K.+NERVOUS+SYSTEM

NERVOUS SYSTEM



__OVERVIEW __
Neurons consist of three parts, the cell body, dendrites, and an axon. Dendrites and axons project from the cell body and can also be called processes. The cell body, which contains a nucleus, is the largest part of a neuron. Also found in the cell body are Nissle bodies. Nissle bodies are areas of Rough ER. When cell bodies are in the central nervous system, they can be found in groups called nuclei. When they are in the peripheral nervous system they are found in groups called ganglia. Dendrites project from the cell body and resemble this tree branches. The dendrites are responsible for taking impulses away from the cell body. Axons can be both very short or very long depending of their final destination in the body. The starting point of the axon, near the cell body, is called the axon hillock. There may also be branches that come off the axon which are called axon collaterals. Now that you know the basic structure of the neuron, we talk about what the neuron does.

Neurons can be identified by either their structure or function. When neurons are identified by their function it all has to do with where their impulses are being sent. Sensory or afferent neurons send their impulses to the central nervous system. Motor or efferent neurons, on the other hand, send their impulses our of the central nervous system and to the intended muscles and glands. Association neurons or interneurons are only found inside the central nervous system and only send their impulses within the central nervous system. Reflexes and voluntary control of the muscles are controlled by somatic motor neurons. Involuntary actions of the smooth muscle, cardiac muscle, and glands are controlled y the autonomic motor neurons. Both sympathetic and parasympathetic neurons are considered autonomic neurons. When identifying a neuron by its structure you look at how many processes project from the cell body. Pseudounipolar neurons that have one process that turns into two. It is called pseudounipolar because at the earliest stages of life it starts with two processes. Pseudounipolar neurons are sensory neurons. Bipolar neurons, located in the retina, have two processes. Finally, multipolar neurons have one axon with several dendrites. An example of a multipolar neuron would be a motor neuron.JM

__SUMMARY __
The nervous system is divided into the central nervous system and the peripheral nervous system. The CNS includes the

brain and spinal cord. The PNS includes the cranial nerves arising from the brain and the spinal nerves arising from the

spinal cord. The nervous system is also composed of only two principal types of cells called neurons and supporting cells.

=__ Neurons __=

Neurons are the basic structural and functional units of the nervous system. They respond to physical and chemical

stimuli, conduct electrochemical impulses, and release chemical regulators. With these activities, neurons enable the

perception of sensory stimuli, learning, memory, and the control of muscles and glands. Many neurons can regenerate

a severed portion or sprout small new branches under certain conditions but most neurons cannot divide by mitosis.

Neurons vary in size and shape but have three regions. 1. cell body. 2. dendrites. 3. axon.

__** Cell Body **__ : the enlarged portion of the neuron that contains the nucleus. Called the nutritional center where

macromolecules are produced. Contains densely staining areas of rough ER known as Nissl bodies not found anywhere

else. Cell bodies in the CNS are clustered into groups called nuclei. Cell bodies in the PNS are clusters called ganglia.

__** Dendrites **__ : thin, branched processes that extend from the cytoplasm of the cell body. Provide a receptive area that

transmits electrical impulses to the cell body.

__** Axon **__ : longer process than the dendrite process that conducts impulses away from the cell body. Vary in length from only

a millimeter long to up to a meter or more. The origin of the axon in the CNS is an expanded region called axon hillock

where nerve impulses originate. Axon collaterals are side branches that may extend from the axon. Axoplasmic flow and

Axonal transport are the two mechanisms that rapidly move proteins and molecules through the axon.



= Classification of Neurons and Nerves =

__** Sensory neuron (afferent neuron): **__ transmit impulses from a sensory receptor into the CNS.

__** Motor neuron (efferent neuron): **__ transmits impulses from the CNS to an effector organ such as a muscle.

__** Association neuron (interneuron): **__ multipolar neuron located entirely within the CNS.

__** Somatic motor neurons: **__ nerve that is responsible for both reflex and voluntary control of skeletal muscles.


 * __ Autonomic motor neruons: __** nerve that stimulates contraction of smooth muscle and cardiac muscle and that stimulates

glandular secretion. May also inhibit contraction.

