Τόμος 28 (2014) – Τεύχος 2 – Άρθρο 3 – Review of Clinical Pharmacology and Pharmacokinetics -Διεθνής Έκδοση – Volume 28 (2014) – Issue 2 – Article 3 Review of Clinical Pharmacology and Pharmacokinetics – International Edition

 

Τίτλος – Title
Κεταμίνη και Ντοπαμινενεργικοί Υποδοχείς
Ketamine and Dopaminergic Receptors
Συγγραφέας – Author

Δημοχρήστος Παπαδημητρίου, Αρετή Κατσούδα, Κατερίνα Κατσαβριά, Αλέξανδρος Μπούκας, Μαρία Μυρωνίδου-Τζουβελέκη
A΄ Εργαστήριο Φαρμακολογίας, Ιατρική Σχολή, Αριστοτέλειο Πανεπιστήμιο, Θεσσαλονίκη, Ελλάς –

Dimochristos Papadimitriou, Areti Katsouda, Katerina Katsavria, Alexandros Boukas, Maria Mironidou-Tjouveleki
A’ Laboratory of Pharmacology, Faculty of Medicine, School of Health Sciences, Aristotle University, Thessaloniki, Greece

Παραπομπή – Citation
Παπαδημητρίου Δ. , Κατσούδα Α. , Κατσαβριά Κ., Μπούκας Α., Μυρωνίδου-Τζουβελέκη Μ.: Κεταμίνη και Ντοπαμινενεργοί Υποδοχείς, Rev. Clin. Pharmacol. Pharmacokinet. Int. Ed. 28: 67-72 (2014)
Papadimitriou D., Katsouda A., Katsavria K., Boukas A., Mironidou-Tjouveleki M..: Ketamine and Dopaminergic Receptors, Rev. Clin. Pharmacol. Pharmacokinet. 28: 67-72 (2014)
Ημερομηνία Δημοσιευσης – Publication Date
01 Οκτωβρίου 2014 – 2014-10-01
Γλώσσα Πλήρους Κειμένου – Full Text Language
Αγγλικά – English
Λέξεις κλειδιά – Keywords
Kεταμίνη, ντοπαμινενεργοί υποδοχείς, ντοπαμίνη, ανταγωνιστής των γλουταμινεργικών υποδοχέων NMDA
Ketamine, dopaminergic receptors, dopamine, NMDA receptor antagonists, N-methyl-D-aspartate (NMDA)
Λοιποί Όροι – Other Terms

