Explain how neurons communicate using acials and neurotransmittertion potents

Explain how neurons communicate using acials and neurotransmittertion potents. the answer must compare and contrast the similarities and differences between these two means of communication

BACKGROUND 

SUBJECT: Under resting conditions, the concentration of sodium ions — shown here in red — is about 10 times higher outside the neuron compared to the concentration inside. At the same time, levels of potassium ions — shown here in blue — are about 15 times higher inside the neuron compared to the extracellular environment. This ion gradient is maintained by the continuous operation of the sodium-potassium ATPase pump, which moves three sodium ions from the inside of the neuron to the outside environment, and at the same time, shifts two potassium ions from outside the neuron to the inside of the cell. Therefore, at each cycle of the sodium-potassium ATPase pump, the cell loses one positively charged ion from the intracellular environment. The action of the sodium-potassium ATPase pump is needed, because there is a constant flow of potassium ions down their concentration gradient from the inside of the neuron to the outside through leaky potassium channels that are situated in the membrane of the neuron. These two processes — diffusion of potassium out of the cell and exchange of intracellular sodium for extracellular potassium by the sodium-potassium ATPase pump — are continuously taking place in the neuron. This ultimately results in more positive charge outside the neuron compared to the inside of the neuron. The difference in charge across the membrane of the neuron is referred to as polarisation. If you subtract the value of all the positive charges inside the neuron — in this case, 30millivolts — from the value of the positive charges outside of the cell — in this case, 100millivolts — there is a difference of minus 70millivolts inside the neuron compared to the outside of the cell. This is called the resting membrane potential of the neuron.

Neurons communicate with each other via action potentials. Action potentials start in the axon hillock at the base of the cell body and then travel down the axon towards the dendrites of the neuron. To understand how an action potential is initiated, we need to look at the plasma membrane of the neuron.At rest, the neuron maintains a constant membrane potential of approximately minus 70 millivolts. Embedded in the membrane of the neuron are ion channels that are sensitive to the voltage of the cell. These channels open only when the voltage in the cell reaches a certain value. They are called voltage-gated ion channels.Voltage-gated sodium channels have both an activation gate and an inactivation gate. At rest, the activation gate is closed and the inactivation gate is open. Voltage-gated potassium channels have only one gate, which opens to allow the flow of potassium ions through the channel and closes to stop the flow of potassium ions.When the membrane potential is minus 70 millivolts, voltage-gated sodium channels are closed and the concentration of sodium outside the cell is higher than inside the cell. When the neuron receives an excitatory signal or stimulus, small amounts of sodium will move down their concentration gradient into the neuron, and the resting potential will start to become less negative.Once the membrane potential reaches a critical threshold of minus 55 millivolts, voltage-gated activation gates in the sodium channel open quickly, allowing sodium to flood into the neuron. As a result of the large influx of positively charged sodium, the neuron loses its negative charge and undergoes depolarisation.When the inside of the neuron becomes highly positive, the pore of the voltage-gated sodium channel is plugged by the inactivation gate, and the flow of sodium into the neuron stops.Eventually, the intracellular environment of the neuron becomes sufficiently positive that voltage-gated potassium channels begin to open slowly. Opening of these channels allows potassium to flow down its concentration gradient, out of the cell. This movement of potassium causes the inside of the neuron to quickly regain its negative charge in a process called repolarisation.In response to the increasingly negative charge inside the neuron, the voltage-gated potassium channels close. Because this process is slow, some potassium ions continue to move outside the cell while the channel is closing. This extra efflux of potassium causes the membrane potential to become more negative than the resting potential of minus 70 millivolts. This process is called hyperpolarisation.During the period of hyperpolarisation, the neuron will not be able to fire another action potential. This is termed the refractory period. Eventually, the action of the sodium potassium ATPase pump will restore the resting membrane potential to minus 70 millivolts, and the neuron will be ready to fire another action potential.The process of depolarisation and repolarisation is referred to as an action potential. A single action potential takes only milliseconds– that is one-thousandth of a second– to complete, enabling the neuron to quickly fire in response to the hundreds of signals it receives every second.

