Neuroscience For Kids

Motor Division

Nociceptor
Choroid plexus is the source for cerebrospinal fluid CSF. The stretch of axon between nodes is called an internode. The same is true for chemical stimuli, since TRPA1 appears to detect both mechanical and chemical changes. Blood vessels appear similar in any region of the brain. This is due to the fact that cell bodies of preganglionic neurons are located in the brain stem nuclei, and also in the lateral grey horns of the 2nd through the 4th sacral segments of the spinal cord; hence, the term craniosacral is often used to refer to the parasympathetic division. The spaces between nerve cell bodies with a feltwork of these axonal and dendritic processes, called neuropil which also includes glial cell processes. Gray matter typically contains both many short-axon neurons and a smaller number of long-axon neurons.

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Neuroplasticity

These reactions have allowed us to survive as a species for thousands of years. As is often the case with the human body, the sympathetic system is perfectly balanced by the parasympathetic division, which returns our system to normal following activation of the sympathetic division.

The parasympathetic system not only restores balance, but also performs other important functions in reproduction, rest and sleep, and digestion. Each division uses different neurotransmitters to perform their actions- for the sympathetic nervous system, norepinephrine and epinephrine are the neurotransmitters of choice, while the parasympathetic division uses acetylcholine to perform its duties.

Neurotransmitters of the Autonomic Nervous System Neurotransmitters Sympathetic Nervous System Parasympathetic Nervous System Acetylcholine preganglionic fibers preganglionic fibers; postganglionic fibers at synapses with effector cells cholinergic Norepinephrine postganglionic fibers at synapses with effector cells adrenergic The above chart describes the major neurotransmitters of the sympathetic and parasympathetic divisions.

There are a few special situations that should be noted: Some sympathetic fibers that innervate sweat glands and blood vessels within skeletal muscles release acetylcholine Cells of the adrenal medulla are closely related to postganglionic sympathetic neurons; they secrete epinephrine and norepinephrine, similarly to postganglionic sympathetic neurons Receptors of the ANS The following chart depicts the receptors of the ANS, including their location: Receptors ANS Division Location Adrenergic or Cholinergic Nicotinic receptors parasympathetic ANS both parasympathetic and sympathetic ganglia; muscle cells Cholinergic Muscarinic receptors M2, M3 affect cardiovascular activity parasympathetic M2- located on the heart acted on by acetylcholine ; M3- located on the arterial tree nitric oxide Cholinergic Alpha 1 receptors sympathetic mainly located on blood vessels; mainly located postsynaptically Adrenergic Alpha 2 receptors sympathetic located presynaptically on the nerve terminal; also located distal to synaptic cleft Adrenergic Beta 1 receptors sympathetic lipocytes; conduction system of the heart Adrenergic Beta 2 receptors sympathetic mainly located on arteries coronary and skeletal muscle Adrenergic Agonist and Antagonist In order to understand how certain drugs affect the autonomic nervous system, it is necessary to define certain terms: Sympathetic agonist sympathomimetic - a drug that stimulates the sympathetic nervous system Sympathetic antagonist sympatholytic - a drug that inhibits the sympathetic nervous system Parasympathetic agonist parasympathomimetic - a drug that stimulates the parasympathetic nervous system Parasympathetic antagonist parasympatholytic - a drug that inhibits the parasympathetic nervous system One way to keep the terms straight is to think of the suffix -mimetic as meaning "mimic"; in other words, it mimics the action.

Responses to Adrenergic Stimulation Adrenergic responses in the body are stimulated by compounds that are chemically similar to adrenalin. Norepinephrine, which is released from sympathetic nerve endings, and epinephrine adrenalin in the bloodstream are the most important adrenergic transmitters.

Adrenergic stimulation can have both excitatory and inhibitory effects, depending on the type of receptor on the effector target organ: For example, when faced with a threatening situation, it makes sense that your heart rate and blood pressure will increase, breakdown of glycogen will occur to provide needed energy and your rate of respiration will increase.

All of these are stimulatory effects. On the other hand, if you are faced with a threatening situation, digestion will not be a priority, thus this function is suppressed inhibited. Responses to Cholinergic Stimulation It is helpful to remember that parasympathetic stimulation is, in general, opposite to the effects of sympathetic stimulation at least on organs that have dual innervations- there are always exceptions to every rule. An example of an exception is the parasympathetic fibers that innervate the heart- inhibition causes slowing of the heart rate.

