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IVMS-Neurotransmitters
IVMS-Neurotransmitters
IVMS-Neurotransmitters
IVMS-Neurotransmitters
IVMS-Neurotransmitters
IVMS-Neurotransmitters
IVMS-Neurotransmitters
IVMS-Neurotransmitters
IVMS-Neurotransmitters
IVMS-Neurotransmitters
IVMS-Neurotransmitters
IVMS-Neurotransmitters
IVMS-Neurotransmitters
IVMS-Neurotransmitters
IVMS-Neurotransmitters
IVMS-Neurotransmitters
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IVMS-Neurotransmitters

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Also see IVMS Neurobiology Review | Overview Notes

Also see IVMS Neurobiology Review | Overview Notes

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  • 1. Neurotransmitters| mic 08-13 1 | P a g e
  • 2. Neurotransmitters| mic 08-13 2 | P a g e
  • 3. Neurotransmitters| mic 08-13 3 | P a g e Neurotransmitter Retrieved and modified from "http://en.wikipedia.org/w/index.php?title=Neurotransmitter&oldid=556935683" Categories:  Neurotransmitters  Molecular neuroscience  Neuroscience Structure of a typical chemical synapse Neurotransmitters are endogenous chemicals that transmit signals from a neuron to a target cell across a synapse.[1] Neurotransmitters are packaged into synaptic vesicles clustered beneath the membrane in the axon terminal, on the presynaptic side of a synapse. They are released into and diffuse across the synaptic cleft, where they bind to specific receptors in the membrane on the postsynaptic side of the synapse.[2] 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. Many 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.[3]
  • 4. Neurotransmitters| mic 08-13 4 | P a g e Discovery Until the early 20th century, scientists assumed that the majority of synaptic communication in the brain was electrical. However, through the careful histological examinations of Ramón y Cajal (1852–1934), a 20 to 40 nm gap between neurons, known today as the synaptic cleft, was discovered. The presence of such a gap suggested communication via chemical messengers traversing the synaptic cleft, and in 1921 German pharmacologist Otto Loewi (1873–1961) confirmed that neurons can communicate by releasing chemicals. Through a series of experiments involving the vagus nerves of frogs, Loewi was able to manually slow the heart rate of frogs by controlling the amount of saline solution present around the vagus nerve. Upon completion of this experiment, Loewi asserted that sympathetic regulation of cardiac function can be mediated through changes in chemical concentrations. Furthermore, Otto Loewi is accredited with discovering acetylcholine (ACh)—the first known neurotransmitter.[4] Some neurons do, however, communicate via electrical synapses through the use of gap junctions, which allow specific ions to pass directly from one cell to another.[5] Identifying neurotransmitters 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. Modern advances in pharmacology, genetics, and chemical neuroanatomy have greatly reduced the importance of these rules. A series of experiments that may have taken several years in the 1960s can now be done, with much better precision, in a few months. Thus, it is unusual nowadays for the identification of a chemical as a neurotransmitter to remain controversial for very long periods of time.
  • 5. Neurotransmitters| mic 08-13 5 | P a g e Types of neurotransmitters 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,[3] 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)  Peptides: somatostatin, substance P, opioid peptides[6]  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,[7] as are some gaseous molecules such as nitric oxide (NO), hydrogen sulfide (H2S), and carbon monoxide (CO).[8] Because they are not packaged into vesicles they are not classical neurotransmitters by the strictest definition, however they have all been shown experimentally to be released by presynaptic terminals in an activity-dependent way. By far the most prevalent transmitter is glutamate, which is excitatory at well over 90% of the synapses in the human brain.[3] 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 dopamine system. The addictive opiate drugs exert their effects primarily as functional analogs of opioid peptides, which, in turn, regulate dopamine levels.
