Ketamine Pain Mechanism

distress is communicated from the headland to other parts of the dead body by the CNS (Central Nervous System) and nerve endings. (Mayer, Mao, Holt, value, 7731-7736) The ligand-gated ion agate lines, also referred to as LGICs, or ionotropic receptors, are a group of intrinsic transmembrane ion channels that are clear in response to binding of a chemical messenger. (Collingridge, Singer, 290-296) (Dickenson, 307-309) (Dickenson, Chapman, Green, 633-638)The ion channel is adjust by a neurotransmitter ligand that is very selective to one or much ions like potassium, sodium, calcium, and chloride. (Kandel, Schwartz, Jessell, 178-180) Such receptors located at synapses converting the chemical signal to an electrical signal in the post-synaptic cell. (Connolly, Wafford, 529-534) The NMDA receptor (N-methyl-D-aspartate) is such an ionotropic receptor for glutamate. (Dingledine, Borges, Bowie, Traynelis, 7-61) (Lodge, Johnson, 81-86) (Meller, 435-436) By roentgen ray crystallograph y, the NMDA receptors have an heterodimer subunits, which are involved in the binding of agonists and antagonists like Ketamine. (Hirota, Lambert, 441-444)This channel complex contributes to excitatory synaptic transmission system at sites byout the brain and the spinal cord, and is modulated by a number of endogenous and exogenous compounds. (Rabben, Skljelbred, Oye, 1060-1066) NMDA receptors play a key role in a childlike range of physiologic and pathologic processes. (Hoffman, Coppejans, Vercauteren, Adriemsen, 240-242) (Klepstadt, Maurset, Moberg, Oye, 513-518) (Coderre, Katz, Vaccarino, Melzack, 259-285) Ketamine is primarily a non-competitive antagonist, which opens in response to binding of glutamate. This NMDA receptor mediates the reduction of upset effects of ketamine at low doses. (Lofwall, Griffiths, Mintzer, 439-449)Evidence for this is reinforced by the fact that naxolone, an opioid antagonist, does not reversal the analgesia. Studies also seem to indicate that k etamine is use dependent meaning it still initiates its blocking action once a glutamate binds to the NMDA receptor. (Sorensen, Bengtsson, Ahlner, Henriksson, Ekselius et al., 1615-1621) At high take aim doses, ketamine has also been found to bind to opioid mu receptors and sigma receptors. Thus, loss of consciousness that occurs may be partially due to binding at the opioid mu and sigma receptors. (Lonnqvist, Norton, 617-621)(Menigaux, Fletcher, Dupont, Guignard, Guirimand, et al. 129-135) (Koppert, Sittl, Scheuber, Alsheimer, Schmelz, 152-159) (Bushell, Endoh, Simen, Ren, Bindokas, 55-64)Works CitedMayer DJ, Mao J, Holt J, Price DD. Cellular tools of Neuropathic Pain, Morphin Tolerance, and their Interactions. Proc. Natl Acac. Sci. USA. 1999, 96(14) 7731-7736.Collingridge G, Singer W. Excitatory amino group Acid sense organs and Synaptic Plasticity. Trends Pharmacol Sci. 1990 11 290-296.Dickenson AH. A cure for wind-up NMDA receptor antagonists as potential analgesics. Trends Pharmacol Sci 1990 11 307-309Dickenson AH, Chapman V and Green GM. The pharmacology of excitatory and inhibitory amino acid-mediated events in the transmission and modulation of pain in the spinal cord. Gen Pharmacol 1997 28 633-638Kandel ER, Schwartz JH, Jessell TM. Principles of Neural Science, fourth ed. McGraw-Hill New York, (2000), pp.178-180Connolly CN, Wafford KA. The Cys-Loop Superfamily of Ligand-Gated Ion Channels the Impact of Receptor Structure on Function. biochemical Society Transactions (2004) Vol. 32 529-534.Dingledine R, Borges K, Bowie D, Taynelis SF. The Glutamate Receptors Ion Channels. Pharmacology Reviews, 1999 51(1) 7-61Lodge D and Johnson KM. Non-Competitive Excitatory Amino Acid Antagonists. Trends Pharmacol Sci 1990 11 81-86Meller ST. Ketamine Relief from Chronic Pain through Actions at the NMDA Receptor? Pain 1996 68 435-436Hirota K, Lambert DG. Ketamine Its Mechanism (s) of Action and its Unusual Clinical Uses. Br. J. Anesth. 1996, 77(4)441-444.Rabben T , Skjelbred P, Oye I. Prolonged Analgesic Effects of Ketamine, an N-Methyl-D-Aspartate Receptor Inhibitor, in Patients with Chronic Pain. The Journal of Pharmacology and Experimental Pharmaceutics. 1999, 289(2)1060-1066.Hoffmann V, Coppejans H, Vercauteren M and Adriaemsen H Successful Treatment of Postherpetic Neuralgia with Oral Ketamine. 1994 Clin J Pain 10 240-242Klepstad P, Maurset A, Moberg ER and Oye I Evidence for a Role for NMDA Receptors in Pain Perception. Eur J Pharmacol 1990 187 513-518Coderre TJ, Katz J, Vaccarino AL and Melzack R. Contribution of Central Neuroplasticity to Pathological Pain A Review of Clinical and Experimental Evidence. 1993 Pain 52 259-285.Lofwall MR, Griffiths RR, Mintzer MZ. Cognitive and immanent Acute Dose Effects of Intramuscular Ketamine in good for you(p) Adults. Ex. Clin. Psychopharmacol. (2006), 14(4)439-449Sorensen J, Bengtsson A, Ahlner J, Henriksson KG, Ekselius L and Bengtsson M. Fibromyalgia. Are there different mechanisms in the proc essing of pain? A double Blind Crossover Comparison of analgesic Drugs. 1997 J Rheumatol 24 1615-1621Lonnqvist PA, Norton NS. Pediatric Day-Case Anesthesia and Pain Control. Curr. Opin. Anaest. (2006), 19(6) 617-621.Menigaux C, Fletcher D, Dupont X, Guignard B, Guirimand F, Chauvin M. The Benefits of Intraoperative Small-Dose Ketamine on surgical Pain after Anterior Cruciate Ligament Repair. Anesth. Analg. 2000 90(1) 129-135Koppert W, Sittl R, Scheuber K,Alsheimer M, Schmeltz M, Schuttler J. Differential Modulation of Remifentanil-Induced Analgesia and Post-Infusion Hyperalgesia by S-Ketamine and Clonidine in Humans. Anesthesiology. 2003, 99(1) 152-159.Bushell T, Endoh T, Simen AA, Ren D, Bindokas VP, Miller RJ. Molecular Components of Tolerance to Opiates In individual(a) Hippocampal Neurons. Mol. Pharmacol. 2002, 61(1) 55-64.