__** Pseudounipolar neurons: **__ single, short process that branches like a T to form a pair of longer processes.

__** Bipolar neurons: **__ have two processes at either end and is typically found in the retina of the eye.


 * __ Multipolar neurons: __** most common, have several dendrites and one axon extending from the cell body.

__** Nerve: **__ bundle of axons located outside the CNS. Most have both motor and sensory fibers and are then called mixed

nerves. Some of the cranial nerves only consist of sensory fibers, which serve as the special senses: sight, hearing, taste

and smell.

= Supporting Cells = Supporting cells aid in the function of neurons and are about 5 times more abundant than neurons. Can divide by mitosis. Supporting cells are derived from the same embryonic tissue layer that produces neurons. In the peripheral nervous system there are two types and in the central nervous system there are four types that are also known as neuroglial or glial cells. Listed below are the different types.

PNS supporting cells
__** Schwann Cells: **__ form myelin sheaths around peripheral axons __** Satellite Cells **__or ganglionic gliocytes: support neuron cell bodies within the ganglia of the PNS. PLEASE CLICK ON PICTURE AND VISIT LINK FOR MORE INFO AND TUTORIALS REGARDING SUPPORTING CELLS.

__** ﻿ CNS supporting cells **__
__** Oligodendrocytes: **__ form myelin sheaths around axons of the CNS. __** Microglia: **__ migrate through the CNS and phagocytose foreign and degenerate material. __** Astrocytes: **__ help regulate the external environment of neurons in the CNS. __** Ependymal cells: **__ line the ventricles of the brain and the central canal of the spinal cord.

//__** Functions of the supporting cells **__//

 * Schwann Cells: PNS ;** Surround axons of all peripheral nerve fibers, forming a neuroilemmal sheath aka sheath of Schwann; wrap around many peripheral fibers to form myelin sheaths aka neurolemmocytes.


 * Satellite Cells: PNS **; support functions of neurons within sensory and autonomic ganglia, aka ganglionic gliocytes.

** Microglia: CNS **; phagocytose pathogens and cellular debris in the CNS.
 * **** ﻿ **** ﻿ **** ﻿ **** ﻿ **** ﻿Oligodendrocytes: CNS **; form myelin sheaths around central axons, producing "white matter" of the CNS.
 * Astrocytes: CNS **; cover capillaries of the CNS and induce the blood-brain barrier; interact metabolically with neurons and modify the extracellular environment of neurons
 * Ependymal Cells: CNS **; form the epithelial lining of brain cavities and the central canal of the spinal cord; cover tufts of capillaries to for choroid plexuses, which are structures that produce cerebrospinal fluid.

=**__ MONOAMINES AS NEUROTRANSMITTERS __**= Monoamines consist of regulatory molecules known as epinephrine, norepinephrine, dopamine and serotonin. Serotonin is derived from tryptophan, while the other molecules are derived from tyrosine and form a subfamily of monoamines called catecholamines. Monoamine neurotransmitters are released by exocytosis from presynaptic vesicles and diffuse across the synaptic cleft then interact with specific receptor proteins in the membrane of the postsynaptic cell. The stimulatory effects of monoamines must be quickly inhibited so as to maintain proper neural control. The action of these are stopped at the synapse by reuptake of the neurotransmitter molecules from the synaptic cleft into the presynaptic axon terminal and then degradation of the monoamine by an enzyme within the axon terminal called monoamine oxidase (MAO). Illustrated above is the process of exocytosis.

