„Legalizować czy nie?” – analiza związku pomiędzy stosowaniem kanabinoli a częstością występowania i obrazem klinicznym zaburzeń psychotycznych

• Authors: Marta Gawłowska , Jolanta Rabe-Jabłońska

Title variants

EN

“To legalize or not to legalize?” – analysis of association between cannabis use and psychosis frequency and clinical manifestation

• Languages of publication: EN PL

Abstracts

EN

The association between cannabis use and psychotic disorders has long been recognized. Among others, it is evidenced that cannabinoids can produce transient positive, negative and cognitive psychotic symptoms in healthy individuals and exacerbate symptoms and trigger relapse on the course of established psychotic disorder. But until recently, little was known about the mechanism, by which these effects are caused. According to the newest research, the mechanism may involve dopamine, GABA or glutamate neurotransmission. As only a small proportion of total population exposed to cannabinoids develops psychotic disorders, it is likely that cannabinoids are not the main causative factor of psychosis but may play a role of significant risk factor that contributes to psychosis manifestation. Such parameters as dose, duration and the age of first exposure to cannabinoids are well established modifying factors of psychosis course, however the mechanisms of this association are still mostly unknown. Recently, more and more attention has been given to the novel hypotheses including the role of cannabinoids on neurodevelopment of central nervous system. It is proved that endocannabinoids may play an important role in such processes as neurogenesis, neural specification, neural maturation, neuronal migration, axonal elongation, and glia formation. Use of exogenous cannabinoids, by disrupting the endocannabinoid system and interfering with neurodevelopmental processes, may provide a mechanism by which exposure to cannabinoids during adolescence may.

PL

Związek pomiędzy zażywaniem kanabinoli a występowaniem zaburzeń psychotycznych jest opisywany od dawna. Udowodniono między innymi, że kanabinole mogą wywoływać przemijające objawy pozytywne, negatywne i poznawcze psychozy u zdrowych osób oraz zaostrzać objawy lub powodować ich nawrót w przebiegu wcześniej rozpoznanych zaburzeń psychotycznych. Jednak nadal niewiele wiadomo o mechanizmach, które powodują powstawanie tych symptomów. Zgodnie z najnowszymi doniesieniami mogą one angażować układy dopaminergiczny, GABA-ergiczny i glutaminergiczny. Ponieważ tylko u części osób zażywających kanabinole rozwijają się objawy psychotyczne, prawdopodobnie substancje te nie stanowią głównego czynnika sprawczego psychozy, lecz mogą stanowić ważny czynnik ryzyka, który przyczynia się do manifestacji jej objawów. Takie wskaźniki, jak dawka, długość stosowania oraz wiek pierwszego kontaktu z kanabinolami, stanowią uznane czynniki modyfikujące przebieg psychozy, jakkolwiek mechanizm tego zjawiska pozostaje w dużym stopniu niejasny. W ostatnim czasie coraz szersze uznanie zyskują nowe hipotezy, zakładające możliwy wpływ kanabinoli na rozwój centralnego układu nerwowego. Istnieją dowody na to, że endogenny układ kanabinoidalny może odgrywać istotną rolę w takich procesach, jak neurogeneza, różnicowanie, dojrzewanie i migracja neuronów, wydłużanie aksonów oraz formowanie struktur gleju. Zażywanie kanabinoidów egzogennych, zaburzając działanie układu endokanabinoidalnego oraz zakłócając procesy neurorozwojowe, może stanowić mechanizm, poprzez który ekspozycja na działanie tych substancji w okresie adolescencji zwiększa ryzyko rozwoju schizofrenii lub innych utrwalonych zaburzeń psychotycznych.

Keywords

EN

cannabinoids   czynnik ryzyka   kanabinole   psychotic disorders   risk factor   schizofrenia   schizophrenia   tetrahydrocannabinol (THC)   tetrahydrokanabinol (THC)   zaburzenia psychotyczne  

Discipline

• MEDICINE: MEDICINE

• Publisher: Medical Communications
• Journal: Psychiatria i Psychologia Kliniczna
• Year: 2010
• Volume: 10
• Issue: 1
• Pages: 38-44

