How does the neural cell work?

By Sergey Skudaev

The human brain is a quite mysterious system. It is comprised of about 10 billions of neural cells or neurons.

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At the beginning it was thought that neurons work as switches. They may be in two states: "on" or "off". If a neuron is "on", it sends signals to the other neurons. When a neuron is "off", it does not send signals. Later, it was discovered that neuron is a very sophisticated system. Hover your mouse over a thumbnail to see a large image.

Neuronal network
Figure 1. Pyramidal Neurons in cat's sensorimotor cortex.
pyramidal neuron N.S.Kositzyn
Figure 2. A pyramidal neuron. N.S.Kositzyn[1]

The Excitatory Tissue and Membrane Potential.

Any excitatory tissue cell has a membrane potential; its cell membrane is negative inside and positive outside. This membrane potential is called Resting Potential. How is it maintained?

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A cell membrane has a sodium-potassium pump, which pumps K+ ions in the cell and Na+ ions out of the cell. If the cell membrane were equally permeable to K+ and Na + ions, K+ ions would passively flow back outside and Na + ions would passively flow back inside to restore original equilibrium.

In fact, a cell membrane is much less permeable to Na + ions than to K+ ions. The membrane has K channels and Na channels. These channels may be closed or opened depending on the membrane potential.

During the Resting Potential, Na channels are closed and K channels are opened. K+ ions flow passively outside and accumulate positive charge. Na + ions cannot flow inside or its flow is insignificant.

When positive K+ ions leave the cell, it becomes negative inside. The negative charge attracts positive K+ ions and some of them flow back inside. When the charge force (inside direction) and the force due to gradient of K+ ions concentration become equal, equilibrium develops. Some insignificant Na+ ions flow decreases membrane potential. That is how Resting Potential is maintained. Please see figure. 3

Membane potentials at rest and exitement

Figure 3. A membane potentials at rest and exitement

When a negatively charge electrode applied to the cell surface, the resting potential starts decreasing. This condition is called depolarization. When depolarization reaches a threshold, Na channels will open in cell membrane. Since Na+ concentration is higher outside the cell than inside the cell, a force due to gradient concentration will make Na+ ions to flow inside. Besides, negative charge inside the cell will attract positive Na+ ions. Both forces make Na+ ions flow inside the cell and Na+ flow becomes much greater than K+ ions flow outside the cell. As a result, the cell membrane becomes positive inside and negative outside. An Action Potential is generated.

Please see figure 3. and 4. A membrane potential is measured by inserting inside the cell a tiny glass capillary filled with the KCL solution. This capillary has a wire inside, which is connected to an amplifier and a display.

Action potential

Figure 4. The Action Potential

The Resting potential of a muscle or neural cell membrane is about 0.09 volt. The Action Potential is about 0.120 volt, depending on type and size of the cell.

Hodgkin and Huxley [3,4,5,6,7] studied membrane potentials on the giant axon of a squid, which is one millimeter in diameter. They changed membrane potentials and found that the permeability of a membrane depends on the membrane potential. Depolarization causes opening Na+ channels and an Action Potential is generated. Then Na+ channels are closing again. K+ ions flow outside becomes greater than Na+ ions flow inside and the membrane potential is restored back to the Resting Potential.

An Action potential in the neuron or the skeletal muscle cell lasts about one millisecond. In the heart or smooth muscle cell the membrane has Ca+ channels. Ca++ channels become opened after opening Na channels. Ca++ ions flow inside and cause muscle contraction. Ca++ channel blockers cause relaxation of vascular smooth muscles and as a result lower blood pressure.

The Neural cell and synapses

A neural cell or neuron has many dendrites, which look like trees and serve for input information. One long outgrowth - axon serves for output information. The body of the neural cell and its dendrites are covered with thousand of synapses, Synapses are contacts from the other neurons.

Dendrites covered by synapses                                synapses

Figure 5. Dendrites covered by synapses. A Synapse. N.S.Kositzyn[1]

Through this synapses dendrites receive messages from the other neurons. These messages can inhibit or increase neuron activity. In the last case, the neuron may generate an action potential, which spreads along the axon.

The Axon terminal forms synapse, a structure comprised of the axon terminal, presynaptic membrane, synaptic cleft and postsynaptic membrane. Please see figure 6.

Synaptic Transmission

Figure 6. The Synaptic Transmission

A synapse contains vesicles with a neurotransmitter. When an action potential reaches the axon terminal , its membrane becomes permeable to Ca++ ions. Ca++ ions flow inside the terminal and cause vesicles to move to the presynapric membrane and release the transmitter in the synaptic cleft. Please see figure 6.