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[] Amanda Rolstad Sources: Fox, Stuart Ira. (2009). //Human Physiology//. New York, NY: McGraw-Hill.
 * ~ Name ||~ Type ||~ Postsynaptic Effect ||~ Location(s) ||~ Function(s) ||
 * [|Dopamine] || Amine || Excitatory || Brain, smooth muscle || Control arousal levels ||
 * [|Serotonin] || Amine || Excitatory || Brain, smooth muscle || Effects on mood, sleep, pain, appetite ||
 * [|Noradrenaline] || Amine || Excitatory || Brain, smooth muscle || Induce arousal, heighten mood ||
 * [|Acetylcholine (ACh)] || Acetic acid || Excitatory & Inhibitory || Parasymathetic nervous system, brainstem || Role in memory, vasodilation ||
 * [|GABA][|§] || amino acid || Inhibitory || Brain || Control anxiety level ||
 * [|Enkephalin (opiate)] || Neuropeptide || Inhibitory || Brain, spinal cord || Reduce stress, promote calm, natural painkiller ||

__ESSENTIAL QUESTIONS __

**Describe how the dendrite or cell body of the postsynaptic neuron is stimulated to send an impulse from the axon hillock to the rest of the neuron.**
Dendrites receive stimuli from other nerves and transmit them through the neuron to the axon. The axon then conducts impulses to the dendrite of another cell. In the first stage of starting an impulse, axon terminals open their voltage-gated Ca2+ channels. The opening of these channels cause neurotransmitters to be released, these neurotransmitters may excite or inhibit the following neurons.The release of these neurotransmitters will diffuse across an area called the synaptic cleft. The synaptic cleft is an area that separates two neurons from each other. Once the neurotransmitters go through the synaptic cleft, they attach themselves to specific receptors on a dendrite or cell body of the postsynaptic neruon. The attachment of the neurotransmitters (chemicals, for ex. acetylcholine which is a common excitatory neurotransmitter) to these certain areas are called ligand-gated channels. This attachment will cause the "gate" to open, and Na+ will enter the neuron and cause depolarization (EPSP). This depolarization then causes the opening of Na+ voltage-gated channels and then K+ channels in the axon hillock. This all leads to the conduction of the action potential to the next neuron and this action potential will continue until it reaches its effector.



**Describe the sequence of events that occur to get an action potential to stimulate the release of neurotransmitters from the presynaptic axon. What happens when the neuron is inhibited?**
First, I am going to tell you what happens to the neuron cell when it goes through a complete action potential cycle. For an action potential in a neuron to begin it must be stimulated to the threshold of -55mv, while the resting membrane potential of a neuron is -70mv. When the neuron is stimulated, Na+ enters by diffusion into the neuron via the Na+ gates. This inward movement of Na+ causes a voltage change in the neuron and it depolarizes to -55mv. Once it hits the -55mv (threshold for an action potential), the Na+ gate closes and no more Na+ is allowed into the neuron (cell). Once the neuron's membrane is at the threshold of -55mv, it begins the stage of re-polarization by opening the K+ gates and K+ flows into the cell and Na+ via the Na+/K+ pump is moved out of the cell. This continues until the cell becomes hyper-polarized, which means that it is now more negative than the resting membrane potential of -70mv. Now, I am going to tell you about what happens to the action potential when a neuron has been stimulated to its threshold of -55mv. The action potential (impulse) moves down the axon to the axon terminals, where it causes the voltage-gated Ca2+ channels to open and Ca2+ enters the the cytoplasm of the axon terminal. The Ca2+, then bonds with a sensor protein in the cytoplasm (believed to be synaptotagmin) in the axon terminal. The bonding of the Ca2+ with the sensor protein, alters the docking location at the end of the neuron, where the synaptic vesicles are docked and they release their neurotransmitters. The release of neurotransmitters from the axon terminal of a pre-synaptic neuron into the space between the two neurons called the synaptic cleft and to the post-synaptic neuron occurs through exocytosis. If a neuron is inhibited, it means that stimulation to that neuron did not meet the threshold of -55mv and therefore no action potential will be generated. It will remain "quiet".

http://faculty.washington.edu/chudler/gif/actionp1.gif

Sources:
Fox, Stuart Ira. (2009). //Human Physiology//. New York, NY: McGraw-Hill.

