That’s scary stuff when you think about it. Now then, I have a non sequitur, and thought I’d like to share with you today if you have a few moments.

Since trains produce vibrational energy which can be viewed on a Richter scale, often in the neighborhood of 1.2 to 2 magnitude, then essentially that is creating lots of little earthquakes, let’s call them swarms of earthquakes every time the train goes by. The train runs up and down the San Andreas Fault in California in some parts. In doing so it jiggles the Earth, and allows the sand to settle. As the sand settles it becomes more compacted with less space in between the granulars, over time this would cause the ground elevation to lower. Interestingly enough many of the cities near where I live are around 10 feet less in elevation than they were 30 years ago.

There are probably two reasons for this, one is that there are lots of golf courses around here and they’ve been taking the groundwater out to water the golf courses, therefore lowering the water table, but also I believe some is due to the earthquakes that we get now and again, the small ones, along with the vibrational energy from the trains which go by every day.

Do trains also help relieve stress from earthquake faults?

They very well might, or in some cases they will increase the stress. This of course, depending on what type of fault it is, and which way the surface waves from the motion of the train are spreading outward. Some might say that the net difference is so little, that it doesn’t matter. Ah but over time, it does matter, and it would change the overall dynamics of the fault and the stress, just as it changes the dynamics of the soil compaction and the settling of the Earth and soil of the terrain.

It does matter, and yet perhaps to protect the railroad industry, I’ve never found or read any solid research, nor can I find anyone that has the knowledge or empirical proof to answer this question. Therefore I’m putting it out to you on the Internet and hopefully you will contact me if you have some information on this topic. You may e-mail me if you have comments, concerns, questions, or other theories of your own along the subject matter.

Source: EzineArticles.com/?expert=Lance_Winslow

Generation of action potential within a neuron

All animal cells are electrically polarized as they maintain a voltage difference known as membrane potential. In case of neurons, axons, dendrites and cell body have different electrical properties. The most excitable part of a neuron is the axon hillock but axon and cell body also become excited. At the axon hillock the resting potential is -70 mV and the threshold potential is -55 mV. Synaptic inputs to the neuron result in depolarization causing the membrane potential to rise or fall. Action potential is produced when enough depolarization accumulates and the membrane potential reaches a threshold value.

Mechanism involved in action potential

Action potential is the result of activity of voltage-gated ion channels present in the plasma membrane of a cell. A voltage-gated ion channel is actually a cluster of proteins that remain embedded in plasma membrane and produces action potential because it can give rise to a positive feedback loop. Membrane potential is responsible for controlling the state of ion channels. Action potential is generated when the positive feedback cycle proceeds with full intensity. The time and amplitude are determined by the bio-physical properties of the voltage-gated ion channels. Several types of ion channels are known that produce positive feedback cycles and ultimately result in the production of these potentials. Voltage-gated sodium channels are involved in generation of faster potentials like those of nerve impulse. Slower ones like those produced in the muscle cells are mediated by the calcium ion channels.The most intensively studied voltage-gated ion channels are the sodium ion channels participating in faster nerve impulse conduction.

Alan Hodgkin and Andrew Huxley received Noble Prize for studying the bio-physical basis of action potential. These channels are also referred to as Nav channels where v stands for voltage. The Nav channels occur in three different states namely, deactivated, activated and inactivated. The channel is permeable to the sodium ions only when it is in activated state. Higher is the membrane potential greater is the probability of activation. Once the channel has entered activated state it will automatically become inactivated and finally deactivated after some time. During an action potential most of the sodium ion channels follow the cycle of deactivation, activation, inactivation and deactivation again. Sodium and potassium ions are the principal ions needed for action potential. Sodium ions enter inside, potassium ions leave the cell thus, maintaining equilibrium. Relatively few ions are needed to cross the membrane and ions that fail to cross the membrane are pumped out again, because the sodium-potassium pump always remains in active state. Calcium and chloride ions are also involved in some types of action potentials especially those occurring in the cardiac muscles and in single-celled alga, Acetabularia.

How a neuron looks like

A neuron is composed of one or more dendrites, a soma, a single axon and one or more axon terminals. Dendrites form protrusions in order to join axon terminals which in turn are responsible for storing the neurotransmitters released by the pre-synaptic neurons. They are also equipped with high concentrations of ligand activated channels to communicate with other neurons. These protrusions have a bulbous neck through which they join the main dendrite. The dendrites then join the soma. Soma bears a nucleus which acts as the regulator of the neuron. The surface of soma is packed with voltage-gated ion channels. These channels actively participate in the transmission of signals generated by the dendrites. From the soma emerges the axon hillock which is characterized by the presence of voltage activated sodium channels.

Immediately following the axon hillock is the axon. Axon is a thin protrusion that travels away from the soma. Axon is covered by a myelin sheath which is composed of Schwann cells which acts as an insulator. This insulation prevents significant signal decay as well as ensures faster signal transmission but does not allow any type of voltage-gated ion channel to be present on the surface of axon. Therefore, regularly spaced patches are present on the membrane which lack insulation and are known as nodes of Ranvier. These nodes are also known as mini axon hillocks as their main function is to boost the signal so that signal decay can be prevented. At its farthest end axon loses its insulation cover and begins to branch into several axon terminals that end in axon terminal buttons. These buttons bear voltage activated calcium channels.