Transmitter molecules passively spread in the synaptic cleft and reach the postsynaptic membrane receptors. Transmitter molecules bind to receptors and change the postsynaptic membrane potential. The message is transferred to the next neuron or muscle cell.

There are many different neurotransmitters or neuromediators: norepinephrine, dopamine, serotonin, acetylcholine, gamma-aminobutiric acid (GABA), glutamine, etc.

Some transmitters affect ion channels, some use a second messager (adenyl cyclase cAMP).

Transmitters can be inhibitory, excitatory or both, depending on receptor type.

Inhibitory mediators increase K+ or Cl - flow, which increase the membrane potential. Excitatory mediators increase Na+ flow and cause depolarization of the membrane, as a result, an action potential may be generated in the neuron if the axon ends on a neuron or in muscle cell if the axon ends on a muscle cell.

Mediators' action is stopped when a mediator molecule is modified by an enzyme, or due to reuptake of mediator molecules by the axon terminal.

In case when mediator is acetylcholine, it is deactivated by acetylcholine esterase. It breaks acetylcholine to choline and acetate. The axon terminal reuptakes choline from synaptic cleft by choline pump and acetylcholine is synthesized again from choline and acetylCoA.

Acetylcholine system is impaired in patients with Alzheimer disease.

There are two acetylcholine receptors: muscarinic and nicotinic. Muscarinic receptors bind muscarin and nicotinic receptors bind nicotine. For example, brain and heart cells have muscarinic receptors and skeletal muscle tissue has nicotinic receptors.

In case, when a mediator is norepinephrine, an axon terminal reuptakes it from synaptic cleft.<.p>

Monoamineoxidase (MAO)is an enzyme that oxidizes norepinephrine. MAO inhibitors are used as antidepressants because they increase the norepinephrine concentration in the brain. Neurons, which synapses produce norepinephrine are located in an area of the brain, which is called "locus coeruleus" (blue spot). It is known that rats with electrodes inserted into the blue spot, or into fibers, which go out of the blue spot, stimulate their own brain. It was established that this brain area belongs to the rewarding system.[2]

Also neurons, which are located in the raphe nuclei of the brain stem, produce serotonin. It is known that the raphe nuclei control sleep. A low serotonin concentration in the brain may cause anxiety and depression. Selective serotonin reuptake inhibitors (SSRIs) inhibit serotonin reuptake from the synaptic cleft and increase serotonin extracellular concentration. SSRI are used as antidepressants in the treatment of depression and anxiety. Lexapro, Selexa and Zoloft are most known SSRI in the USA.

Norepinephrine receptors are divided on two types: alpha and beta. There are two types of alpha receptors excitatory alpha1, inhibitory alpha2 and three types of beta receptors: excitatory beta1, inhibitory beta2, beta3. The heart has beta1 receptors that is why beta blockers decrease heart rate.

Dopamine receptors are divided on two types: D1 and D2. Substantia Nigra in the brain stem contains neurons, which axon terminals produce dopamine. An excess of dopamine production is related to schizophrenia. The lack of dopamine production is observed in Parkinsonism.

Understanding of mechanisms of the synaptic transmission and metabolism of neuromediators will help us to develop new safe medications and to understand conditions underlying different psychotic or somatic diseases.

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2. Catherine H Bielajew, Tamara Harris. Self-Stimulation: A Rewarding Decade J. Psychiatr Neurosci, Vol.16, No 3, 1991

3. Huxley AL and Hodgkin AF. Measurement of Current-Voltage Relations in the Membrane of the Giant Axon of Loligo. Journal of Physiology 1: 424-448, 1952.

4. Huxley AL and Hodgkin AF. Currents Carried by Sodium and Potassium Ions Through the Membrane of the Giant Axon of Loligo. Journal of Physiology 1:449-472, 1952.

5. Huxley AL and Hodgkin AF. The Components of Membrane Conductance in the Giant Axon of Loligo. Journal of Physiology 1: 473-496, 1952 (c).

6. Huxley AL and Hodgkin AF. The Dual Effect of Membrane Potential on Sodium Conductance in the Giant Axon of Loligo. Journal of Physiology 1: 497-506,1952.

7. Huxley AF and Hodgkin AL. A Quantitative Description of Membrane Currentand Its Application to Conduction and Excitiation in Nerve. Journal of Physiology 1: 500-544, 1952.