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Neurotransmitter 3D Animation
on Tuesday, December 21, 2010




Neurotransmitters are endogenous chemicals which transmit signals from a neuron to a target cell across a synapse. Neurotransmitters are packaged into synaptic vesicles clustered beneath the membrane on the presynaptic side of a synapse, and are released into the synaptic cleft, where they bind to receptors in the membrane on the postsynaptic side of the synapse. Release of neurotransmitters usually follows arrival of an action potential at the synapse, but may also follow graded electrical potentials. Low level "baseline" release also occurs without electrical stimulation. Neurotransmitters are synthesized from plentiful and simple precursors, such as amino acids, which are readily available from the diet and which require only a small number of biosynthetic steps to convert. The chemical identity of neurotransmitters is often difficult to determine experimentally. For example, it is easy using an electron microscope to recognize vesicles on the presynaptic side of a synapse, but it may not be easy to determine directly what chemical is packed into them. The difficulties led to many historical controversies over whether a given chemical was or was not clearly established as a transmitter. In an effort to give some structure to the arguments, neurochemists worked out a set of experimentally tractable rules. According to the prevailing beliefs of the 1960s, a chemical can be classified as a neurotransmitter if it meets the following conditions: * There are precursors and/or synthesis enzymes located in the presynaptic side of the synapse. * The chemical is present in the presynaptic element. * It is available in sufficient quantity in the presynaptic neuron to affect the postsynaptic neuron; * There are postsynaptic receptors and the chemical is able to bind to them. * A biochemical mechanism for inactivation is present. There are many different ways to classify neurotransmitters. Dividing them into amino acids, peptides, and monoamines is sufficient for some classification purposes. Major neurotransmitters: * Amino acids: glutamate, aspartate, D-serine, γ-aminobutyric acid (GABA), glycine * Monoamines and other biogenic amines: dopamine (DA), norepinephrine (noradrenaline; NE, NA), epinephrine (adrenaline), histamine, serotonin (SE, 5-HT), melatonin * Others: acetylcholine (ACh), adenosine, anandamide, nitric oxide, etc. In addition, over 50 neuroactive peptides have been found, and new ones are discovered regularly. Many of these are "co-released" along with a small-molecule transmitter, but in some cases a peptide is the primary transmitter at a synapse. β-endorphin is a relatively well known example of a peptide neurotransmitter; it engages in highly specific interactions with opioid receptors in the central nervous system. Single ions, such as synaptically released zinc, are also considered neurotransmitters by some[by whom?], as are some gaseous molecules such as nitric oxide (NO) and carbon monoxide (CO). These are not classical neurotransmitters by the strictest definition, however, because although they have all been shown experimentally to be released by presynaptic terminals in an activity-dependent way, they are not packaged into vesicles. By far the most prevalent transmitter is glutamate, which is excitatory at well over 90% of the synapses in the human brain. The next most prevalent is GABA, which is inhibitory at more than 90% of the synapses that do not use glutamate. Even though other transmitters are used in far fewer synapses, they may be very important functionally—the great majority of psychoactive drugs exert their effects by altering the actions of some neurotransmitter systems, often acting through transmitters other than glutamate or GABA. Addictive drugs such as cocaine and amphetamine exert their effects primarily on the dop

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Cystic fibrosis is a disease passed down through families that causes thick, sticky mucus to build up in the lungs, digestive tract, and other areas of the body. It is one of the most common chronic lung diseases in children and young adults. It is a life-threatening disorder.

M.Torabi Nami MD, PhDc Department of Neuroscience Institute for Cognitive Science Studies (ICSS), Tehran 15948 Iran Torabi_m@iricss.org Abstract Sleepiness, tiredness and fatigue are complaints which must be thoroughly analyzed to eliminate blur and ambiguity. Physiological sleepiness (“sleep pressure”) increases while being awake and additionally underlies the circadian rhythm with a lower threshold to fall asleep during night time. Excessive daytime sleepiness (EDS) is considered normal only after sleep deprivation. Clinically, EDS manifests by frequents daytime napping and/or reduced alertness with automatic behavior or - in its extreme form - in recurrent attacks of sudden, uncontrollable compulsion to sleep also in inappropriate situations (= “sleep attacks”). EDS is “objectively” addressed by measuring the mean sleep latency to four to five nap opportunities throughout the day using the multiple sleep latency test (MSLT) or the maintenance of wakefulness test (MWT). EDS denotes both, a ready entrance into sleep as well as difficulty in staying awake during daytime or accordingly in inappropriate situations. These two partially independent aspects of EDS are separately assessed by the “passive” MSLT and the “active” MWT respectively. For that reason the MSLT and MWT only weakly correlate with each other when tested over a broad range of patients with EDS. It is important to keep in mind, that these tests are importantly influenced by a great variety of factors such as mood, anxiety, and motivation. “Vigilance” comprises wakefulness, alertness and attention and therefore is more than just the reciprocal to sleepiness. Cognitive performance tasks such as Steer Clear Reaction Time Test (SCRTT) or driving simulators require the complete integrity of vigilance to achieve normal results. Hypersomnia is usually broadly defined as the combination of abnormally prolonged night-time sleep (regularly >10 h) with EDS during ≥1 months. On the other hand, the term hypersomnia has also been used in a narrower scene for the isolated abnormality of a prolonged night-time sleep need (>10 h). “Tiredness”, also in colloquial language often used for sleepiness, in a broader sense also describes the feeling of lack of energy, motivation and initiative. These patients seek rest rather than sleep. They often cannot fall asleep when given the opportunity in spite of feeling tired, and hence, in an MSLT, do not show an abnormally short sleep latency. Furthermore, tiredness (and fatigue) as opposed to sleepiness has a mental (“central”) and physiological (bodily or “peripheral”) component, which the patients can readily distinguish. Patients with insomnia, mild sleep apnea syndrome, or depression rather suffer from mental tiredness than sleepiness during the day. The simple subjective self-assessment using the Epworth Sleepiness Scale (ESS) quite reliably differentiates between sleepiness and mental tiredness (without sleepiness), which makes it a widely used test. The term “fatigue” is also heterogeneously used. In physiology the “fatigue” implied a “time on task performance decrement” to describe decreasing muscle force during a sustained physical effort. In clinical medicine one distinguishes physical (“peripheral”) from mental (“central”) fatigue and the term usually denotes a chronic and more abnormal situation than tiredness. In a broad sense “fatigue” implies a deficiency in coping satisfactorily with mental and physical work load. The chronic fatigue syndrome entails both mental as well as a physical fatigue (so called “leaden paralysis” of limbs). Depressive states are often associated with insomnia and fatigue, but there are also cases with hypersomnia rather than insomnia ( non organic hypersomnia , “atypical depression” or “hypersom

