In the CNS, the links are complex. A pulse from one neuron to another may be from the axon to the cell body, from the axon to the dendrites (a afferent branch of a neuron), is transmitted from the cell body to the cell body or dendrite to dendrite. A neuron receives many same-excitatory and inhibitory impulses from other neurons and integrates them to different discharge patterns. (Editor’s note: A neuron can simultaneously many – receive impulses from other neurons and integrate them at different discharge patterns – excitatory and inhibitory.)

A neuron generates an action potential and forward it to its axon further, then this signal is transmitted via a synapse by release of a neurotransmitter, a reaction in another neuron, or an effector cell (eg. B. muscle cells, most of exocrine and endocrine cells ) triggers. Depending on the involved neurotransmitters and from the receptor, the signal can stimulate or inhibit the postsynaptic cell. In the CNS, the links are complex. A pulse from one neuron to another may be from the axon to the cell body, from the axon to the dendrites (a afferent branch of a neuron), is transmitted from the cell body to the cell body or dendrite to dendrite. A neuron receives many same-excitatory and inhibitory impulses from other neurons and integrates them to different discharge patterns. (Editor’s note: A neuron can be many simultaneously – receive pulses from other neurons and integrating these into different discharge patterns – excitatory and inhibitory.) Forwarding the propagation of an action potential along an axon is effected electrically by the exchange of Na + – and K + ions on the axonal membrane. A particular neuron generates after each stimulus always the same action potential and directs it at a constant speed through the axon on. The speed depends on the axon diameter and the degree of myelination and varies from 1-4 m / s in thin unmyelinated up to 75 m / s in large myelinated fibers. The propagation speed is faster in myelinated fibers, because the myelin sheath has regular constrictions (Node of Ranvier) where the axon is uncovered. The electrical impulse jumps from one constriction to the next, skipping over the myelinated section of the axon. Therefore disturbing diseases that affect the myelin sheath (eg. As multiple sclerosis), the impulse conduction and cause a variety of neurological symptoms. Synaptic Transmission The pulse transmission takes place chemically, by the release of specific neurotransmitters from the nerve terminal (axon terminal). Neurotransmitters diffuse across the synaptic cleft and bind to specific receptors in the short term of the adjacent neuron or effector cell. Depending on the receptor, the answer may be excitatory or inhibitory. A synapse type, the electrical synapse, operates without neurotransmitters. About ion channels the cytoplasm of the presynaptic with the postsynaptic neuron is directly connected. This type of transmission is the fastest. The nerve cell bodies produce enzymes that synthesize most neurotransmitters; these are stored in vesicles in the nerve terminal (s. neurotransmission). The transmitter amount in a vesicle (usually several thousand molecules) corresponds to a Quantum. An action potential arrives at the axon terminal opens axonal calcium channels; by the calcium influx neurotransmitter molecules from many vesicles are released by fusing the vesicle membrane in each case with the membrane of the axon terminal. Characterized an opening is generated, so that the molecules may be delivered by exocytosis into the synaptic cleft. Neurotransmission by incoming action potentials axonal calcium channels are opened (not shown). Ca ++ activates the release of neurotransmitters (NT) from the vesicles, where they are stored. The neurotransmitter molecules get into the synaptic cleft. Some bind to postsynaptic receptors and initiate a response from the downstream cell. The others will be pumped back into the axon and stored or diffuse into the surrounding tissue. The neurotransmitters amount in the axon terminal is typically independent of the neuronal activity. It is held by modification of the uptake of neurotransmitter precursors or by the activity of enzymes that are involved in the synthesis or degradation of neurotransmitters, relatively constant. The stimulation of