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You remember where your N methyl D aspartate or NMDA receptors are?
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∙ 15y ago
the brain
Wiki User
∙ 15y ago
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What is acethylcoline?
I assume you mean Acetylcholine. Acetylcholine (often abbreviated ACh) is a neurotransmitter in both the peripheral nervous system (PNS) and central nervous system (CNS) in many organisms including humans. Acetylcholine is one of many neurotransmitters in the autonomic nervous system (ANS) and the only neurotransmitter used in the somatic nervous system. It is also the neurotransmitter in all autonomic ganglia. Acetylcholine has functions both in the peripheral nervous system (PNS) and in the central nervous system (CNS) as a neuromodulator. In the PNS, acetylcholine activates muscles, and is a major neurotransmitter in the autonomic nervous system. In the CNS, acetylcholine and the associated neurons form a neurotransmitter system, the cholinergic system, which tends to cause excitatory actions. In the peripheral nervous system, acetylcholine activates muscles, and is a major neurotransmitter in the autonomic nervous system. . When acetylcholine binds to acetylcholine receptors on skeletal muscle fibers, it opens ligand gated sodium channels in the cell membrane. Sodium ions then enter the muscle cell, stimulating muscle contraction. Acetylcholine, while inducing contraction of skeletal muscles, instead induces decreased contraction in cardiac muscle fibers. This distinction is attributed to differences in receptor structure between skeletal and cardiac fibers. In the autonomic nervous system, acetylcholine is released in the following sites: * all pre- and post-ganglionic parasympathetic neurons * all preganglionic sympathetic neurons ** preganglionic sympathetic fibers to suprarenal medulla, the modified sympathetic ganglion; on stimulation by acetylcholine, the suprarenal medulla releases epinephrine and norepinephrine * some postganglionic sympathetic fibers ** sudomotor neurons to sweat glands. In the central nervous system, ACh has a variety of effects as a neuromodulator, e.g., for plasticity and excitability. Other effects are arousal and reward. == Acetylcholine and the associated neurons form a neurotransmitter system, the cholinergic system. It originates mainly in pontomesencephalotegmental complex, basal optic nucleus of Meynert and medial septal nucleus, and projects axons to vast areas of the brain: * The pontomesencephalotegmental complex acts mainly on M1 receptors in the brainstem . * Basal optic nucleus of Meynert acts mainly on M1 receptors in the neocortex. * Medial septal nucleus acts mainly on M1 receptors in the hippocampus and neocortex. == ACh is involved with synaptic plasticity, specifically in learning and short-term memory. Acetylcholine has been shown to enhance the amplitude of synaptic potentials following long-term potentiation in many regions, including the dentate gyrus, CA1, piriform cortex, and neocortex. This effect most likely occurs either through enhancing currents through NMDA receptors or indirectly by suppressing adaptation. The suppression of adaptation has been shown in brain slices of regions CA1, cingulate cortex, and piriform cortex, as well as in vivo in cat somatosensory and motor cortex by decreasing the conductance of voltage-dependent M currents and Ca2+-dependent K+ currents. == Acetylcholine also has other effects on excitability of neurons. Its presence causes a slow depolarization by blocking a tonically-active K+ current, which increases neuronal excitability. It appears to be a paradox, however, that ACh increases spiking activity in inhibitory interneurons while decreasing strength of synaptic transmission from those cells. This decrease in synaptic transmission also occurs selectively at some excitatory cells: For instance, it has an effect on intrinsic and associational fibers in layer Ib of piriform cortex, but has no effect on afferent fibers in layer Ia. Similar laminar selectivity has been shown in dentate gyrus and region CA1 of the hippocampus. One theory to explain this paradox interprets acetylcholine neuromodulation in the neocortex as modulating the estimate of expected uncertainty, acting counter to norepinephrine (NE) signals for unexpected uncertainty. Both would then decrease synaptic transition strength, but ACh would then be needed to counter the effects of NE in learning, a signal understood to be 'noisy'. This information along with diagrams and much more can be found at Wikipedia.com
List all the essential neurotransmitters?