References

• 1. Hibell B., Andersson B., Ahlstrom S. i wsp.: The 1999 ESPAD Report: Alcohol and Other Drug Use Among Students in 30 European Countries. The Swedish Council for Information on Alcohol and Other Drugs (CAN) and The Pompidou Group at the Council of Europe. Stockholm 2000.
• 2. Webb E., Ashton C.H., Kelly P., Kamali F.: Alcohol and drug use in UK university students. Lancet 1996; 348: 922-925.
• 3. Fergusson D.M., Horwood L.J.: Cannabis use and dependence in a New Zealand birth cohort. N. Z. Med. J. 2000; 113: 156-158.
• 4. D’Souza D.C.: Cannabinoids and psychosis. Int. Rev. Neu-robiol. 2007; 78: 289-326.
• 5. Smith M.J., Thirthalli J., Abdallah A.B. i wsp.: Prevalence of psychotic symptoms in substance users: a comparison across substances. Compr. Psychiatry 2009; 50: 245-250.
• 6. Carney M.W, Bacelle L., Robinson B.: Psychosis after cannabis abuse. Br. Med. J. (Clin. Res. Ed.) 1984; 288: 1047.
• 7. Chopra G.S., Smith J.W: Psychotic reactions following cannabis use in East Indians. Arch. Gen. Psychiatry 1974; 30: 24-27.
• 8. Gerra G., Zaimovic A., Gerra M.L. i wsp.: Pharmacology and toxicology of Cannabis derivatives and endocannabi-noid agonists. Recent Pat. CNS Drug Discov. 2010; 5: 46-52.
• 9. Marinol product monograph (Sanofi-Canada), Rev 1996. W: Gillis M.C. (red.): CPS Compendium of Pharmaceuticals and Specialities. Wyd. 33, Canadian Pharmacists Association, Ottawa 1998: 941-942.
• 10. Jones R.T., Stone G.C.: Psychological studies of marijuana and alcohol in man. Psychopharmacologia 1970; 18: 108-117.
• 11. Melges F.T., Tinklenberg J.R., Hollister L.E., Gillespie H.K.: Marihuana and temporal disintegration. Science 1970; 168: 1118-1120.
• 12. Leweke F.M., Schneider U., Thies M. i wsp.: Effects of synthetic A9-tetrahydrocannabinol on binocular depth inversion of natural and artificial objects in man. Psychopharmacology (Berl.) 1999; 142: 230-235.
• 13. D’Souza D.C., Perry E., MacDougall L. i wsp.: The psychotomimetic effects of intravenous delta-9-tetrahydrocannabinol in healthy individuals: implications for psychosis. Neuropsychopharmacology 2004; 29: 1558-1572.
• 14. Andreasson S., Allebeck P., Engstrom A., Rydberg U.: Cannabis and schizophrenia. A longitudinal study of Swedish conscripts. Lancet 1987; 2: 1483-1486.
• 15. Zammit S., Allebeck P, Andreasson S. i wsp.: Self reported cannabis use as a risk factor for schizophrenia in Swedish conscripts of 1969: historical cohort study. BMJ 2002; 325: 1199.
• 16. Arseneault L., Cannon M., Poulton R. i wsp.: Cannabis use in adolescence and risk for adult psychosis: longitudinal prospective study. BMJ 2002; 325: 1212-1213.
• 17. Fergusson D.M., Horwood L.J., Swain-Campbell N.R.: Cannabis dependence and psychotic symptoms in young people. Psychol. Med. 2003; 33: 15-21.
• 18. Weiser M., Knobler H.Y., Noy S., Kaplan Z.: Clinical characteristics of adolescents later hospitalized for schizophrenia. Am. J. Med. Genet. 2002; 114: 949-955.
• 19. van Os J., Bak M., Hanssen M. i wsp.: Cannabis use and psychosis: a longitudinal population-based study. Am. J. Epidemiol. 2002; 156: 319-327.
• 20. Henquet C., Krabbendam L., Spauwen J. i wsp.: Prospective cohort study of cannabis use, predisposition for psychosis, and psychotic symptoms in young people. BMJ 2005; 330: 11.
• 21. Moore T.H., Zammit S., Lingford-Hughes A. i wsp.: Cannabis use and risk of psychotic or affective mental health outcomes: a systematic review. Lancet 2007; 370: 319-328.
• 22. Freund T.F., Katona I., Piomelli D.: Role of endogenous cannabinoids in synaptic signaling. Physiol. Rev. 2003; 83: 1017-1066.
• 23. Hermann H., Marsicano G., Lutz B.: Coexpression of the cannabinoid receptor type 1 with dopamine and serotonin receptors in distinct neuronal subpopulations of the adult mouse forebrain. Neuroscience 2002; 109: 451-460.
• 24. Meschler J.P., Howlett A.C.: Signal transduction interactions between CBj cannabinoid and dopamine receptors in the rat and monkey striatum. Neuropharmacology 2001; 40: 918-926.
