potential of the sarcolemma(the membrane)


Neurotransmitters categorized as inhibitory are expected to?

Inhibitory neurotransmitters prevent the firing of neurons by binding with certain receptors, causing the influx of chloride ions to hyperpolarize the neuron. When this happens, it requires a much larger excitatory signal to override the inhibitory effects in order to allow the neuron to fire.


What is the role of calcium in synaptic activity?

In a classic synapse, calcium's main role is to trigger the release of chemicals (called neurotransmitters) from the presynaptic neuron. How calcium does this is well established and is achieved through voltage-gated calcium channels located on the membrane of the presynaptic terminal. These channels open in response to membrane depolarization, the type of signal carried by an action potential. The whole process goes something like this: When an action potential arrives at the presynaptic terminal, it depolarizes the membrane sufficiently to open voltage-gated calcium channels. The calcium gradient across the membrane is such that when these channels open, an inward calcium current is produced, with calcium rapidly entering the cell. Calcium is rapidly bound by a presynaptic intracellular protein called synaptotagmin. Synaptotagmin is considered a calcium sensor that triggers a host of downstream events. Ultimately, synaptotagmin activation results in the fusion of neurotransmitter vesicles with the presynaptic membrane. These vesicles fuse with the membrane through interactions between v- and t-snares (the "v" and "t" stand for "vesicular" and "target", respectively) causing the release of neurotransmitters into the space between the pre- and postsynaptic terminal. Individual molecules of neurotransmitter diffuse across this space, called the synaptic cleft, and ultimately bind to receptors on the postsynaptic cell membrane. Since calcium triggers the conversion of an electrical signal (the action potential) into a chemical one (the release of neurotransmitters), calcium can be thought of as the trigger for electrochemical transduction (the term literally means the conversion of electrical into chemical information). Note that calcium's role is not limited to the presynaptic terminal; plenty of other synaptic phenomena rely on calcium. For example, at the specialized synapses between neurons and muscle cells (called the neuromuscular junction), binding of the neurotransmitter acetylcholine to the muscle cell triggers a rise in calcium within the muscle cell, which ultimately leads to muscle contraction. Another example occurs in the brain and involves a postsynaptic receptor called the NMDA receptor. Activation of this receptor also produces a rise in intracellular calcium in the postsynaptic cell which contributes to a number of interesting phenomena, notably learning and memory.