Acetylcholine - synthesized from Choline, Lecithin, and panthothenic acid (B5), or Diethylaminoethanol (DMAE) - Arousal and orgasm - voluntary muscular control and proper tone - enhance energy and stamina - memory - long-term planning - mental focus Dopamine - synthesized from amino acid Levodopa - Alertness - Motivation - motor control - immune function - Ego hardening, confidence, optimism - Sexual Desire - Fat gain and loss - lean muscle gain - Bone density - ability to sleep soundly - Inhibits prolactin - thinking, planning, and problem solving - Aggression - Increase psychic and creative ability - Reduction of compulsivety - Salience and paranoia - Processing of pain - Increase sociability Serotonin (5-HT) - Synthesized from amino acid L-tryptophan with co-factor Niacin (B3), through the intermediate 5-hydroxytryptophan (5-HTP) - Decrease thought - Anaesthesize emotions - Decrease Agression and anger - Decrease Anxiety - Promote satiety and decrease appetite - Elevates Pain threshold - Reduces compulsivety/impulsivety - Decrease Sexual Desire - Orgasm - Thermoregulation (5-HT1A) - Stimulate Emesis (5-HT3) - Cerebrospinal fluid secretion (5-HT2C) - Platelate aggregation (5-HT2A) - Smooth muscle contraction, vasoconstriction, and vasodilation (5-HT2A) - Release oxytocin (5-HT1A) - Learning (5-HT2A & 5-HT4) - Memory (5-HT4) - Neuronal excitation (5-HT2A, 5-HT3, & 5-HT4) - GI motility (5-HT4) - Neuronal inhibition (5-HT1A) - Cerebral vasoconstriction (5-HT1D) - Pulmonary vasoconstriction (5-HT1B) - Presynaptic inhbition (5-HT1B) Norepinephrine - Synthesized from Dopamine with co-factor of vitamin C through the intermediate DOPAC. - Increase physical energy - Reduce compulsivety - Increase heart rate - Increase BP - Aggression - Alertness - Wakefulness/sleep cycle - Memory and learning - Orgasm - Decrease blood flow to extremities - Increase heart rate - Maintenance of attention - Orgasm - Cerebral plasticity Epinephrine - Synthesized from Norepinephrine. Also know as adrenaline, acts as both neurotransmitter and hormone. Oxidizes into Adrenochrome. - increases supply of oxygen and glucose to brain and muscles - Surpresses digestion - Increase heart rate and stroke volume - Pupil dilation - constricts arterioles in skin and GI tract - Dilates arterioles in skeletal muscles - Elevates blood sugar levels GABA - synthesized from glutamate - Reduce physical tension - Reduce Anxiety - Reduce Insomnia - Elevates pain threshold - Reduces blood pressure - Decrease heart rate - Reduce compulsivety Prolactin - Inhibition of Dopamine - Decreases sex hormones - estrogen in women, testosterone in men - Stimulates proliferation of oligodendrocyte precursor cells. These cells differentiate into oligodendrocytes, the cells responsible for the formation of myelin coatings on axons in the central nervous system. Nitric oxide - vasodilation, thins blood - reduces platelate stickiness, blood coagulation, wound healing - vasopressin release - stimulation of guanyl cyclase > GTP > cGMP. GMP lays a role in the relaxation of smooth muscle (including penis to facilitate erection), the inhibition of platelet aggregation and participates in signal transduction within the nervous system. Moreover, cGMP is involved in the regulation of the water and electrolyte balance as well as in the metabolism of the bone. cGMP is also involved in retinal phototransduction--that is the conversion of a light signal received by a nerve receptor, to an electrical signal transmitted to the brain. This might help explain transcendental vision, that is the radical increase in visual acuity and sensory perception in general. - involved in apoptosis, and DNA breakage and mutation - enables macrophages to kill tumor cells and bacteria Histamine - synthesized from L-histidine with co-factors folic acid, niacin, and copper. H1 - Vasodilation - Bronchoconstriction - Smooth muscle activation - separation of endothelial cells (responsible for hives) - Pain and itching due to insect stings - Allergic rhinitis - Motion sickness H2 - stimulates gastric acid secretion - Potent stimulant of cAMP production - increases the intracellular Ca2+ concentrations and release Ca2+ from intracellular stores. H3 - presynaptically inhibits the release of a number of other neurotransmitters including, but probably not limited to dopamine, histamine, GABA, acetylcholine, noradrenaline, and 5-HT. It leads to inhibition of the formation of cAMP H4 - H4 Receptors mediate Chemotaxis and Calcium Mobilization of Mast Cells Vasopressin - Water retention - raises blood pressure by inducing moderate vasoconstriction (AVPR1A) - Platellate aggregation (AVPR1A) - involved in aggression, blood pressure regulation and temperature regulation. - It has been implicated in memory formation, including delayed reflexes, image, short- and long-term memory (controversial) - increases peripheral vascular resistance and thus increases arterial blood pressure - adrenocorticotropic hormone secretion in response to stress (AVPR1B) - social interpretation of olfactory cues (AVPR1B) - Gluconeogenesis (AVPR1A) - Social Recognition (AVPR1A) - Increases mental clarity and memory when used as nootropic Oxytocin - spontaneous erections and orgasm - water retention (slight) - inhibition of adrenocorticotropic hormone, cortisol, and vasopressin - bonding - decreased repetitive behaviors and improved interpretation of emotions - Maternal behaviour - increased trust and reduced fear - Affecting generosity by increasing empathy during perspective taking. - inhibition of development of tolerance to various drugs (opiates, cocaine, alcohol), and reduced withdrawals. - impair learning and memory retrieval in certain aversive memory tasks Endocannabinoids - synthesized from an essential fatty acid. Endogenous cannabinoids include anandamine, 2-AG, Noladin Ether, NADA, and OAD - reduce GABA release in interneurons of the basolateral amygdala, thereby helping to extinguish the fear-conditioned response. - Memory - Development of opiate tolerance - control of appetite and food intake - long term potentiation Endogenous opioids - Include Enkephalin, Beta-endorphin, Dynorphin, Endomorphin, Nociceptin, opiorphin, and morphine. Enkephalin is the ligand for delta receptors and also has a high affinity for Mu-opioid receptors. Dynorphin is the ligand for kappa receptors. Beta-endorphin has an affinity for mostly Mu, but also delta and kappa. Endomorphin is the ligand for Mu. Nociceptin for ORL receptors. Opiorphin is found in saliva and inhibits the enzyme that breaks down Enkephalin and B-Endorphin called Enkephalinase. Little is know about the role of Morphine in the body, but speculating from the effects of exogenous morphine, it would bind to Mu-receptors. Mu-1 - Supraspinal Analgesia - Physical dependence Mu-2 - Respiratory depression - Miosis - Euphoria - Reduced GI motility - Physical dependence Kappa - Spinal Analgesia - Sedation - Inhibition of vasopressin release - Miosis Delta - Anti-depressant effects - Analgesia - Physical dependence ORL - Depression - Appetite - Anxiety - Development of tolerance to mu-agonists Sigma Receptors - Little is know about these enigmatic receptors, but possible ligands include DHEA (sigma 1), and endogenous N, N-DMT with slight affinity for both sigma receptors. Effects of sigma receptor stimulation include: - hypertonia (increased muscle tension) - tachycardia - tachypnea (increased breathing rate) - mydriasis (pupil dilation) - Euphoria or dysphoria - anti-depressant effects Other neurotransmitters include Glycine Glutamate and Aspartate - excitatory neurotransmitters that bind to the NMDA receptor. Can be synthesized from L-glutamine, glucose, or lipids. A metabolite of tryptophan in the absence of Niacin may produce kyunerinic acid, is also an NMDA excitatory neurotransmitter. Melatonin - Synthesized from the methylation of serotonin. Regulates circadian rhythms and has powerful anti-oxidant effects. Trace Amines - Include tryptamine, Phenylethylamine, tyramine, octopamine, 3-iodothyronamine, and others. Bind to the TAAR receptors. GHB - bind to GHB receptor(s), and GABAb subunit receptor. Niacin - Also know as vitamin B3, also acts as a neurotransmitter Orexin - Also know as hypocretin. Plays a role in wakefullness and appetite. - Yan Niemczycki Note: There are four criteria by which neurotransmitters are defined. 1. It must be synthesized in the presynaptic cell. 2. It must be released by the presynaptic terminal in sufficient quantities to produce a measurable effect on the postsynaptic cell. 3. When administered artificially, it mimics natural release. 4. A specific, known mechanism exists for it to be removed from the synaptic cleft. Of all the neurochemicals listed here, the following ten actually fit this definition. The remainder are all neuromodulators. 1. Glutamate 2. GABA 3. Glycine 4. Epinephrine (adrenaline) 5. Norepinephrine (noradrenaline) 6. Dopamine 7. Serotonin 8. Acetylcholine 9. Histamine 10. ATP/adenosine
Which part of the body is most affected by alcohol?