• 25. French E.D., Dillon K., Wu X.: Cannabinoids excite dopamine neurons in the ventral tegmentum and substantia nigra. Neuroreport 1997; 8: 649-652.
• 26. Gessa G.L., Melis M., Muntoni A.L., Diana M.: Cannabinoids activate mesolimbic dopamine neurons by an action on cannabinoid CBj receptors. Eur. J. Pharmacol. 1998; 341: 39-44.
• 27. Chen J., Paredes W, Lowinson J.H., Gardner E.L.: Delta 9-tetrahydrocannabinol enhances presynaptic dopamine efflux in medial prefrontal cortex. Eur. J. Pharmacol. 1990; 190: 259-262.
• 28. Fadda P., Scherma M., Spano M.S. i wsp.: Cannabinoid selfadministration increases dopamine release in the nucleus accumbens. Neuroreport 2006; 17: 1629-1632.
• 29. Bossong M.G., van Berckel B.N., Boellaard R. i wsp.: A9-tet-rahydrocannabinol induces dopamine release in the human striatum. Neuropsychopharmacology 2009; 34: 759-766.
• 30. D’Souza D.C., Braley G., Blaise R. i wsp.: Effects of haloperi-dol on the behavioral, subjective, cognitive, motor, and neuroendocrine effects of A-9-tetrahydrocannabinol in humans. Psychopharmacology (Berl.) 2008; 198: 587-603.
• 31. Egerton A., Allison C., Brett R.R., Pratt J.A.: Cannabinoids and prefrontal cortical function: insights from preclinical studies. Neurosci. Biobehav. Rev. 2006; 30: 680-695.
• 32. Laviolette S.R., Grace A.A.: The roles of cannabinoid and dopamine receptor systems in neural emotional learning circuits: implications for schizophrenia and addiction. Cell. Mol. Life Sci. 2006; 63: 1597-1613.
• 33. Pistis M., Porcu G., Melis M. i wsp.: Effects of cannabinoids on prefrontal neuronal responses to ventral tegmental area stimulation. Eur. J. Neurosci. 2001; 14: 96-102.
• 34. Yang C.R., Seamans J.K., Gorelova N.: Developing a neuronal model for the pathophysiology of schizophrenia based on the nature of electrophysiological actions of dopamine in the prefrontal cortex. Neuropsychopharmacology 1999; 21: 161-194.
• 35. Monory K., Blaudzun H., Massa F. i wsp.: Genetic dissection of behavioural and autonomic effects of 9-tetrahydrocannabinol in mice. PLoS Biol. 2007; 5: e269.
• 36. Hajos N., Katona I., Naiem S.S. i wsp.: Cannabinoids inhibit hippocampal GABAergic transmission and network oscillations. Eur. J. Neurosci. 2000; 12: 3239-3249.
• 37. Hoffman A.F., Lupica C.R.: Mechanisms of cannabinoid inhibition of GABAA synaptic transmission in the hippocampus. J. Neurosci. 2000; 20: 2470-2479.
• 38. Hajos M., Hoffmann WE., Kocsis B.: Activation of cannabinoid-1 receptors disrupts sensory gating and neuronal oscillation: relevance to schizophrenia. Biol. Psychiatry 2008; 63: 1075-1083.
• 39. Robbe D., Montgomery S.M., Thome A. i wsp.: Cannabinoids reveal importance of spike timing coordination in hippocampal function. Nat. Neurosci. 2006; 9: 1526-1533.
• 40. Domenici M.R., Azad S.C., Marsicano G. i wsp.: Cannabinoid receptor type 1 located on presynaptic terminals of principal neurons in the forebrain controls glutamatergic synaptic transmission. J. Neurosci. 2006; 26: 5794-5799.
• 41. Takahashi K.A., Castillo P.E.: The CB1 cannabinoid receptor mediates glutamatergic synaptic suppression in the hippocampus. Neuroscience 2006; 139: 795-802.
• 42. Auclair N., Otani S., Soubrie P., Crepel F.: Cannabinoids modulate synaptic strength and plasticity at glutamatergic synapses of rat prefrontal cortex pyramidal neurons. J. Neurophysiol. 2000; 83: 3287-3293.
• 43. Azad S.C., Eder M., Marsicano G. i wsp.: Activation of the cannabinoid receptor type 1 decreases glutamatergic and GABAergic synaptic transmission in the lateral amygdala of the mouse. Learn. Mem. 2003; 10: 116-128.
• 44. Misner D.L., Sullivan J.M.: Mechanism of cannabinoid effects on long-term potentiation and depression in hippocampal CA1 neurons. J. Neurosci. 1999; 19: 6795-6805.
• 45. Robbe D., Alonso G., Duchamp F. i wsp.: Localization and mechanisms of action of cannabinoid receptors at the glutamatergic synapses of the mouse nucleus accumbens. J. Neurosci. 2001; 21: 109-116.