  • 6. Neurotransmitters| mic 08-13 6 | P a g e Excitatory and inhibitory Some neurotransmitters are commonly described as "excitatory" or "inhibitory". The only direct effect of a neurotransmitter is to activate one or more types of receptors. The effect on the postsynaptic cell depends, therefore, entirely on the properties of those receptors. It happens that for some neurotransmitters (for example, glutamate), the most important receptors all have excitatory effects: that is, they increase the probability that the target cell will fire an action potential. For other neurotransmitters, such as GABA, the most important receptors all have inhibitory effects (although there is evidence that GABA is excitatory during early brain development). There are, however, other neurotransmitters, such as acetylcholine, for which both excitatory and inhibitory receptors exist; and there are some types of receptors that activate complex metabolic pathways in the postsynaptic cell to produce effects that cannot appropriately be called either excitatory or inhibitory. Thus, it is an oversimplification to call a neurotransmitter excitatory or inhibitory—nevertheless it is convenient to call glutamate excitatory and GABA inhibitory so this usage is seen frequently. Actions Main article: Neuromodulation As explained above, the only direct action of a neurotransmitter is to activate a receptor. Therefore, the effects of a neurotransmitter system depend on the connections of the neurons that use the transmitter, and the chemical properties of the receptors that the transmitter binds to. Here are a few examples of important neurotransmitter actions:  Glutamate is used at the great majority of fast excitatory synapses in the brain and spinal cord. It is also used at most synapses that are "modifiable", i.e. capable of increasing or decreasing in strength. Excess glutamate can overstimulate the brain and causes seizures.[ Modifiable synapses are thought to be the main memory-storage elements in the brain. Excessive glutamate release can lead to excitotoxicity causing cell death.  GABA is used at the great majority of fast inhibitory synapses in virtually every part of the brain. Many sedative/tranquilizing drugs act by enhancing the effects of GABA. Correspondingly glycine is the inhibitory transmitter in the spinal cord.  Acetylcholine is distinguished as the transmitter at the neuromuscular junction connecting motor nerves to muscles. The paralytic arrow-poison curare acts by blocking transmission at these synapses. Acetylcholine also operates in many regions of the brain, but using different types of receptors, including nicotinic and muscarinic receptors.[9]  Dopamine has a number of important functions in the brain; this includes regulation of motor behavior, pleasures related to motivation and also emotional arousal. It plays a critical role in the reward system; people with Parkinson's
  • 7. Neurotransmitters| mic 08-13 7 | P a g e disease have been linked to low levels of dopamine and people with schizophrenia have been linked to high levels of dopamine.[10]  Serotonin is a monoamine neurotransmitter. Most is produced by and found in the intestine (approximately 90%), and the remainder in central nervous system neurons. It functions to regulate appetite, sleep, memory and learning, temperature, mood, behaviour, muscle contraction, and function of the cardiovascular system and endocrine system. It is speculated to have a role in depression, as some depressed patients are seen to have lower concentrations of metabolites of serotonin in their cerebrospinal fluid and brain tissue.[11]  Substance P is an undecapeptide responsible for transmission of pain from certain sensory neurons to the central nervous system. It also aids in controlling relaxation of the vasculature and lowering blood pressure through the release of nitric oxide.[12]  Opioid peptides are neurotransmitters that act within pain pathways and the emotional centers of the brain; some of them are analgesics and elicit pleasure or euphoria.[13] Neurons expressing certain types of neurotransmitters sometimes form distinct systems, where activation of the system affects large volumes of the brain, called volume transmission. Major neurotransmitter systems include the noradrenaline (norepinephrine) system, the dopamine system, the serotonin system and the cholinergic system. Drugs targeting the neurotransmitter of such systems affect the whole system; this fact explains the complexity of action of some drugs. Cocaine, for example, blocks the reuptake of dopamine back into the presynaptic neuron, leaving the neurotransmitter molecules in the synaptic gap longer. Since the dopamine remains in the synapse longer, the neurotransmitter continues to bind to the receptors on the postsynaptic neuron, eliciting a pleasurable emotional response. Physical addiction to cocaine may result from prolonged exposure to excess dopamine in the synapses, which leads to the downregulation of some postsynaptic receptors. After the effects of the drug wear off, one might feel depressed because of the decreased probability of the neurotransmitter binding to a receptor. Prozac is a selective serotonin reuptake inhibitor (SSRI), which blocks re-uptake of serotonin by the presynaptic cell. This increases the amount of serotonin present at the synapse and allows it to remain there longer, hence potentiating the effect of naturally released serotonin.[14] AMPT prevents the conversion of tyrosine to L-DOPA, the precursor to dopamine; reserpine prevents dopamine storage within vesicles; and deprenyl inhibits monoamine oxidase (MAO)-B and thus increases dopamine levels. Diseases may affect specific neurotransmitter systems. For example, Parkinson's disease is at least in part related to failure of dopaminergic cells in deep-brain nuclei, for example the substantia nigra. Levodopa is a precursor of dopamine, and is the most widely used drug to treat Parkinson's disease.