presynaptic receptors may reduce the presynaptic neurotransmitter synthesis, a blockage can reinforce them. The neurotransmitter receptor interaction must be terminated quickly to allow very quick and repetitive activation of the receptors. Neurotransmitters can be processed by interaction with receptors as follows: you are either using active, ATP-dependent processes quickly into the presynaptic nerve endings transported back (recovery); or they are degraded by enzymes in the vicinity of the receptors; or they diffuse into the environment and be removed. Neurotransmitter molecules that are included in the nerve ending again, are stored in vesicles for reuse. Receptors neurotransmitter receptors are protein complexes that span the cell membrane. They determine whether a neurotransmitter excitatory or inhibitory effect. Receptors are continuously stimulated by neurotransmitters or drugs, they are insensitive (down-regulated); Receptors are not stimulated by their neurotransmitter or chronic inhibited by drugs are hypersensitive (upregulated). The downgrades or upregulation of receptors influences the development of tolerance and physical dependence. These concepts are particularly important in organ or tissue transplantation, in which the receptors are removed by denervation their neurotransmitters. Withdrawal symptoms may be explained at least partly by a rebound phenomenon due to altered Rezptoraffinit√§t or density. Most neurotransmitters interact primarily with postsynaptic receptors, some receptors are presynaptic but localized and provide fine tuning of neurotransmitter release. One class of receptors which are ionotropic receptors (eg., N-methyl-D-aspartate, kainate, quisqualate, nicotinic acetylcholine, glycine, and ?-aminobutyric acid [GABA] receptors), ion channels open, when a neurotransmitter, binds to it and give us a very quick response. (Editor’s note: Instead of “quisqualate receptors” is the name now probably “AMPA receptors”.) In the second class of receptors, the metabotropic receptors (e.g., serotonergic, ?- and ?-adrenergic and dopaminergic receptors.), Takes place the interaction of receptor-coupled G-proteins, thereby (a second messenger such as cAMP) is activated, another molecule which is in the cell via protein phosphorylation and / or calcium release a cascade of events in motion; mediated second messenger cellular changes take place slowly and allow fine tuning of the neurotransmitter schnellenionotropen answer. (Note / the editorial correction: Because the receptor is linked to the G protein, does not take place a direct interaction with the neurotransmitter.) The vast majority of neurotransmitter activates a specific receptor and not a second messenger. Important neurotransmitters and receptors At least 100 substances can act as neurotransmitters; about 18 are more important. Many are found in slightly different forms. Glutamate and aspartate These amino acids are the major excitatory neurotransmitter in the CNS. They occur in the cortex, cerebellum and spinal cord. In the neurons of the synthesis of nitric oxide (NO) increases glutamate response. Excessive glutamate stimulation can be toxic by increasing intracellular calcium, free radicals and the proteinase activity. These neurotransmitters may contribute to the development of tolerance in opioid therapy and mediate hyperalgesia. in NMDA (N-methyl-D-aspartate) receptors and non-NMDA receptors are classified glutamate receptors. Phencyclidine (PCP, also known as “angel dust”) and memantine (used in dementia therapy) bind to NMDA Rezeptoren.GABA GABA is the major inhibitory neurotransmitter in the brain. It is an amino acid that is derived from glutamate by decarboxylation using glutamate decarboxylase. After receptor interaction GABA is actively transported back into the nerve ending and metabolized. Glycine, which resembles GABA in his activity, used primarily in neurons (Renshaw) cells of the spinal cord and in circuits relax the antagonistic muscles,. GABA receptors are classified as GABA (activating chloride channels) and GABA (metabotropic receptor). At GABAA receptors sit at different neuroactive substances, including benzodiazepines, barbiturates, picrotoxin, and muscimol. GABAB receptors are activated by baclofen, which is used for the treatment of muscle spasms (z. B. in multiple