CANNASTRESS

Involvement of the endocannabinoid system in posttraumatic stress disorder

 Coordinatore MAX PLANCK GESELLSCHAFT ZUR FOERDERUNG DER WISSENSCHAFTEN E.V. 

 Organization address address: Hofgartenstrasse 8
city: MUENCHEN
postcode: 80539

contact info
Titolo: Ms.
Nome: Silvia
Cognome: Juckoff
Email: send email
Telefono: +49 89 30622474
Fax: +49 89 30622444

 Nazionalità Coordinatore Germany [DE]
 Totale costo 168˙794 €
 EC contributo 168˙794 €
 Programma FP7-PEOPLE
Specific programme "People" implementing the Seventh Framework Programme of the European Community for research, technological development and demonstration activities (2007 to 2013)
 Code Call FP7-PEOPLE-2013-IEF
 Funding Scheme MC-IEF
 Anno di inizio 2014
 Periodo (anno-mese-giorno) 2014-07-01   -   2016-06-30

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    MAX PLANCK GESELLSCHAFT ZUR FOERDERUNG DER WISSENSCHAFTEN E.V.

 Organization address address: Hofgartenstrasse 8
city: MUENCHEN
postcode: 80539

contact info
Titolo: Ms.
Nome: Silvia
Cognome: Juckoff
Email: send email
Telefono: +49 89 30622474
Fax: +49 89 30622444

DE (MUENCHEN) coordinator 168˙794.40

Mappa


 Word cloud

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aftermath    glutamate    disorder    evidence    therapeutic    cb    health    endocannabinoid    involvement    ptsd    traumatic   

 Obiettivo del progetto (Objective)

'Posttraumatic stress disorder (PTSD) belongs to the most frequent anxiety disorders. It develops in the aftermath of a traumatic life event and represents a clear public health problem. In spite of its increasing incidence, there are no established effective treatments for this disorder. In addition, even though a broad body of evidence concerning neurobiological correlates of this illness, the pathomechanisms of PTSD is still poorly understood. Therefore, there is a need to identify new therapeutic targets/strategies for PTSD. Interestingly, only 10-15 percent of the people confronted with a trauma develop PTSD in its aftermath. This points to the existence of highly efficient “salutogenic” (i.e. health promoting) factors. With the help of animal models we have accumulated preliminary evidence that the endocannabinoid system of the brain plays an important role in the modulation of processes occurring in PSTD and is pointed out as a potential therapeutic target for this neuropsychiatric disorder. The involvement of ECS in the development of PTSD symptoms seems to critically depend on the neuronal population affected. For instance, CB1 on glutamatergic neurons constrain the expression of fear responses, once the averseness of the test situation has surpassed a certain threshold. Therefore, the general objective of this research proposal is to unravel the time point, sites and consequences of attenuated CB1 buffered glutamate signalling in a mouse model of PTSD. To address this issue, we will combine genetic, in vivo imaging, electrophysiology, behavioural and biochemical studies in mice. The achievement of these objectives will provide new insights into the mechanisms underling the involvement of endocannabinoid system into the adverse consequences of a traumatic experience that might lead to the development of new therapeutic approaches for the treatment of PTSD that are based on downscaling glutamate release at presynaptic terminals.'

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