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Prevention of Post-Traumatic Stress Disorder

Potential „morning-after pill“ sucessfully tested in animal model

Scientists at the Max Planck Institute of Psychiatry have recently identified the neuropeptide Corticotropin-releasing hormone (CRH) as an important factor for developing a post-traumatic stress disorder (PTSD). This discovery opens up a new pharmacological strategy for prevention of consequential mental damage after traumas by means of the so-called CRHR1-antagonists. During the test treatment on „traumatized“ mice, these pharmaceutical products reduced the appearance of disease-specific symptoms, such as anxiety, startle response and trauma-associated memory formation.

 

Exposure to a traumatic event can trigger off a particularly severe type of psychiatric disorder in human beings, the post-traumatic stress disorder. Currently, classical antidepressants are used for medical treatment. It would, however, be better to prevent the development of a PTSD by taking disease-preventive pharmaceuticals directly after the trauma. In order to understand the neuobiological basics of the PTSD, the research group of Carsten Wotjak explores the development of the disease in an animal model. He has succeeded in establishing a mouse model which takes the essential, disease-specific criteria of the psychiatric disorder into account.

 

In a recently published study, the scientists have shown that CRH and its receptor CRHR1 are involved in the symptomatology of PTSD as main regulators of the neuronal stress reaction. Indeed, traumatized mice lacking CRHR1 do not show increased startle response and have a reduced trauma-associated memory formation.

With this evidence, so-called CRHR1-antagonists (i.e. substances which can specifically block the CRHR1) are gaining increasing importance as possible therapeutic agents of the PTSD. In fact, treatment with CRHR1-antagonists leads to a reduction of the trauma-associated memory and the unspecific stress reaction in traumatized wild-type animals provided that it is performed within the first week after the trauma.

 

 

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Figure legend: After a trauma, an elevated signal transmission at the CRHR-receptors of the forebrain can be observed. As a consequence of this, traumatic memory contents are reinforced and maintained over a long period of time through an increased availability of glutamatergic GluR1-receptors. This process can be influenced pharmacologically to the effect that the blockade of the CRHR1-receptors during the first week after the trauma will result in a significantly reduced memory of the trauma, counteracting the development of a PTSD. 

„In view of the lack of psychopharmacological possibilities of prevention, the results from the animal experiments about the CRHR1-blocking during a sensitive phase after a trauma - quasi as a „morning-after pill“ - might represent a new promising approach for the clinical practise. In future, the „first aid kit“ might then include a CRHR1-antagonist which might prevent traumatized people from developing a PTSD after having taken their medicine for several days“, Carsten Wotjak, group leader at the Max Planck Institute of Psychiatry, explains.

 

 

Original publication:

Thoeringer CK, Henes K, Eder M, Dahlhoff M, Wurst W, Holsboer F, Deussing JM, Moosmang S, Wotjak CT.

Consolidation of remote fear memories involves corticotropin releasing hormone (CRH) receptor type 1-mediated enhancement of AMPA receptor GluR1 signaling in the dentate gyrus

Neuropsychopharmacology. 2011 Oct 26. doi: 10.1038/npp.2011.256.

 

 

For further information, please contact:

Dr. Barbara Meyer

Public relations

Max Planck Institute of Psychiatry

Phone: +49 89 30622-616

Fax: +49 89 30622-348

Email: bmeyer[a]mpipsykl.mpg.de


Date of press release: 02.12.2011