Medical Hypotheses
Volume 56, Issue 6 , Pages 638-643, June 2001

Are cannabinoid receptor knockout mice animal models for schizophrenia?

Praxis für Innere Medizin, Adliswil, Switzerland

Received 21 September 2000; accepted 19 October 2000.

Abstract 

Schizophrenia is a devastating psychiatric disorder with a high prevalence worldwide. There is therefore a need for animal models allowing the development of new therapeutic interventions and reliable diagnostic tests. In the temporal domain, cannabinoid receptor gene (CB1) knockout mice exhibit behavioural alterations, which parallel symptoms in schizophrenia, cannabis intoxication and dopamine D2 activation. While a specific nucleotide homology between CB1 and D2 accounts for the pathophysiology, pre-inserted spirochaetal DNA on the polyadenylation signal of CB1 reveals the aetiology of schizophrenia. If, in analogy to thalassaemia, mutations occur within this 3′ regulatory domain, the genetic expression of CB1 is disrupted and sequential information lost in time. CB1, previously unrecognized as a candidate gene, thus unifies the different aspects of schizophrenic psychosis: cannabis-induced model psychosis, disrupted information processing, spatio-temporal distortions and other psychotic symptoms, disturbed neuronal migration, schizophrenic brain disorder, familial transmission, and prenatal infection byBorrelia burgdorferi .

No full text is available. To read the body of this article, please view the PDF online.

To access this article, please choose from the options below

Login to an existing account or Register a new account.

  • Purchase this article for 31.50 USD (You must login/register to purchase this article)

    Online access for 24 hours. The PDF version can be downloaded as your permanent record.

  • Subscribe to this title

    Get unlimited online access to this article and all other articles in this title 24/7 for one year.

  • Claim access now

    For current subscribers with Society Membership or Account Number.

  • Visit SciVerse ScienceDirect to see if you have access via your institution.
 

PII: S0306-9877(00)91261-1

doi:10.1054/mehy.2000.1261

Medical Hypotheses
Volume 56, Issue 6 , Pages 638-643, June 2001