άρθρο επισκόπησης
review article

Περίληψη – Summary
Η κεταμίνη είναι μια μοναδική χημική ουσία που αλληλεπιδρά με τον οργανισμό σε πολλά επίπεδα. Η κεταμίνη χρησιμοποιείται ως ένα αναισθητικό, αναλγητικό-παυσίπονο, αλλά είναι επίσης μια ουσία με ψυχεδελική επίδραση. Η κεταμίνη αλληλεπιδρά κυρίως με το γλουταματεργικό σύστημα, αλλά τα αποτελέσματά της μπορεί να συμβάλλουν κατά πάσα πιθανότητα σε μια γενική αναστάτωση των νευροχημικών συστημάτων ενός οργανισμού. Έμμεση αλληλεπίδραση με το ντοπαμινεργικό σύστημα έχει αποδειχθεί. Η κεταμίνη ενεργεί σε προσυναπτικό επίπεδο, προκαλώντας αύξηση της συγκέντρωσης ντοπαμίνης στον εξωκυττάριο χώρο. Όσον αφορά την άμεση αλληλεπίδραση μεταξύ κεταμίνης και υποδοχέων ντοπαμίνης, πειράματα που πραγματοποιήθηκαν in vitro προσδιόρησαν ότι η κεταμίνη είχε μια agonist-like δράση στους ντοπαμινεργικούς D2 υποδοχείς. Μελέτες in vivo δεv oδήγησαν σε οποιαδήποτε άμεση αλληλεπίδραση της κεταμίνης με τους ντοπαμινεργικούς υποδοχείς . Το άρθρο επιχειρεί να διερευνήσει τις μελέτες σχετικά με το ντοπαμινεργικό σύστημα και την κεταμίνη και εκθέτει τις υπάρχουσες πληροφορίες, εστιάζοντας στην άμεση αλληλεπίδραση που αναδύεται μεταξύ κεταμίνης και ντοπαμινεργικών υποδοχέων.
Ketamine is a unique chemical substance that interacts with the organism at many levels. Ketamine is used as an anaesthetic, analgesic – painkiller, but it is also a substance with psychedelic effects. Ketamine interacts mainly with the glutamatergic system, as a noncompetitive NMDA glutamatergic receptor antagonist, but its effects can be contributed probably to an overall disruption of the neurochemical systems of an organization. Indirect interaction with the dopaminergic system is proven. Ketamine acts at a presynaptic level, causing an increase in extracellular dopamine concentration. Regarding the direct interaction between ketamine and dopamine receptors, experiments conducted in vitro indicated that ketamine had an agonist-like action on dopaminergic D2 receptors. In vivo studies did not result in any direct ketamine-dopaminergic receptors interactions. This paper attempts to explore the studies concerning dopaminergic system and ketamine and exhibit the existent information focusing on the direct interaction that emerges between ketamine and dopaminergic receptors.
Αναφορές – References
  1. The WHO: Expert Committee on Drug Dependence (34th), Critical review of KETAMINE (2006)
  2. Morgan C.J., Curran H.V.: Ketamine use: a review. Addiction 107: 27-38 (2012)
  3. Rang H.P., Dale M.M., Ritter J.M., Moyr P.K.: Pharmacology. Chapter 35. General anaesthetic agents. p.550 (2007)
  4. Kopsky D.J., Keppel Hesselink J.M., Bhaskar A., Hariton G., Romanenko V., Casale R.: Analgesic effects of topical ketamine. Minerva Anestesiol. [Epub ahead of print] (2014 May 22)
  5. Bergman S.A.: Ketamine: review of its pharmacology and its use in pediatric anesthesia. Anesth. Prog. 46: 10-20 (1999)
  6. Cengiz P., Gokcinar D., Karabeyoglu I., Topcu H., Cicek G.S., Gogus N.: Intraoperative low-dose ketamine infusion reduces acute postoperative pain following total knee replacement surgery: a prospective, randomized double-blind placebo-controlled trial. J. Coll. Physicians Surg. Pak, 24(5): 299-303 (2014)
  7. Behaeen K., Soltanzadeh M., Nesioonpour S., Ebadi A., Olapour A., Aslani S.M.: Analgesic effect of low dose subcutaneous ketamine administration before and after cesarean section. Iran Red Crescent Med. J. 16(3): 15506 (2014)
  8. Dalgarno P.J., Shewan D.: Illicit use of ketamine in Scotland. J. Psychoactive Drugs 28(2): 191-199 (1996)
  9. Shewan D., Dalgarno P.: Ecstasy and neurodegeneration. …such as ketamine. BMJ 313(7054): 424 (1996)
  10. Krystal J.H., Karper L.P., Seibyl J.P., Freeman G.K., Delaney R., BremnerJ.D., Heninger G.R., Bowers M.B.Jr, Charney D.S.: Subanesthetic effects of the noncompetitive NMDA antagonist, ketamine, in humans. Psychotomimetic, perceptual, cognitive, and neuroendocrine responses. Arch. Gen. Psychiatry 51: 199-214 (1994)
  11. Newcomer J.W., Farber N.B., Jevtovic-Todorovic V., Selke G., Melson A.K., Hershey T., Craft S., Olney J.W.: Ketamine-induced NMDA receptor hypofunction as a model of memory impairment and psychosis. Neuropsychopharmacology 20: 106-118 (1999)
  12. Morgan C.J., Mofeez A., Brandner B., Bromley L., Curran H.V.: Acute effects of ketamine on memory systems and psychotic symptoms in healthy volunteers. Neuropsychopharmacology 29: 208-218 (2004)
  13. Hashimoto K.: The R-Stereoisomer of Ketamine as an Alternative for Ketamine for Treatment-resistant Major Depression. Clin. Psychopharmacol. Neurosci. 12(1): 72-73 (2014)
  14. Naughton M., Clarke G., O′Leary O.F., Cryan J.F., Dinan T.G.: A review of ketamine in affective disorders: Current evidence of clinical efficacy, limitations of use andpre-clinical evidence on proposed mechanisms of action. J. Affect. Disorders 156: 24-35 (2014).
  15. Harrison N.L, Simmonds M.A.: Quantitative studies on some antagonists of N-methyl D-aspartate in slices of rat cerebral cortex. Br. J. Pharmacol. 84(2): 381-391 (1985)
  16. Anis N.A., Berry S.C., Burton N.R., Lodge D.: The dissociative anaesthetics, ketamine and phencyclidine, selectively reduce excitation of central mammalian neurones by N-methyl-aspartate. Br. J. Pharmacol. 79: 565-575 (1983)
  17. Duncan G.E., Miyamoto S., Leipzig J.N., Lieberman J.A.: Comparison of brain metabolic activity patterns induced by ketamine, MK-801 and amphetamine in rats: support for NMDA receptor involvement in responses to subanesthetic dose of ketamine. Brain Res. 843: 171-183 (1999)
  18. Lodge D., Johnson K.M.: Noncompetitive excitatory amino acid receptor antagonists. Trends Pharmacol Sci. 11: 81-86 (1990)
  19. MacDonald J.F., Miljkovic Z., Pennefather P.: Use-dependent block of excitatory amino acid currents in cultured neurons by ketamine. J. Neurophysiol. 58: 251-266 (1987)
  20. Hirota K., Sikand K.S., Lambert D.G.: Interaction of ketamine with mu2 opioid receptors in SH-SY5Y human neuroblastoma cells. J. Anesth. 13(2): 107-109 (1999)
  21. Smith A.J., Pekoe G.M., Monroe P.J., Martin L.L., Cabral M.E.Y., Crisp T.: Ketamine analgesia in rats may be mediated by an interaction with opiate receptors. Domino EF (ed) Status of ketamine in anesthesiology. Ann. Arbor: 199-209 (1990)
  22. Hustveit O., Maurset A., Oye I.: Interaction of the chiral forms of ketamine with opioid, phencyclidine, sigma and muscarinic receptors. Pharmacol. Toxicol, 77: 355-359 (1995)
  23. Narita M., Yoshizawa K., Aoki K., Takagi M., Miyatake M., Suzuki T.: A putative sigma1 receptor antagonist NE-100 attenuates the discriminative stimulus effects of ketamine in rats. Addict. Biol. v.4: 373-376 (2001)