  • 8. Neurotransmitters| mic 08-13 8 | P a g e A brief comparison of the major neurotransmitter systems follows: Neurotransmitter systems System Origin [15] Effects[15] Noradrenaline system locus coeruleus  arousal  reward Lateral tegmental field Dopamine system dopamine pathways:  mesocortical pathway  mesolimbic pathway  nigrostriatal pathway  tuberoinfundibular pathway motor system, reward, cognition, endocrine, nausea Serotonin system caudal dorsal raphe nucleus Increase (introversion), mood, satiety, body temperature and sleep, while decreasing nociception.rostral dorsal raphe nucleus Cholinergic system pontomesencephalotegmental complex  learning  short-term memory  arousal  reward basal optic nucleus of Meynert medial septal nucleus Common neurotransmitters Category Name Abbreviation Metabotropic Ionotropic Small: Amino acids Aspartate - - Neuropeptides N- Acetylaspartylglutamate NAAG Metabotropic glutamate receptors; selective agonist of mGluR3 - Small: Amino acids Glutamate (glutamic acid) Glu Metabotropic glutamate receptor NMDA receptor, Kainate receptor, AMPA receptor Small: Amino acids Gamma-aminobutyric acid GABA GABAB receptor GABAA, GABAA-ρ receptor Small: Amino acids Glycine Gly - Glycine receptor Small: Acetylcholine Acetylcholine Ach Muscarinic acetylcholine receptor Nicotinic acetylcholine receptor Small: Monoamine (Phe/Tyr) Dopamine DA Dopamine receptor - Small: Monoamine Norepinephrine NE Adrenergic -
  • 9. Neurotransmitters| mic 08-13 9 | P a g e Category Name Abbreviation Metabotropic Ionotropic (Phe/Tyr) (noradrenaline) receptor Small: Monoamine (Phe/Tyr) Epinephrine (adrenaline) Epi Adrenergic receptor - Small: Monoamine (Phe/Tyr) Octopamine - - Small: Monoamine (Phe/Tyr) Tyramine - Small: Monoamine (Trp) Serotonin (5- hydroxytryptamine) 5-HT Serotonin receptor, all but 5- HT3 5-HT3 Small: Monoamine (Trp) Melatonin Mel Melatonin receptor - Small: Diamine (His) Histamine H Histamine receptor - PP: Gastrins Gastrin - - PP: Gastrins Cholecystokinin CCK Cholecystokinin receptor - PP: Neurohypophyseals Vasopressin AVP Vasopressin receptor - PP: Neurohypophyseals Oxytocin OT Oxytocin receptor - PP: Neurohypophyseals Neurophysin I - - PP: Neurohypophyseals Neurophysin II - - PP: Neuropeptide Y Neuropeptide Y NY Neuropeptide Y receptor - PP: Neuropeptide Y Pancreatic polypeptide PP - - PP: Neuropeptide Y Peptide YY PYY - - PP: Opioids Corticotropin (adrenocorticotropic hormone) ACTH Corticotropin receptor - PP: Opioids Dynorphin - - PP: Opioids Endorphin - - PP: Opioids Enkephaline - - PP: Secretins Secretin Secretin receptor - PP: Secretins Motilin Motilin receptor - PP: Secretins Glucagon Glucagon receptor - PP: Secretins Vasoactive intestinal peptide VIP Vasoactive intestinal peptide receptor -
  • 10. Neurotransmitters| mic 08-13 10 | P a g e Category Name Abbreviation Metabotropic Ionotropic PP: Secretins Growth hormone- releasing factor GRF - - PP: Somatostatins Somatostatin Somatostatin receptor - SS: Tachykinins Neurokinin A - - SS: Tachykinins Neurokinin B - - SS: Tachykinins Substance P - - PP: Other Bombesin - - PP: Other Gastrin releasing peptide GRP - - Gas Nitric oxide NO Soluble guanylyl cyclase - Gas Carbon monoxide CO - Heme bound to potassium channels Other Anandamide AEA Cannabinoid receptor - Other Adenosine triphosphate ATP P2Y12 P2X receptor Precursors of neurotransmitters While intake of neurotransmitter precursors does increase neurotransmitter synthesis, evidence is mixed as to whether neurotransmitter release (firing) is increased. Even with increased neurotransmitter release, it is unclear whether this will result in a long-term increase in neurotransmitter signal strength, since the nervous system can adapt to changes such as increased neurotransmitter synthesis and may therefore maintain constant firing.[16] Some neurotransmitters may have a role in depression, and there is some evidence to suggest that intake of precursors of these neurotransmitters may be useful in the treatment of mild and moderate depression.