sclerosis) .Serotonin serotonin (5-hydroxytryptamine, 5-HT) is in the raphe nuclei and centerline neurons of the pons and the upper brainstem synthesized. Tryptophan is hydroxylated using the tryptophan hydroxylase to 5-hydroxytryptophan, then decarboxylated to serotonin. The serotonin levels are controlled by the uptake of tryptophan and intraneuronal monoamine oxidase (MAO), which degrades serotonin. Ultimately, serotonin 5-hydroxyindoleacetic acid in the urine as (5-HIAA) is excreted. Serotonergic (5-HT) receptors (at least 15 subtypes) are classified as 5-HT1 (4 subtypes), 5-HT2 and 5-HT3 receptors. Selective serotonin receptor agonists (eg. As sumatriptan) can migraines durchbrechen.Acetylcholin acetylcholine is the main transmitters of the bulbospinalen motoneurons, the autonomous preganglionic fibers of the postganglionic cholinergic (parasympathetic) fibers and many neurons in the CNS (eg. B. basal ganglia, motor cortex) , It is synthesized by acetylcholine from choline and acetyl-CoA. Its activity is quickly terminated by the local hydrolysis to choline and acetate by acetylcholinesterase. Acetylcholine levels are regulated by the acetylcholine and choline. In patients with Alzheimer’s dementia, the levels of this neurotransmitter are reduced. Cholinergic receptors are classified as nicotinic N1 (in the adrenal medulla and autonomic ganglia) or N2 (in skeletal muscle) or muscarinic M1-M5 (widespread in the CNS). M1 receptors are found in the autonomic nervous system, in the striatum, cortex and hippocampus; M2 receptors are found in the autonomic nervous system, the heart, in the intestinal smooth muscle, interacts in the hindbrain and Kleinhirn.Dopamin dopamine with receptors in some peripheral nerve fibers and many central neurons (eg. As in the substantia nigra, the midbrain, the ventral tegmental area and hypothalamus). The amino acid tyrosine is taken up by dopaminergic neurons and converted using the tyrosine to 3,4-dihydroxyphenylalanine (dopa); this is decarboxylated by aromatic L -Aminos√§uredecarboxylase to dopamine. After release and interaction with receptors, dopamine is active again incorporated into the nerve terminal (reuptake). Tyrosine hydroxylase and MAO (degrades dopamine) regulate the levels of dopamine in the nerve endings. Dopaminergic receptors are classified as D1-D5. D3 and D4 receptors play a role in the mind control (and are, of importance. B. in schizophrenia), the D2 receptor activation controls the extrapyramidal system. However receptor affinity does not mean the predictions of the functional response (intrinsic activity), for example. with a strong affinity for the D3 receptor as ropinirole has an intrinsic activity by the activation of D2 receptors auf.Noradrenalin norepinephrine is the neurotransmitter of postganglionic sympathetic fibers, and most of many central neurons (z. B. in locus coeruleus and hypothalamus). The precursor Tyrosine is converted to dopamine, which is hydroxylated by dopamine-?-hydroxylase to norepinephrine. After release and receptor interaction, a part of noradrenaline by means of catechol-O-methyltransferase (COMT) is broken, the rest becomes active again added to the nerve ending and degraded by MAO. Tyrosine hydroxylase, dopamine-?-hydroxylase and MAO regulate the intra euro neuronal noradrenaline. Adrenergic receptors are classified as ?1 (postsynaptic in the sympathetic system), ?2 (presynaptically in the sympathetic system and postsynaptic in the brain), ?1 (the heart) or ?2 (in other sympathetically innervated structures) .Endorphine enkephalins and endorphins and enkephalins are opioids. Endorphins are large polypeptides that can activate many central neurons (eg. As in the hypothalamus, amygdala, thalamus and locus coeruleus). The cell body contains large polypeptide Pro-Opiomelanokortin, the precursor of ?-, ?- and ?-endorphins. This polypeptide is transported along the axon and cleaved into fragments; one of which is the ?-endorphin contained in neurons that project to the periaqueductal gray to limbic structures and most catecholamine-containing neurons in the brain. After release and interaction with the receptors ?