24 Nakao S., Miyamoto E., Masuzawa M., Kambara T., Shingu K.: Ketamine-induced c-Fos expression in the mouse posterior cingulate and retrosplenial cortices is mediated not only via NMDA receptors but also via sigma receptors. Brain Res. 926: 191-196 (2002)

  1. Pharmaceutical Society of Australia. 2.1.1 IV general anaesthetics. Australian Medicines Handbook. Australian Medicines Handbook Pty Ltd. p. 13. (2011)
  2. Vallone D., Picetti R., Borrelli E.: Structure and function of dopamine receptors. Neurosci. Biobehav. Rev. 24: 125-132 (2000)
  3. Stuart C., Sealfon C., Olanow C.: Dopamine receptors: from structure to behavior. Trends Neurosci. 23: 34-40. (2000)
  4. Emilien G., Maloteaux J.M., Geurts M., Hoogenberg K., Cragg S.: Dopamine receptors – physiological understanding to therapeutic intervention potential. Pharmacol. Ther. 84: 133-156 (1999)
  5. Jaber M., Robinson S.W., Missale C., Caron M.G.: Dopamine Receptors and Brain Function. Nruropharmacology 35: 1503-1519 (1996)
  6. Smith Y. Kieval J.Z.: Anatomy of the dopamine system in the basal ganglia. Trends Neurosci. 23: 28-33 (2002)
  7. Breier A., Adler C.M., Weisenfeld N., Su T.P., Elman I., Picken L., Malhotra A.K., Pickar D.: Effects of NMDA antagonism on striatal dopamine release in healthy subjects: application of a novel PET approach. Synapse 29: 142-147 (1998)
  8. Lorrain D.S., Baccei C.S., Bristow L.J., Anderson J.J., Varney M.A.: Effects of ketamine and N-methyl-D-aspartate on glutamate and dopamine release in the rat prefrontal cortex: modulation by a group II selective metabotropic glutamate receptor agonist LY379268. Neuroscience 117: 697-706 (2003)
  9. Moghaddam B., Adams B., Verma A., Daly D.: Activation of glutamatergic neurotransmission by ketamine: a novel step in the pathway from NMDA receptor blockade to dopaminergic and cognitive disruptions associated with the prefrontal cortex. J. Neurosci. 17: 2921-2927 (1997)
  10. Usun Y., Eybrard S., Meyer F., Louilot A.: Ketamine increases striatal dopamine release and hyperlocomotion in adult rats after postnatal functional blockade of the prefrontal cortex. Behav. Brain Res. 256: 229-237 (2013)
  11. Jedema H.P., Moghaddam B.: Characterization of excitatory amino acid modulation of dopamine release in the prefrontal cortex of conscious rats. J. Neurochem. 66(4): 1448-1453 (1996)
  12. Tso M.M., Blatchford K.L., Callado L.F., McLaughlin D.P., Stamford J.A.: Stereoselective effects of ketamine on dopamine, serotonin and noradrenaline release and uptake in rat brain slices. Neurochem. Int. 44: 1-7 (2004)
  13. Aquilonius S.M, Bertröm K., Eckernäs S.-Å., Hartvig P., Leenders K.L., Lundquist H., Antoni G., Gee A., Rimland A., Uhlin J., Långström B.: In vivo evaluation of striatal dopamine reuptake sites using 11C-nomifensine and positron emission tomography. Acta Neurol. Scand. 76(4): 237-315 (1987)
  14. Tan S., Lam W.P., Wai M.S.M., Yu W.H.A., Yew D.T.: Chronic Ketamine Administration Modulates Midbrain Dopamine System in Mice. PLoS ONE 7(8):e43947. doi:10.1371/journal.pone.0043947. (2013)
  15. Fukuchi M., Fujii H., Takachi H., Ichinose H., Kuwana Y., Tabuchi A., Tsuda M.: Activation of tyrosine hydroxylase (TH) gene transcription induced by brain-derived neurotrophic factor (BDNF) and its selective inhibition through Ca(2+) signals evoked via the N-methyl-D-aspartate (NMDA) receptor. Brain Res. 1366: 18-26 (2010)
  16. Kapur S., Seeman P.: Ketamine has equal affinity for NMDA receptors and the high-affinity state of the dopamine D2 receptor. Biol. Psychiatry 49(11): 954-957 (2001)