[16][17] Dopamine precursors L-DOPA, a precursor of dopamine that crosses the blood–brain barrier, is used in the treatment of Parkinson's disease. Norepinephrine precursors For depressed patients where low activity of the neurotransmitter norepinephrine is implicated, there is only little evidence for benefit of neurotransmitter precursor administration. L-phenylalanine and L-tyrosine are both precursors for dopamine, norepinephrine, and epinephrine. These conversions require vitamin B6, vitamin C, and S-adenosylmethionine. A few studies suggest potential antidepressant effects of L- phenylalanine and L-tyrosine, but there is much room for further research in this area.[16]
  • 11. Neurotransmitters| mic 08-13 11 | P a g e Serotonin precursors Administration of L-tryptophan, a precursor for serotonin, is seen to double the production of serotonin in the brain. It is significantly more effective than a placebo in the treatment of mild and moderate depression.[16] This conversion requires vitamin C.[11] 5-hydroxytryptophan (5-HTP), also a precursor for serotonin, is also more effective than a placebo.[16] Degradation and elimination A neurotransmitter must be broken down once it reaches the post-synaptic cell to prevent further excitatory or inhibitory signal transduction. For example, acetylcholine (ACh), an excitatory neurotransmitter, is broken down by acetylcholinesterase (AChE). Choline is taken up and recycled by the pre-synaptic neuron to synthesize more ACh. Other neurotransmitters such as dopamine are able to diffuse away from their targeted synaptic junctions and are eliminated from the body via the kidneys, or destroyed in the liver. Each neurotransmitter has very specific degradation pathways at regulatory points, which may be the target of the body's own regulatory system or recreational drugs. References 1. "Neurotransmitter" at Dorland's Medical Dictionary 2. Elias, L. J, & Saucier, D. M. (2005). Neuropsychology: Clinical and Experimental Foundations. Boston: Pearson 3. Robert Sapolsky (2005). "Biology and Human Behavior: The Neurological Origins of Individuality, 2nd edition". The Teaching Company. "see pages 13 & 14 of Guide Book" 4. Saladin, Kenneth S. Anatomy and Physiology: The Unity of Form and Function. McGraw Hill. 2009 ISBN 0-07-727620-5 5. "Junctions Between Cells". Retrieved 2010-11-22. 6. http://www.ncbi.nlm.nih.gov/pubmed/38738 7. Kodirov,Sodikdjon A., Shuichi Takizawa, Jamie Joseph, Eric R. Kandel, Gleb P. Shumyatsky, and Vadim Y. Bolshakov. Synaptically released zinc gates long- term potentiation in fear conditioning pathways. PNAS, October 10, 2006. 103(41): 15218-23. doi:10.1073/pnas.0607131103 8. Nitric oxide and other gaseous neurotransmitters 9. http://www.ebi.ac.uk/interpro/potm/2005_11/Page2.htm 10.Schacter, Gilbert and Weger. Psychology.United States of America.2009.Print. 11.a b University of Bristol. "Introduction to Serotonin". Retrieved 2009-10-15. 12.http://www.wellnessresources.com/health_topics/sleep/substance_p.php 13.Schacter, Gilbert and Weger. Psychology. 2009.Print. 14.Yadav, V. et al; Ryu, Je-Hwang; Suda, Nina; Tanaka, Kenji F.; Gingrich, Jay A.; Schütz, Günther; Glorieux, Francis H.; Chiang, Cherie Y. et al. (2008). "Lrp5
  • 12. Neurotransmitters| mic 08-13 12 | P a g e Controls Bone Formation by Inhibiting Serotonin Synthesis in the Duodenum". Cell 135 (5): 825–837. doi:10.1016/j.cell.2008.09.059. PMC 2614332. PMID 19041748. 15.Rang, H. P. (2003). Pharmacology. Edinburgh: Churchill Livingstone. pp. 474 for noradrenaline system, page 476 for dopamine system, page 480 for serotonin system and page 483 for cholinergic system. ISBN 0-443-07145-4. 16. Meyers, Stephen (2000). "Use of Neurotransmitter Precursors for Treatment of Depression". Alternative Medicine Review 5 (1): 64–71. PMID 10696120. 17. Van Praag, HM (1981). "Management of depression with serotonin precursors". Biol Psychiatry 16 (3): 291–310. PMID 6164407. External links  Molecular Expressions Photo Gallery: The Neurotransmitter Collection  Brain Neurotransmitters  Endogenous Neuroactive Extracellular Signal Transducers  Neurotransmitter at the US National Library of Medicine Medical Subject Headings (MeSH)  neuroscience for kids website  brain explorer website  wikibooks cellular neurobiology Supplemental: An overview of neurotransmitters for non-biomedical science learners