Alcohol is permeable to many areas of the brain. However, the main areas affected are: 1) the neocortex - alcohol inhibits activity in the neocortex, responsible for higher-level thinking and execution; 2) the hippocampus - by inhibiting NMDA receptors and increasing GABA-A receptor activity in this region, memory impairment results. In high enough doses, even blackouts can occur, whereby short-term to long-term memory consolidation has been effectively blocked altogether; 3) the cerebellum - inhibiting this region, primarily via GABA-A receptor modulation, reduces fine movement abilities, posture, coordination, etc..; 4) osmoreceptors in the hypothalamus - this results in poor modulation of ADH (antidiuretic hormone), resulting in increased urination and poor water retention, leading to dehydration; 5) in high enough doses, even the lowest regions of the brain can be affected, leading to unconsciousness, coma, or death
What kinds of cells are there in the human body?
cellular structure, cellular function, tissue, systems of organs of human body, acetylcholine, action potential, alveolus, bone, centriole, chloroplast, chromosome, cilium, clathrin, desmosome, digestive, ear, endocrine, endocytosis, endoplasmic reticulum, epithel, epithelial cell, erythrocyte, exocytosis, eye, gap junction, glutamate ion channel, Golgi body, hearing, heart, inner ear, liver, lung, lymph, megakaryocites, meiosis, microtubule, mitochondrion, mitosis, motor proteins, muscle spindle, nerve cell, neuron, NMDA ion channel, nose, olfactory, organ of balance, pacinian corpuscle, papilla, pituitary, platelets, reproductive system, respiratory system , ribosome, sensory cells, skeleton, skin, sodium ion channel, stem cells, synapse, taste, teeth, tight junction, tongue taste areas, tooth, touch, urinary system, white blood cells
What group does Ketamine belong to?
Ketamine is in a group of medications known as N-methyl d-aspartate (NMDA) receptor antagonists, and is legally used as an anesthetic for humans and animals.
Is ketamine an agonist or antagonist?
Ketamine is an antagonist at the N-methyl-D-aspartate (NMDA) receptor in the brain. It blocks the action of glutamate, an excitatory neurotransmitter, leading to its dissociative and anesthetic effects.
How is the Ketamine used?
It is used as a dissociative anaesthetic in surgery. By this, it doesn't actually stop pain, so much as it "shifts" consciousness, allowing for a sort of disconnected state. The same is said of out-of-body experiences, which are controlled by the same neurochemical mechanism. It is able to do this by blocking (antagonizing) NMDA (N-methyl-D-aspartate) receptors used in glutaminergic neurotransmission.
How is the drug ketamine used?
It is used as a dissociative anaesthetic in surgery. By this, it doesn't actually stop pain, so much as it "shifts" consciousness, allowing for a sort of disconnected state. The same is said of out-of-body experiences, which are controlled by the same neurochemical mechanism. It is able to do this by blocking (antagonizing) NMDA (N-methyl-D-aspartate) receptors used in glutaminergic neurotransmission.
How do you lower opioid tolerance?