41 Kapur S., Seeman P.: NMDA receptor antagonists ketamine and PCP have direct effects on the dopamine D2 and serotonin 5-HT2 receptors – implications for models of schizophrenia. Mol. Psychiatry 7: 837-844 (2002)

  1. Seeman P., Ko F., Tallerico T.: Dopamine receptor contribution to the action of PCP, LSD and ketamine psychotomimetics. Molecular Psychiatry 10: 877-883 (2005)
  2. Ko F., Seeman P., Sun W.S., Kapur S.: Dopamine D2 receptors internalize in their low-affinity state. NeuroReport 13: 1017-1020 (2002)
  3. Gardner B., Strange P.G.: Agonist action at D2(long) dopamine receptors: ligand binding and functional assays. Br. J. Pharmacol. 124: 978-984 (1998)
  4. Seeman P., Guan H.C.: Phencyclidine and glutamate agonist LY379268 stimulate dopamine D2High receptors: D2 basis for schizophrenia. SYNAPSE 62: 819-828 (2008)
  5. Jordan S., Chen R., Fernalld R., Johnson J., Regardie K., Kambayashi J., Tadori Y., Kitagawa H., Kikuchi T.: In vitro biochemical evidence that the psychotomimetics phencyclidine, ketamine and dizocilpine (MK-801) are inactive at cloned human and rat dopamine D2 receptors. Eur. J. Pharmacol. 540: 53-56 (2006)
  6. Odagaki Y., Toyoshima R.: Dopamine D2 receptor-mediated G protein activation assessed by agonist-stimulated [35S]guanosine 5′-O-(γ-thiotriphosphate) binding in rat striatal membranes. Prog. Neuro-Psychopharmacol. Biol. Psychiatry 30: 1304-1312 (2006)
  7. Seeman P., Guan H.C., Hibert H.: Dopamine D2High receptors stimulated by phencyclidines, lysergic acid diethylamide, salvinorin A, and modafinil. Synapse 63(8): 698-704 (2009)
  8. Seeman P., Ulpian C., Wreggett K.A., Wells J.W.: Dopamine receptor parameters detected by [3H]spiperone depend on tissue concentration: Analysis and examples. J. Neurochem. 43: 221-235 (1984)

50. George S.R., Watanabe M., Di Paolo T., Falardeau P., Labrie F., Seeman P.: The functional state of the dopamine receptor in the anterior pituitary is in the high affinity form. Endocrinology 117: 690-697 (1985)

Σχετικές Εργασίες – Relative Papers

Online ISSN 1011-6575

 

Bookmark the permalink.

Comments are closed.