__SUMMARY __ Stimulation all starts with an action potential in the axon. The axon in the presynaptic neuron releases a neurotransmitter that binds to a receptor protein located in the postsynaptic neuron. A neurotransmitter is released when the membranes of the vesicle and the axon join together in a process called exocytosis. The release of the neurotransmitter is triggered by the influx of Ca+ into the axon by way of the voltage-gated Ca+ channels. This means there are more synaptic vesicles going through exocytosis which means there are more neurotransmitters being released. The more action potentials there are in the presynaptic axon, the more stimulation there is in the postsynaptic neuron. The ligand of the receptor protein the part of the protein that is specifically designed for that particular neurotransmitter. When the ligand and the neurotransmitter bind together ion channels in the postsynaptic neuron are caused to open. We call theses channels ligand regulated or chemically regulated gates. Voltage-gated channels, which open due to depolarization, are found mostly in the axons. Chemically or ligand regulated gates, which respond to postsynaptic receptor proteins and neurotransmitter ligands binding together, are found mainly in the postsynaptic membrane. Depolarization is often a product of a chemical or ligand regulated gate. When this depolarization happens it is called excitatory postsynaptic potential or EPSP. EPSP happens because the membrane potential is moving closer to an action potential. EPSPs are created in the dendrite when there is a synapse between an axon and a dendrite. The EPSPs must initialize the production of an action potential in the axon, where there is a lot of voltage-gated Na+ and K+ channels. How many action potentials will be fired by the axon will depend on the amount of depolarization by the EPSPs. When a cell experiences hyperpolarization it causes the neuron to have a more difficult time to produce an action potential because the membrane potential ends up farther away from the threshold required. This is also called an inhibitory postsynaptic potential or IPSP. EPSPs and IPSPs are antagonistic of each other. Once an action potential has been produced they will continue to regenerate themselves. They are an all or nothing deal. Once an action potential has been sent there is no turning back. Resting membrane potential for a neuron is -70mV. During resting membrane potential the charge inside the membrane has a more negative charge than the outside of the membrane. The Na+/K+ pumps play a large role in maintaining resting membrane potential. For every two K+ ions that are being let in the membrane, the pump allows three Na+ ions out thus creating a larger amount of Na+ outside the cell and more K+ inside the cell. When the neuron experiences an influx of Na+, depolarization occurs. When the threshold is met the voltage-gated Na+ channels will open allowing a large amount of Na+ to enter the cell. As depolarization continues even more Na+ channels will open causing the membrane potential to go all the way from -70mV to +30mV. After the cell has undergone depolarization it will then go through repolarization. During repolarization the voltage-gated Na+ channels that were previously open for depolarization will quickly shut. Now the voltage-gated K+ channels will open and the K+ will quickly leave the cell due to the electrochemical gradient, this will cause the neuron to return to it's resting membrane potential.JM

__APPLICATION __ As a nurse we will all be working with **MAO (monoamine oxidase) inhibitors**. It is important to understand how these work because not only will we be administering them but we will also need to be careful for the many drugs that cannot be given with them.

MAO inhibitors are drugs that block monoamine oxidase from degrading monoamine neurotransmitters. Since MAO inhibitors prevent the breakdown of monoamine, there is an increased amount of neurotransmitters in the synaptic cleft, which promotes their effects on the body.

MAO inhibitors treat conditions which can be serious without treatment. They are helpful in the treatment of //depression//. This would suggest that there is a deficiency in monoamine neurotransmission with depression. They are also used to treat //Parkinson's Disease//. MAO inhibitors enhance the action of dopamine at the synapse.

A serious side effect we will need to watch for as nurses from MAO inhibitors is a severe hypertensive crisis. This can also be provoked by a diet that is high in tyramine. Tyramine can be found in cheese, preserved meat, certain fish and some other foods. JD If I were a nurse that was going to be working with surgical patients I would need to know that the numbing happens due to the fact that action potentials can not be produced because the membrane is not able to complete the depolarization cycle. JM



http://upload.wikimedia.org/wikipedia/commons/thumb/c/cd/MonoamineOxidase-1GOS.png/220px-MonoamineOxidase-1GOS.png

