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1. A neurotransmitter (NT) released from another cell (or in some cases the same cell) will diffuse across the synaptic cleft and bind to a recipient receptor.

2. The receptor will then change it's permeability to certain ions in the extracellular fluid, allowing the ions to flux into the cell (the exception here would be pharmacological agents designed to occupy the receptor without leading to a conformation change)

3. The influx of ions will alter the membrane potential. If the NT is inhibitory (e.g. GABA), then the GABA receptor that it binds to will increase its permeability to negatively charged ions (chloride) and thereby lower the local resting membrane potential (which is normally -70mV). If the NT is excitatory (e.g. glutamate) then the glutamte receptor (AMPA or NMDA) will increase its permeability to positively charged ions (sodium) which will increase the resting membrane potential from -70mV.

4. If enough NTs bind then the local membrane potentials will summate - and in the case of excitatory NTs - cause the membrane potential to change (by opening of voltage-gated ion channels) to around 0-20mV leading to an action potential

5. The action potential, which is generated in an 'all or none fashion' at the axon hillock, will then propagate all the way down the axon to the axon terminal causing the release of stored NTs (although not all NTs are stored - e.g. NOS)

6. NTs released from the presynaptic cell will then diffuse across the synaptic cleft and bind their postsynaptic receptor (normally located on a dendrite, although also located on the cell body themselves) and the whole process starts all over again

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15y ago
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11y ago

Voltage-gated sodium ion channels open, causing an influx of sodium ions into the axon, resulting in a shift from a negative (-70 mV) resting potential to a positive action potential.

This triggers adjacent, downstream voltage-gated sodium ion channels to open, continuing the process down the axon.

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12y ago

the inside of the membrane temporarily becomes more positive than the outside,reversing the resting potential

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14y ago

Please in very simple terms explain the changes in a neuron during an action potential

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Q: What happens to the membrane potential of a neuron during an action potential?
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Related questions

Why does the polarity of a cell membrane reverse during an action potential?

During an action potential the neuron receives a stimulus causing the cell membrane to become more permeable to sodium than potassium, calling the polarity to change.


What happens in the neurolemma as the result of an action potential?

It provides insulation to the axons and dendrites during depolarization or action potential.


During an action potential hyperpolarization beyond more negative to the resting membrane potential is primarily due to?

Potential hyperpolarization are more negative to the resting membrane potential because of voltage. This is taught in biology.


Which is the first step in a neuron production of an action potential?

Depolarization is the first event in action potential. During depolarization, the sodium gates open and the membrane depolarizes.


During action potential transmission many ions cross the neuronal membrane at right angles to the membrane what travels along the membrane and acts as the signal?

neurotransmitters


What is in the cell membrane that can be opened or close?

There is more potassium inside the cell during a resting period...as an action potential occurs, the cell becomes depolarized, or in other words there is an influx of sodium, allowing the membrane to open. As the action potential comes to an end, the cell repolarizes, meaning the levels of sodium rush outside of the cell again, while the potassium flows back in. As another action potential takes place, this happens over again.


What is the charge on the inside membrane during the resting membrane potential?

The resting membrane potential of a typical neuron is around -65mV


What ion is rapidly moving into the cell during the depolarization period of an action potential?

Sodium.A positive ion (cation) that enters the cell (influx) rapidly when the membrane threshold is reached and the voltage gated sodium channels open.This occurs during the rising phase of an action potential, i.e. membrane depolarization beyond the threshold for activation.


What happens during the refractory period?

The voltage-gated Na+ channels get deactivated, thus the sodium ions cannot diffuse into the cell and cause depolarisation and this also provides time for the membrane to prepare for its second action potential.


What is the process called when sodium NA is pumped out of a nerve cell?

during action potentials, sodium and potassium cross the membrane of the synapse after the threshold of membrane potential is reached. There, sodium leaves the synapse and the membrane potential is now positive. this is known as depolarization. then during repolarization, the sodium channels close and the potassium channels open to stabilize the membrane potential. during this time, a second action potential cannot occur and this is an evolutionary advantage because it allows rest in the nerve cells and it allows the membrane potential to equalize.


Is an action spike an impulse created by an excitable membrane when it reaches the threshold?

Yes, during th rising phase of an action potential you will see the spike which is representative of the threshold (all or none) occuring.


What is the electrical charge of an action potential?

The electrical potential of the cell body changes during an action potential from a negative potential of around -70 mV to a positive potential of +40 mV. The resting potential, however, remains constant.