The importance of being fully informed about serious heart conditions like atrial fibrillation

Holoprosencephaly (HPE, once known as arhinencephaly) is a cephalic disorder in which the prosencephalon (the forebrain of the embryo) fails to develop into two hemispheres. Normally, the forebrain is formed and the face begins to develop in the fifth and sixth weeks of human pregnancy. The condition also occurs in other species, as with Cy, the Cyclops kitten.

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Lo Que Todos Necesitan Saber Sobre La Presión Arterial Alta

Si le han dicho que tiene presión arterial alta, usted puede decir, "Pero me siento muy bien!" Esto se debe a que la hipertensión o la presión arterial alta no tiene síntomas visibles. Es por eso que se la describe a menudo como el "asesino silencioso". No hay achaques o limitaciones físicas sólo porque tiene la presión arterial alta. Entonces, por qué siquiera preocuparse?

La hipertensión afecta a uno de cada tres adultos estadounidenses, y muchas de estas personas ni siquiera saben que la tienen. Además, aquellos con presión arterial alta tienen también un mayor riesgo de tener el colesterol alto.

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The incidence of digitalis toxicity has declined in recent years, due to decreased use of this drug along with improved technology for monitoring of drug levels and increased awareness of drug interactions. Nevertheless, cardiac glycoside toxicity continues to be a problem in the United States because of the wide use of digoxin (a preparation of digitalis) and its narrow therapeutic window. Digitalis is a plant-derived cardiac glycoside commonly used in the treatment of chronic heart failure (CHF), atrial fibrillation, and reentrant supraventricular tachycardia.[1, 2] Digoxin is the only available preparation of digitalis in the United States. (See Etiology and Epidemiology.) Cardiac glycosides are found in certain flowering plants, such as oleander and lily-of-the-valley. Indigenous people in various parts of the world have used many plant extracts containing cardiac glycosides as arrow and ordeal poisons. The ancient Egyptians used squill (Urginea maritime) as a medicine. The Romans employed it as a diuretic, heart tonic, emetic, and rat poison. Digitalis, or foxglove, was mentioned in the year 1250 in the writings of Welsh physicians. Fuchsius described it botanically 300 years later and named it Digitalis purpurea. William Withering published his classic account of foxglove and some of its medical uses in 1785, remarking upon his experience with digitalis. He recognized many of the signs of digitalis toxicity, noting, "The foxglove, when given in very large and quickly repeated doses, occasions sickness, vomiting, purging, giddiness, confused vision, objects appearing green or yellow; increased secretion of urine, slow pulses, even as low as 35 in a minute, cold sweats, convulsions, syncope, death." (See Presentation and Workup.) During the early 20th century, as a result of the work of Cushny, Mackenzie, Lewis, and others, the drug was gradually recognized as specific for treatment of atrial fibrillation. Only subsequently was the value of digitalis for treatment of CHF established. Cardiac glycosides enhance cardiac contractility and slow conduction through the atrioventricular (AV) junction by increasing vagal tone.[3] (See Etiology.) Cardiac glycoside toxicity has been known to result from ingestion of some plants, including yellow oleander (Thevetia peruviana) and foxglove, and a similar toxidrome has been associated with the use of herbal dietary supplements that contain cardiac glycosides. Digoxin is among the top 50 prescribed drugs in the United States.[4] In 2011, the American Association of Poison Control Centers reported 1601 single exposures to cardiac glycoside drugs.[5] Cardiac glycosides account for 2.6% of toxic plant exposures in the United States.[6, 7] Most of these exposures are in children.[7] (See Epidemiology.) Digoxin-specific fragment antigen-binding (Fab) antibody fragments have contributed significantly to the improved morbidity and mortality of toxic patients since their approval in 1986 by the US Food and Drug Administration (FDA). (See Prognosis, Treatment, and Medication.)