Sympathetic nerves stimulate constriction of blood vessels throughout the alimentary tract, resulting in decreased blood flow to the salivary glands, which in turn causes thicker saliva. Parasympathetic nerves stimulate the secretion of watery saliva. Thus, the two divisions act differently, but in a complementary fashion. Cooperative Effects of Both Divisions Cooperation between the sympathetic and parasympathetic divisions of the ANS can best be seen in the urinary and reproductive systems: Reproductive system- sympathetic fibers stimulate ejaculation of semen and reflex peristalsis in females; parasympathetic fibers cause vasodilation, ultimately resulting in erection of the penis in males and the clitoris in females Urinary system- sympathetic fibers stimulate the urinary urge reflex by increasing bladder tone; parasympathetic nerves promote contraction of the urinary bladder Organs Without Dual Innervation Most organs of the body are innervated by nerve fibers from both the sympathetic and parasympathetic nervous system.

There are a few exceptions: How does the body regulate their action? The body achieves control through increasing or decreasing of the tone of the sympathetic fibers firing rate.

By controlling the stimulation of sympathetic fibers, the action of these organs can be regulated. Stress and ANS When a person is placed in a threatening situation, messages from the sensory nerves are carried to the cerebral cortex and limbic system the "emotional" brain and also to the hypothalamus.

The anterior portion of the hypothalamus excites the sympathetic nervous system. The medulla oblongata contains centers that control many functions of the digestive, cardiovascular, pulmonary, reproductive and urinary systems. The vagus nerve which has both sensory and motor fibers supplies sensory input to these centers through its afferent fibers.

The medulla oblongata is itself regulated by the hypothalamus, the cerebral cortex and the limbic system. Thus there are several areas involved in the body's response to stress. When a person is exposed to extreme stress picture a terrifying situation that occurs without warning, such as a wild animal poised to attack you , the sympathetic nervous system may become completely paralyzed so that its functions cease completely.

The person may be frozen in place, unable to move. They may lose control of their bladder. This is due to an overwhelming number of signals that the brain must "sort" and a corresponding tremendous surge of adrenalin. Thankfully, most of the time we are not exposed to stress of this magnitutude and our autonomic nervous system functions as it should!

It is sometimes caused by failure of baroreceptors to sense and respond to low blood pressure caused by blood pooling in the legs. Horner syndrome- symptoms include decreased sweating, drooping eyelid and pupil constriction affecting one side of the face.

It is caused by damage to the sympathetic nerves that supply the eyes and face. Hirschsprung's disease- also referred to as congenital megacolon, this disorder features dilation of the colon and severe constipation. It is caused by a lack of parasympathetic ganglia in the wall of the colon. Vasovagal syncope- a common cause of fainting, vasovagal syncope occurs when the ANS abnormally responds to a trigger disturbing sights, straining at stool, standing for prolonged periods by slowing the heart rate and dilating the blood vessels in the legs, allowing blood to pool in the lower extremities, resulting in a rapid drop in blood pressure.

Raynaud's phenomenon- this disorder frequently affects young women, causing discoloration of the fingers and toes, and occasionally the ears and other areas of the body. It is caused by extreme vasoconstriction of peripheral blood vessels resulting from hyperactivation of the sympathetic nervous system.

It is often precipitated by stress and cold. Spinal shock- caused by severe injury or damage to the spinal cord, spinal shock may cause autonomic dysreflexia, characterized by sweating, severe hypertension and loss of bowel or bladder control resulting from sympathetic stimulation below the level of the spinal cord injury that is unchecked by the parasympathetic nervous system. Autonomic Neuropathy Autonomic neuropathies are a collection of conditions or diseases that affect sympathetic or parasympathetic neurons or sometimes both.

They may be hereditary present from birth and passed down from an affected parent or acquired later in life. The autonomic nervous system controls many body functions, therefore autonomic neuropathies may cause any number of symptoms and signs that may be elicited through exam or laboratory studies.

Sometimes only a single nerve of the ANS is affected; however, physicians must watch for development of symptoms stemming from involvement of other areas of the ANS. Autonomic neuropathies can cause a wide variety of clinical symptoms.

These symptoms are dependent upon which nerves of the ANS are affected. Symptoms may be widely variable and can affect almost all body systems: Alcoholism- chronic ethanol alcohol exposure may lead to impaired axonal transport and damage to cytoskeletal properties. Alcohol has been shown to be toxic to both peripheral and autonomic nerves. Amyloidosis- in this condition, insoluble proteins are deposited within various tissues and organs; autonomic dysfunction is common in both primary and hereditary amyloidosis.

The immune system wrongfully identifies body tissues as foreign and attempts to destroy them, leading to widespread damage to nerves. Diabetes-neuropathy occurs commonly in diabetes, affecting both sensory and motor nerves; diabetes is the most common cause of AN.