  • 13. Neurotransmitters| mic 08-13 13 | P a g e Source: http://www.integrativepsychiatry.net/neurotransmitter.html The Four Major Neurotransmitters Neurotransmitters are powerful chemicals that regulate numerous physical and emotional processes such as mental performance, emotional states and pain response. Virtually all functions in life are controlled by neurotransmitters. They are the brain's chemical messengers.Interactions between neurotransmitters, hormones, and the brain chemicals have a profound influence on overall health and well-being. When our concentration and focus is good, we feel more directed, motivated, and vibrant. Unfortunately, if neurotransmitter levels are inadequate these energizing and motivating signals are absent and we feel more stressed, sluggish, and out-of-control. Proteins, minerals, vitamins,carbohydrates, and fats are the essential nutrients that make up your body. Proteins are the essential components of muscle tissue, organs, blood, enzymes, antibodies, and neurotransmitters in the brain. Your brain needs the proper nutrients everyday in order to manufacture proper levels of the neurotransmitters that regulate your mood. Neurotransmitter Effects: Control the appetite center of the brain Stimulates Corticotropin Releasing Factor, Adrenalcorticotropic Hormone, & Cortisol Regulate male and female sex hormone Regulates sleep Modulate mood and thought processes Controls ability to focus, concentrate, and remember things The Mind Body Connection The chemistry of our bodies can alter, and be altered by our every thought and feeling. Our bodies and our minds are truly interconnected, the health of one depends on the health of the other.
  • 14. Neurotransmitters| mic 08-13 14 | P a g e There are many biochemical neurotransmitter imbalances that result in mental health symptoms such as:  *Adrenal dysfunction  *Blood sugar imbalance  *Food and Chemical allergy  *Heavy Metal Toxicity  *Hormone imbalance  *NutritionalDeficiency  *Serotonin/Dopamine/Noradrenalin imbalance  *Stimulant and drug intoxication  *Under or overactive thyroid Neurotransmitter Imbalances Disrupted communication between the brain and the body can have serious effects to ones health both physically and mentally. Depression, anxiety and other mood disorders are thought to be directly related to imbalances with neurotransmitters. The four major neurotransmitters that regulate mood are Serotonin, Dopamine, GABA and Norepinephrine. The Inhibitory System is the brains braking system, it prevents the signal from continuing. The inhibitory system slows things down. Serotonin and GABA are examples of inhibitory neurotransmitters. GABA (Gamma amino butyric acid) GABA is the major inhibitory neurotransmitter in the central nervous system. It helps the neurons recover after transmission, reduces anxiety and stress.It regulates norepinephrine, adrenaline, dopamine, and serotonin, it is a significant mood modulator. Serotonin imbalance is one of the most common contributors to mood problems. Some feel it is a virtual epidemic in the United States. Serotonin is key to our feelings of happiness and very important for our emotions because it helps defend against both anxiety and depression. You may have a shortage of serotonin if you have a sad depressed mood, anxiety, panic attacks, low energy, migraines, sleeping problems, obsession or compulsions, feel tense and irritable, crave sweets, and have a reduced interest in sex. Additionally, your hormones and Estrogen levels can affect serotonin levels and this may explain why some women have pre-menstrual and menopausal mood problems. Moreover, daily stress can greatly reduce your serotonin supplies.