Opioid Tolerance has been shown to be regulated by NMDA receptors. When somebody takes an opioid glutamate is released in the brain and binds to the NMDA receptors causing an increase in opioid tolerance. There have been several studies that show that taking and opioid with a NMDA antagonist (a drug that blocks NMDA receptors, effectively "turning them off") prevents the development of opioid tolerance. An accessible NMDA antagonist is DXM or Dextromethorphan which is found in many different cold medicine preparations. Be careful if taking a multiple ingredient cold medicine as many contain acetaminophin and other ingredients that can be dangerous if taken in high doses. Hope this helps, I included a link to a study if your interested. http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=2045628
What is ligand gated ion channel?
Ionotropic receptors are ligand-gated or transmitter gated ion channels. The binding of a neurotransmitter or other ligand to a particular site on a domain of a protein in the receptor causes a conformational change in the protein subunits. This allows a certain ion to pass through, poteitally potassium, sodium or chloride. There are two types of ionotropic receptors, non-NMDA and NMDA. Both are ligand gated receptors, however the NMDA is also voltage gated.
What 's a angel dust?
Angel Dust is the street term for Phencyclidine (PCP). PCP is a powerful dissociative anesthetic and hallucinogen which antagonizes NMDA receptors.
Why are there no pain receptors in the brain?
There are pain receptors in the brain. In fact if the brain didn't get and give the message to you that you were in pain it wouldn't register. The reason why we feel pain is to alert us that something is wrong and needs to be tended to. A nociceptor is a sensory receptor that responds to potentially damaging stimuli by sending nerve signals to the spinal cord and brain. This causes the perception of pain. There are also proteins in your brain called NMDA receptors which allow your neurons to communicate with each other. The neurons talk to each other which in turn reaches the NMDA receptors. The NMDA listens to the neurons and if sufficiently excited ions are expelled from a channel of receptors. Calcium ions then flow through the channel into the listening neuron at the synapse (pathway between the neurons) causing the pathway to be strengthened and giving you a loud signal (hot stove = pain!).
How does a depressant affect the brain function?
They affect GABA, NMDA, opiod, adrenergic, histamine and acetylcholine receptors in your brain. Depressants can effect other parts of your brain aswell, these are just the parts of it that actually cause the depressant effects of the drugs. Alcohol for example effects the GABA, NMDA, acetylcholine and serotonin receptors but it's effect on the serotonin receptor doesn't cause any depressant effect but rather adds to the euphoric effects of alcohol.
What has the author Jeffrey R Gingrich written?
Jeffrey R. Gingrich has written: 'Unique domain anchoring of Src to synaptic NMDA receptors via the mitochondrial protein NADH dehydrogenase subunit 2'
Does blocking receptors reduce action potentials?
Yes it reduces the chance of action potenctial to happen. The NMDA receptor is normally block be a Mg molecule. To unblock it the neuron must "fire" (generate action potencial).
How does Alcohol affects the Brain?
The primary mechanism by which alcohol affects brain function is via its interaction with a class of inhibitory receptors, called 'GABA receptors' (GABA stands for Gamma-AminoBuytric Acid, which is a type of inhibitory neurotransmitter). Normally when GABA binds to its receptor, the neuron's activity is reduced. Since alcohol enhances the way GABA works at this receptor, the net effect at the level of a single cell is an increase in inhibition.In addition, ethanol (alcohol) antagonizes (blocks) NMDA receptors. NMDA is N-methyl-D-aspartate and is a receptor type that both NMDA and glutamate bind with, allowing for short-term memory to be consolidated as long-term memory. As such, excessive alcohol consumption can induce a "blackout" state, whereby a person has no memory of events while intoxicated.In general, alcohol reduces activity in the neocortex (responsible for higher-level thinking) and the cerebellum (responsible for coordination, posture, and fine movement). Higher concentrations of alcohol affect more of these areas in greater degrees. And, with extreme intoxication, it will affect the lower brain areas responsible for consciousness, and can even lead to a coma or death.it slows down your brain. you don't think as fast. some connections are even disabled which means your not thinking about certain things as much if at all. this allows you to feel more relaxed. too much alcohol slows down your brains so much that it impairs your vision and memory and how you process information. this is why drunk driving is dangerous. your brain cannot process or calculate driving as well as when your not drunk.