__CASE STUDY __ **[|The Soccer Mom: A Case Study on the Nervous system]** __**Part One: At the Soccer Game **__ **1.What problems does Phyllis seem to be experiencing? ** Phyllis’ husband mentioned that she has had a lack of concentration at work and forgot to pick up the kids one day last week. Today she has had fainting spells, and feels unfocused and disorientated. **2. Which of these problems could be caused by dehydration? ** Fainting, being unfocused and disorientated can be caused from dehydration. **3. Which of these problems might make you consider that there’s something more going on? Why?** Fainting would make me think that something more serious was going on. With a low blood pressure an individual may experience syncope. Fainting results from an overstimulation of the autonomic nervous system that results in a drop in blood pressure and a slowed heart rate. **4. Suppose Phyllis does have a more serious problem. Can you think of any neurological problems that could be the cause of these symptoms? ** <span style="font-family: 'Times New Roman',Times,serif; font-size: 110%;">Multiple Sclerosis and Parkinson’s disease.

__**<span style="font-family: 'Times New Roman',Times,serif; font-size: 110%;">Part Two: The Doctor Visit **__

<span style="font-family: 'Times New Roman',Times,serif; font-size: 110%;">A new symptom Phyllis mentioned is that her fingers are going numb sometimes.
 * <span style="font-family: 'Times New Roman',Times,serif; font-size: 110%;">1. What new signs or symptoms have been revealed? **

<span style="font-family: 'Times New Roman',Times,serif; font-size: 110%;">Yes, her symptoms of being fatigued and being unable to concentrate can be attributed to depression.
 * <span style="font-family: 'Times New Roman',Times,serif; font-size: 110%;">2. Could any of Phyllis’s symptoms be attributed to depression? If so, which? **

<span style="font-family: 'Times New Roman',Times,serif; font-size: 110%;">A decrease in monoamine transmission can contribute to clinical depression.
 * <span style="font-family: 'Times New Roman',Times,serif; font-size: 110%;">3. What neurotransmitters are thought to be involved in depression? **

<span style="font-family: 'Times New Roman',Times,serif; font-size: 110%;">Multiple sclerosis and Parkinson’s disease are debilitating diseases where individuals are unable to have motor function and end up in a wheelchair.
 * <span style="font-family: 'Times New Roman',Times,serif; font-size: 110%;">4. What neurological disorders could have put her grandfather in a wheelchair? **

<span style="font-family: 'Times New Roman',Times,serif; font-size: 110%;">Multiple sclerosis. Symptoms can vary, but include weakness and fatigue and sensory disturbances of the limbs. <span style="font-family: 'Times New Roman',Times,serif; font-size: 110%;">Parkinson’s disease. Symptoms can include postural instability or impaired balance and coordination, and possibly depression.
 * <span style="font-family: 'Times New Roman',Times,serif; font-size: 110%;">5. Could any of these neurological disorders explain one or more of Phyllis’ symptoms? **

<span style="font-family: 'Times New Roman',Times,serif; font-size: 110%;">Parkinson’s disease is an inherited disease. Multiple sclerosis is not an inherited disease, but a variation in genetics has been shown to increase the risk of developing the disease.
 * <span style="font-family: 'Times New Roman',Times,serif; font-size: 110%;">6.Could Phyllis have inherited any of these disorders? **

<span style="font-family: 'Times New Roman',Times,serif; font-size: 110%;">Neurological testing that tests mental status, cranial nerve function, strength, coordination, reflexes and sensation. This information can help to determine if a problem exists and the clinical location.
 * <span style="font-family: 'Times New Roman',Times,serif; font-size: 110%;">7. If you were in Dr. Warner’s position, what tests might you suggest to confirm (or not) this diagnosis? **

__**<span style="font-family: 'Times New Roman',Times,serif; font-size: 110%;">Part Three: Diagnostic Tests **__


 * <span style="font-family: 'Times New Roman',Times,serif; font-size: 110%;">1. Test your knowledge of the function of chemical synapses by filling in the flow diagram to the right. **