-endorphin is hydrolyzed by peptidases. Met-enkephalin and Leu-enkephalin are small polypeptides which occur in many central neurons (z. B. in globus pallidus, thalamus, caudate nucleus and the periaqueductal gray). Your predecessor, proenkephalin is synthesized in the cell body and then cleaved by specific peptidases in active peptides. These substances are also located in the spinal cord, where they modulate pain signals. The neurotransmitter for pain signals in the dorsal horn of the spinal cord are glutamate and substance P. enkephalins reduce the number of released neurotransmitter and hyperpolarize the postsynaptic membrane, reducing it the generation of action potentials and the perception of pain at the level of the dentate gyrus. After release and interaction with peptidergic receptors enkephalins into smaller are inactive hydrolyzed peptides and amino acids. Since exogenous enkephalins are inactivated very rapidly, these substances are not clinically useful. Stable molecules (eg., Morphine) are instead used as analgesics. Endorphin-enkephalin (opioid) receptors are classified as ?1 and ?2 (manipulation of sensorimotor integration and analgesia), ?1 and ?2 (influence of motor integration, cognitive function, and analgesia) and ?1, ?2 and ?3 (influencing the regulation of water supply, analgesia and food intake). ? receptors are currently not classified as opioid receptors and are mostly located in the hippocampus and bind PCP. New results suggest the presence of a lot more receptor subtypes with pharmacologic implications: The molecular precursor components of the receptor protein can be regrouped during the receptor synthesis to produce different receptor variants (eg 27 splice variants of the ?-opioid receptor.). Likewise 2 receptors can be combined (dimerize) to a new receptor to bilden.Weitere neurotransmitter dynorphins are a group of 7 peptides with similar amino acid sequences. They are like the enkephalins opioids. Substance P, a peptide, comes in central neurons (in the habenula, substantia nigra, basal ganglia, the medulla oblongata and in the hypothalamus) and is a highly concentrated in the dorsal root ganglia. The release is triggered by intense afferent painful stimuli. Substance P modulates the neuronal response to pain and mood; modulating nausea and vomiting by the activation of NK1A receptors, which are localized in the brain stem. Nitric oxide (NO) is an unstable gas, which mediates many neuronal processes. It is produced from arginine by means of NO synthase. Neurotransmitters that increase the intracellular Ca ++ (z. B. substance P, glutamate, acetylcholine) stimulate NO synthesis in neurons that express NO synthase. NO may be an intracellular signaling molecule; it can diffuse out of a cell in a second neuron and trigger physiological responses (eg. as long-term potentiation [gain of the pre- and postsynaptic responses-a form of learning]), or NMDA receptor-mediated neurotoxicity amplify (z. B. for Parkinson’s disease, stroke, Alzheimer’s dementia). Substances with less well-studied role in neurotransmission are histamine, vasopressin, vasoactive intestinal peptide, carnosine, bradykinin, cholecystokinin, bombesin, somatostatin, corticotropin releasing factor, neurotensin, and possibly adenosine. change with faulty neurotransmission disorders associated disorders or substances, production, release, uptake, degradation or re-uptake of neurotransmitters or the number and affinity of receptors, neurological or psychiatric symptoms can cause and disease (s. Examples of associated with faulty neurotransmission disorders) cause , Drugs that modify neurotransmission can, many of these disorders alleviate (z. B. Parkinson’s disease, depression). Overview of neurotransmission (cholinergic synapse) var model = {videoId: ‘4605501853001’ playerId: ‘H1xmEWTatg_default’ imageUrl: ‘http://f1.media.brightcove.com/8/3850378299001/3850378299001_4829229477001_CH19-57-AbnormalHemostasis.jpg? pubId = 3850378299001 & videoId = 4605501853001 ‘, title:’ Overview of neurotransmission (cholinergic synapse) ‘description:’ u003Ca id = “v37896572 ” class = “”anchor “” u003e u003c / a u003e u003cdiv class = “”para “” u003e u003cp u003eEin neuron passes information to another neuron at a synapse. The neuron that transmits information is called a presynaptic neuron and the neuron that receives the information is the postsynaptic neuron. Let’s see what happens during a cholinergic synapse

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