Multiple system atrophy-this is a neurological disorder causing degeneration of nerve cells, causing alterations in autonomic functions and problems with movement and balance. Nerve damage- nerves may be damaged as a result or trauma or surgery, resulting in autonomic dysfunction.

Medications-medications used therapeutically to treat other disorders may affect the ANS. The following are some examples: Drugs that increase sympathetic activity sympathomimetics: Diabetes is by far the largest contributing factor to AN and puts individuals with the disease at high risk for AN. Diabetics can reduce their risk of AN by controlling their blood sugars carefully to prevent damage to their nerves. Smoking, consuming alcohol regularly, hypertension, hypercholesteremia high blood cholesterol and obesity may also increase the risk of developing AN, so these factors should be controlled as much as possible to reduce the risk of developing AN.

Treatment of autonomic dysfunction is largely dependent on the cause of AN. When treatment of the underlying cause is not possible, physicians will attempt various therapies to mitigate symptoms of AN: Integumentary system- itching pruritis may be treated using medications or may be combated by moisturizing the skin, which may be the primary cause of pruritis; hyperalgesia of the skin may be treated with medications such as gabapentin, a medication used to treat neuropathy and nerve pain.

Cardiovascular system-symptoms of orthostatic hypotension may be improved by wearing compression stockings, increasing fluid intake, increasing salt in the diet and medications that regulate blood pressure i.

Tachycardia may be treated with beta blockers. Patients should be counseled to avoid sudden position changes. Gastrointestinal system- patients may be counseled to eat small, frequent meals if they have gastroparesis. Medications may sometimes be helpful in increasing motility i. Increasing fiber in the diet may help with constipation. Bowel retraining is also sometimes helpful for the treatment of bowel issues.

Map expansion, the fourth type of neuroplasticity, entails the flexibility of local brain regions that are dedicated to performing one type of function or storing a particular form of information. This phenomenon usually takes place during the learning and practicing of a skill such as playing a musical instrument.

Specifically, the region grows as the individual gains implicit familiarity with the skill and then shrinks to baseline once the learning becomes explicit.

Implicit learning is the passive acquisition of knowledge through exposure to information, whereas explicit learning is the active acquisition of knowledge gained by consciously seeking out information. But as one continues to develop the skill over repeated practice, the region retains the initial enlargement.

Map expansion neuroplasticity has also been observed in association with pain in the phenomenon of phantom limb syndrome. The relationship between cortical reorganization and phantom limb pain was discovered in the s in arm amputees. Later studies indicated that in amputees who experience phantom limb pain, the mouth brain map shifts to take over the adjacent area of the arm and hand brain maps.

In some patients, the cortical changes could be reversed with peripheral anesthesia. Some of the earliest applied research in neuroplasticity was carried out in the s, when scientists attempted to develop machines that interface with the brain in order to help blind people. The machine consisted of a metal plate with vibrating stimulators. A camera was placed in front of the patient and connected to the vibrators.

The camera acquired images of the room and translated them into patterns of vibration, which represented the physical space of the room and the objects within it. After patients gained some familiarity with the device, their brains were able to construct mental representations of physical spaces and physical objects.

Thus, instead of visible light stimulating their retinas and creating a mental representation of the world, vibrating stimulators triggered the skin of their backs to create a representation in their visual cortices. A similar device exists today, only the camera fits inside a pair of glasses and the sensory surface fits on the tongue. Today neuroscientists are developing machines that bypass external sense organs and actually interface directly with the brain.

For example, researchers implanted a device that monitored neuronal activity in the brain of a female macaque monkey. Thus, the monkey became capable of moving a robot arm with its thoughts. This means that the motor cortex does not control the details of limb movement directly but instead controls the abstract parameters of movement, regardless of the connected apparatus that is actually moving. For humans, however, less-invasive forms of brain-computer interfaces are more conducive to clinical application.

For example, researchers have demonstrated that real-time visual feedback from functional magnetic resonance imaging fMRI can enable patients to retrain their brains and therefore improve brain functioning. Patients with emotional disorders have been trained to self-regulate a region of the brain known as the amygdala located deep within the cerebral hemispheres and believed to influence motivational behaviour by self-inducing sadness and monitoring the activity of the amygdala on a real-time fMRI readout.

Stroke victims have been able to reacquire lost functions through self-induced mental practice and mental imagery. This kind of therapy takes advantage of neuroplasticity in order to reactivate damaged areas of the brain or to deactivate overactive areas of the brain. Today researchers are investigating the efficacy of these forms of therapy for individuals who suffer not only from stroke and emotional disorders but also from chronic pain, psychopathy, and social phobia.

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