Excitatory postsynaptic potential, axon hillock, sodium, threshold, adjacent (NM), nodes of Ranvier (M), synapse

<span style="font-family: 'Times New Roman',Times,serif; font-size: 110%;">Myelin is either a Schwann cell or an oligodendrocyte.
 * <span style="font-family: 'Times New Roman',Times,serif; font-size: 110%;">1. What type of cell is myelin? **

<span style="font-family: 'Times New Roman',Times,serif; font-size: 110%;">It covers and insulates the axons of neurons.
 * <span style="font-family: 'Times New Roman',Times,serif; font-size: 110%;">2. What is the function of myelin in nerve cells? **

<span style="font-family: 'Times New Roman',Times,serif; font-size: 110%;">Once an action potential is generated, consequent action potentials are generated in the Nodes of Ranvier.
 * <span style="font-family: 'Times New Roman',Times,serif; font-size: 110%;">3. In myelinated axons, where are action potentials generated? **

<span style="font-family: 'Times New Roman',Times,serif; font-size: 110%;">Voltage gated sodium channels are highly concentrated in the nodes of Ranvier.
 * <span style="font-family: 'Times New Roman',Times,serif; font-size: 110%;">4. Where, then, are voltage gated sodium channels concentrated in myelinated axons? **

<span style="font-family: 'Times New Roman',Times,serif; font-size: 110%;">Multiple sclerosis is a chronic and degenerating disease that progressively destroys the myelin sheaths of neurons in the CNS. The myelin sheaths harden into scleroses which prohibits the normal conduction of impulses thus resulting in a progressive loss of functions.
 * <span style="font-family: 'Times New Roman',Times,serif; font-size: 110%;">5. What happens to myelin in people who suffer from multiple sclerosis? **

<span style="font-family: 'Times New Roman',Times,serif; font-size: 110%;">The presence of myelin basic protein in the cerebrospinal fluid indicates a breakdown of the central nervous system myelin.
 * <span style="font-family: 'Times New Roman',Times,serif; font-size: 110%;">6. Why is there an elevated level of myelin basic protein in the cerebrospinal fluid? **

<span style="font-family: 'Times New Roman',Times,serif; font-size: 110%;">The myelin sheaths that normally conduct the action potentials from one node to the next are unable to conduct the impulses. The impulses slow down and eventually stop conducting through the neurons.
 * <span style="font-family: 'Times New Roman',Times,serif; font-size: 110%;">7. What would be the effect on action potential conduction at a region of axon where the disease had its effect? **

<span style="font-family: 'Times New Roman',Times,serif; font-size: 110%;">Finger movement and control would be decreased, because the message our brain is sending to our fingers is not getting to them. The coordination for activities such as writing, crocheting, or even picking up objects would decrease.
 * <span style="font-family: 'Times New Roman',Times,serif; font-size: 110%;">8. What effect would this have on the coordination of movements if this took place in areas involved in motor control of finger movements? **

<!--[if gte mso 10]> __**<span style="font-family: 'Times New Roman',Times,serif; font-size: 110%;">Part Four: The Diagnosis **__

I think that because the myelin sheaths are gradually demyelinated, the sodium channels will also gradually decrease their output of sodium because of the decrease in impulses, decreases the action potentials of the neuron.
 * 1. During remission, axons affected by the disorder regain their function. If voltage-gated sodium channels are concentrated in certain regions of the myelinated axon prior to the disease, what do you think happens to these sodium channels after multiple sclerosis has had its effect? **

Physical therapy can help with returning function after an attack and prevent new attacks. It can also help with preventing disability by keeping the body in motion as long as possible. The weekly interferon beta injections will be effective in decreasing new attacks in relapsing-remitting MS. She may be experiencing a relapse now, so the corticosteroids are effective short term for the relief of symptoms.
 * 2. How would these three treatments (physical therapy, weekly injections of interferon beta, and corticosteroids) help to control Phyllis’s symptoms? **

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[] Multiple_sclerosis Fox, Stuart Ira. (2009). //Human Physiology//. New York, NY: McGraw-Hill.
 * Sources:**