Initiation of nerve impulse transmission

The basic requirement for action potential to be produced is that the membrane potential must be above the threshold value so the neurons may fire. They are initiated by the excitatory postsynaptic potentials from the pre-synaptic neuron. These pre-synaptic neurons are responsible for the secretion of the neurotransmitter molecules which then bind to the receptors present on the post-synaptic cells. This binding opens different types of ion channels. Opening of the ion channels changes the permeability of the membrane. If binding increases the voltage then the synapse is said to be excitatory and if it decreases the voltage then it is inhibitory. Some fraction of the excitatory voltage may also reach the axon hillock where it depolarizes the membrane so that a new action potential may be initiated. It is very important that the excitatory potentials from several synapses must work together simultaneously at the same time so that new action potentials may be provoked. Excitable cells are in direct contact with each other through gap junctions and the free flow of ions enables faster transmission. Larger currents do not generate larger potentials. The frequency of the action potential is however dependent upon the intensity of the stimulus.

Sensory neurons and pacemaker potentials

In sensory neurons, external signals like pressure, temperature, light or sound also control opening and closing of the ion channels. The voltage changes may be excitatory or inhibitory. All sensory neurons do not convert these external signals into action potentials as some lack axons but they can convert the signals into neurotransmitters. It can be illustrated by taking the example of retina of the human eye where initial photoreceptor cells, bipolar and horizontal cells play no role in the generation of the action potential but only few amacrine cells and ganglion cells participate in the production of the action potential which later travels towards the optic nerve.

Phases of neurotransmission

The track followed by the action potential can be divided into five phases namely, the rising phase, peak phase, falling phase, undershoot phase and the refractory period. During the rising phase the membrane potential undergoes depolarization and reaches its peak termed as the peak phase. The peak phase is followed by the falling phase characterized by the negative membrane potential which enters the undershoot phase with highest negativity. Finally undershoot phase ends into the refractory period which is a stage at which action potential cannot be provoked. The course of action potential is determined by the combined action of opening and closing of the voltage-gated ion channels in response to the changes in the membrane potential.

Propagation

The action potential generated at the axon hillock propagates in the form of a wave all along the axon. As the current moves forward it depolarizes the adjacent areas of the membrane. If the stimulus is very strong then it also affects the neighboring patches of the membrane to produce action potential. The basic mechanism of nerve impulse propagation was first demonstrated by Alam Lloyd Hodgkin in 1937. There are many types of voltage-activated potassium channels in the neurons which inactivate fast, others inactivate slowly and some do not undergo inactivation at all. All the neuronal voltage-activated sodium channels in general undergo inactivation within milliseconds. The current flowing through the action potential travels in both directions along the axon.

Myelin and saltatory conduction

For faster and efficient transduction of the electrical signals some neurons are covered with myelin sheaths. Myelin is a multilamellar membrane that wraps around the axon except at the nodes of Ranvier. This myelin sheath is produced by the combined activity of the Schwann cells of the peripheral nervous system and the oligodendrites of the central nervous system. This sheath reduces the membrane capacitance and thus, increases the membrane resistance resulting in the faster saltatory movement of the action potential. Myelination is chiefly found in the vertebrates but it has also been observed in shrimps. All neurons in vertebrates are not myelinated for example, axons of the autonomous nervous system. Myelin sheath prevents escape and entry of the ions along the axonal segments and also increases the conduction velocity of the action potential. The mean conduction velocity of an action potential may vary from 1 m/s to 100 m/s.

Termination

Action potentials that reach the synaptic knobs are responsible for the release of neurotransmitters in the synaptic cleft. Neurotransmitters are the molecules that open the ion channels of the post-synaptic cell. The arrival of the action potential results in the opening of the voltage-sensitive calcium channels. The influx of the calcium ions causes the neurotransmitter filled vesicles to migrate towards the cell surface so that their contents can be released in the synaptic cleft. This complex process is inhibited by neurotoxins like tetanospasmin and botulinum that cause tetanus and botulism. Some synapses connect pre-synaptic and post-synaptic cells together. Electrical synapses ensure faster transmission as they do not require slow diffusion of the neurotransmitters across the synaptic cleft. The best examples of the electrical synapses are the escape reflexes of retina of vertebrates.

Cardiac action potentials

The cardiac action potential is different from that produced in a neuron as it has an extended plateau. The plateau is formed by the opening of the calcium ion channels that hold the membrane at the equilibrium potential even when the sodium channels have undergone inactivation. It plays an important role in co-ordinating the contraction of the heart. The cardiac cells of the sinoatrial node produce the pacemaker potential for the synchronization of the heart. The action potential of these cells propagates through the atrioventricular (AV) node which acts as a media for impulse transduction between the atria and the ventricles. The action potential generated in the AV node travels through bundle of His and reaches the Purkinje fibers. Several substances for example, quinidine and beta blockers are known to inhibit the cardiac action potentials.

Muscular action potentials

The action potential initiated in a skeletal muscle cell is similar to that initiated in a neuron. They are provoked by the depolarization of the membrane that result in the opening of the voltage-activated sodium channels which later become inactivated and finally the membrane undergoes repolarization by the releasing potassium ions. The resting potential is generally maintained at -90 mV. The muscle action potential lasts for 2-4 ms and the absolute refractory period is of 1-3 ms with the conduction velocity of 5 m/s. This results in the liberation of calcium ions that are made free from the tropomyosin and finally muscle contraction takes place.

Plant action potentials

Plant and fungal cells are also known to show electrically excitable behavior. The plant action potentials differ from that provoked in an animal cell by the fact that depolarization in the plant cell is not initiated by the uptake of sodium ions but by the release of chloride ions. Release of the potassium ions is a common feature among both types of cells.

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Forensic science is a competitive and challenging field, but if you are truly determined to succeed, you can make this career happen. During college, it will be essential to find a related internship to gain as much hands-on experience as you can. Also, talk to your faculty members about opportunities to sit in on an autopsy or shadow a forensic scientist for a day.