• 46. Arendt M., Mortensen P.B., Rosenberg R. i wsp.: Familial predisposition for psychiatric disorder: comparison of subjects treated for cannabis-induced psychosis and schizophrenia. Arch. Gen. Psychiatry 2008; 65: 1269-1274.
• 47. Corcoran C.M., Kimhy D., Stanford A. i wsp.: Temporal association of cannabis use with symptoms in individuals at clinical high risk for psychosis. Schizophr. Res. 2008; 106: 286-293.
• 48. Kristensen K., Cadenhead K.S.: Cannabis abuse and risk for psychosis in a prodromal sample. Psychiatry Res. 2007; 151: 151-154.
• 49. Henquet C., Rosa A., Krabbendam L. i wsp.: An experimental study of catechol-O-methyltransferase Val158Met moderation of A-9-tetrahydrocannabinol-induced effects on psychosis and cognition. Neuropsychopharmacology 2006; 31: 2748-2757.
• 50. Veling W, Mackenbach J.P., van Os J., Hoek H.W: Cannabis use and genetic predisposition for schizophrenia: a case-control study. Psychol. Med. 2008; 38: 1251-1256.
• 51. Caspi A., Moffitt T.E., Cannon M. i wsp.: Moderation of the effect of adolescent-onset cannabis use on adult psychosis by a functional polymorphism in the catechol-O-methyl-transferase gene: longitudinal evidence of a gene X environment interaction. Biol. Psychiatry 2005; 57: 1117-1127.
• 52. Munafo M.R., Attwood A.S., Flint J.: Neuregulin 1 genotype and schizophrenia. Schizophr. Bull. 2008; 34: 9-12.
• 53. Boucher A.A., Arnold J.C., Duffy L. i wsp.: Heterozygous neuregulin 1 mice are more sensitive to the behavioural effects of A9-tetrahydrocannabinol. Psychopharmacology (Berl.) 2007; 192: 325-336.
• 54. Comings D.E., Muhleman D., Gade R. i wsp.: Cannabinoid receptor gene (CNR1): association with IV drug use. Mol. Psychiatry 1997; 2: 161-168.
• 55. Schmidt L.G., Samochowiec J., Finckh U. i wsp.: Association of a CB1 cannabinoid receptor gene (CNR1) polymorphism with severe alcohol dependence. Drug Alcohol Depend. 2002; 65: 221-224.
• 56. Seifert J., Ossege S., Emrich H.M. i wsp.: No association of CNR1 gene variations with susceptibility to schizophrenia. Neurosci. Lett. 2007; 426: 29-33.
• 57. Ujike H., Takaki M., Nakata K. i wsp.: CNR1, central canna-binoid receptor gene, associated with susceptibility to hebephrenic schizophrenia. Mol. Psychiatry 2002; 7: 515-518.
• 58. Zammit S., Spurlock G., Williams H. i wsp.: Genotype effects of CHRNA7, CNR1 and COMT in schizophrenia: interactions with tobacco and cannabis use. Br. J. Psychiatry 2007; 191: 402-407.
• 59. Galve-Roperh I., Aguado T., Palazuelos J., Guzman M.: The endocannabinoid system and neurogenesis in health and disease. Neuroscientist 2007; 13: 109-114.
• 60. Aguado T., Palazuelos J., Monory K. i wsp.: The endocannabinoid system promotes astroglial differentiation by acting on neural progenitor cells. J. Neurosci. 2006; 26: 1551-1561.
• 61. Berghuis P., Rajnicek A.M., Morozov Y.M. i wsp.: Hardwiring the brain: endocannabinoids shape neuronal connectivity. Science 2007; 316: 1212-1216.
• 62. Mulder J., Aguado T., Keimpema E. i wsp.: Endocannabinoid signaling controls pyramidal cell specification and long-range axon patterning. Proc. Natl Acad. Sci. USA 2008; 105: 8760-8765.
• 63. Rice D., Barone S. Jr: Critical periods of vulnerability for the developing nervous system: evidence from humans and animal models. Environ. Health Perspect. 2000; 108 supl. 3: 511-533.
• 64. Buckley P.F., Mahadik S., Pillai A., Terry A. Jr: Neurotroph-ins and schizophrenia. Schizophr. Res. 2007; 94: 1-11.
• 65. D’Souza D.C., Pittman B., Perry E., Simen A.: Preliminary evidence of cannabinoid effects on brain-derived neurotrophic factor (BDNF) levels in humans. Psychopharmacology (Berl.) 2009; 202: 569-578.
• 66. Angelucci F., Ricci V, Spalletta G. i wsp.: Reduced serum concentrations of nerve growth factor, but not brain-derived neurotrophic factor, in chronic cannabis abusers. Eur. Neuropsychopharmacol. 2008; 18: 882-887.

• Document Type: article