Movement of Na⁺ ions into the neuron causes the neuron to undergo depolarisation. (b) Movement of K⁺ ions out of the neuron causes repolarisation.

The action potential is initiated at the base of the cell body in the axon hillock. As you saw in Section 1.4, the signal will then be transmitted down the axon. However, the myelin covering does not allow for the exchange of ions across the cell membrane. How then does the action potential propagate to the end of the axon? Small gaps in the myelin, called nodes of Ranvier, allow ion movement across the axon membrane at these sites. This effectively permits the action potential to ‘jump’ from one node to another, thereby allowing the signal to be transmitted very quickly. This type of transmission is called saltatory conduction (Figure 2.1). Information is coded by the frequency of the firing of action potentials (i.e. the number of spikes over a given period of time), rather than the size of the action potential, which is always the same.

Image transcription text

opening of Nat depolarisation occurs and an channels action potential is generated myelin Ranvier Ranvier
Ranvier node I node II node Ill depolarisation skips along the axon from one node of Ranvier to the other…
…resulting in the rapid transmission of nerve impulses over long distances

Figure 2.1:Schematic diagram showing saltatory conduction of an action potential along the axon.

PROFESSOR: At an excitatory synapse, binding of the neurotransmitter to its receptors on the postsynaptic neuron will cause channels that are permeable to cations, like sodium, to open. Positively charged ions will enter the neuron and raise the resting membrane potential, bringing it closer to the critical threshold of minus 55millivolts that will trigger an action potential. At an inhibitory synapse, binding of the neurotransmitter to its receptors on the postsynaptic neuron will cause channels that are permeable to anions, like chloride, to open. Negatively charged ions will enter the neuron and lower the resting membrane potential, moving it further away from the critical threshold and decreasing the probability that the neuron will fire an action potential.

2.1.2   Neurotransmitters and synaptic transmission

In the previous section, you saw how a neuron fires an action potential in response to an excitatory stimulus. How do neurons pass along information about a stimulus to other cells? Most neurons are physically separated from other cells by a small gap called the synapse. Although this space is very small (about 20 nm wide), it is too big for the electrical signal to cross. Therefore, the electrical signal is converted into a chemical signal at the nerve terminal via the release of a neurotransmitter.

Many different compounds can act as neurotransmitters and some of the most common are listed below (Figure 2.2).

Figure 2.2 Word cloud of the main chemical neurotransmitters in the CNS and PNS.

Long description

Individual neurons synthesise a particular neurotransmitter (e.g. dopamine) and are classified accordingly (e.g. a dopaminergic neuron).

It is important to note that a single neuron communicates with hundreds of other neurons and therefore constantly receives both excitatory and inhibitory signals. Summation is the process by which the neuron ‘sums up’ all the excitatory and inhibitory signals it receives over a period of time. If the overall sum is sufficient to raise the membrane potential above the critical threshold, the neuron will fire an action potential. An example of how the membrane potential of a single neuron changes in response to binding of excitatory and inhibitory neurotransmitters

It is the combination of different excitatory and inhibitory neurotransmitters and the myriad of corresponding receptors on billions of cells that gives rise to the immense processing power of the human brain.

Chemicals that mimic the shape of a neurotransmitter may also bind to the postsynaptic receptors and alter neuronal activity. For example, alcohol, which is able to cross the BBB, can bind to GABA receptors and imitate its inhibitory actions, thereby producing a feeling of disinhibition at low concentrations, but nausea and even death at higher doses (Davies, 2003).

Similarly, most antidepressant drugs act by either preventing the reuptake or breakdown of neurotransmitters such as noradrenaline and serotonin, thereby increasing the amount of time that the postsynaptic neuron is activated.

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