  • 15. Neurotransmitters| mic 08-13 15 | P a g e The Excitatory Neurotransmitter System can be related to your car's accelerator. It allows the signal to go. When the excitatory neurotransmitter system is in drive your system gets all reved up for action. Without a functioning inhibitory system to put on the brakes, things (like your mood) can get out of control Epinephrine also known as adrenaline is a neurotransmitter and hormone essential to metabolism. It regulates attention, mental focus, arousal, and cognition. It also inhibits insulin excretion and raises the amounts of fatty acids in the blood. Epinephrine is made from norepinephrine and is released from the adrenal glands. Low levels have been can result in fatigue, lack of focus, and difficulty losing weight. High levels have been linked to sleep problems, anxiety and ADHD. Dopamine is responsible for motivation, interest, and drive. It is associated with positive stress states such as being in love, exercising, listening to music, and sex . When we don't have enough of it we don't feel alive, we have difficulty initiating or completing tasks, poor concentration, no energy, and lack of motivation. Dopamine also is involved in muscle control and function. Low Dopamine levels can drive us to use drugs (self medicate), alcohol, smoke cigarettes, gamble, and/or overeat. High dopamine has been observed in patients with poor GI function, autism, mood swings, psychosis, and children with attention disorders. Glutamate is the major excitatory neurotransmitter in the brain. It is required for learning and memory. Low levels can lead to tiredness and poor brain activity. Increased levels of glutamate can cause death to the neurons (nerve cells) in the brain. Dysfunction in glutamate levels are involved in many neurodegenerative diseases such as Alzheimer's disease, Parkinson's, Huntington's, and Tourette's. High levels also contribute to Depression, OCD, and Autism. Histamine is most commonly known for it's role in allergic reactions but it is also involved in neurotransmission and can affect your emotions and behavior as well. Histamine helps control the sleep-wake cycle and promotes the release of epinephrine and norepinephrine. High histamine levels have been linked to obsessive compulsive tendencies, depression, and headaches.Low histamine levels can contribute to paranoia, low libido, fatigue, and medication sensitivities. Norepinephrine also known as noradrenaline is a excitatory neurotransmitter that is produced by the adrenal medulla or made from dopamine. High levels of norepinephrine are linked to anxiety, stress, high blood pressure, and hyperactivity. Low levels are linked to lack of energy, focus, and motivation. PEA is an excitatory neurotransmitter made from phenylalanine. It is important in focus and concentration. High levels are observed in individuals experiencing "mind racing", sleep problems, anxiety, and schizophrenia. Low PEA is associated with difficulty paying attention or thinking clearly, and in depression.
  • 16. Neurotransmitters| mic 08-13 16 | P a g e Neurotransmitter Levels Neurotransmitter levels can now be determined by a simple and convenient urine test collected at home. Knowing your neurotransmitter levels can help you correct a problem today or prevent problems from occuring in the future. For many years, it has been known in medicine that low levels of these neurotransmitters can cause many diseases and illnesses. A Neurotransmitter imbalance can cause:  Depression  Anxiety  Attention deficit/ADHD  Panic Attacks  Insomnia  Irritable bowel  PMS/ Hormone dysfunction  Fibromyalgia  Obesity  Eating disorders  Obsessions and Compulsions  Adrenal dysfunction  Psychosis  Early Death  Chronic Pain  Migraine Headaches What causes a neurotransmitter imbalance? Prolonged periods of stress can deplete neurotransmitters levels. Our fast paced, fast food society greatly contributes to these imbalances.

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