PhD Scientific Days 2017

Oral Presentations: Neurosciences

Endocannabinoid interactions in the regulation of behavioral responses to trauma

Előadó neve

Dr. Balogh, Zoltán, PhD

Előadó munkahelye

Institute of Experimental Medicine - Hungarian Academy of Sciences, Deparment of Behavioural Neurobiology

Előadó telefonszáma

+36303170091

Előadó e-mail címe

balogh.zoltan@koki.mta.hu

Az előadás címe

Endocannabinoid interactions in the regulation of behavioral responses to trauma

Szerző(k) neve és munkahelye

Zoltán Balogh1, 2; László Szente1; Zoltán Kristóf Varga1, 2; László Biró1, 2; József Haller1; Manó Aliczki1
1 Laboratory of Behavioural and Stress Studies, Department of Behavioural Neurobiology, Institute of Experimental Medicine, Hungarian Academy of Sciences, Budapest, Hungary
2 Janos Szentagothai Doctoral School of Neurosciences, Semmelweis University, Budapest, Hungary

Témacsoport

neurosciences

Szekció

Oral Presentations: Neurosciences

Data of the presenter

Doctoral School: Janos Szentagothai Doctoral School of Neurosciences Program: Neuroendocrinology Supervisors: Dr. József Haller, Dr. Manó Aliczki E-mail address: balogh.zoltan@koki.mta.hu

Text of the abstract

Introduction: Endocannabinoid signaling affects behavioral responses to traumatic events, however, the specific roles and possible interactions of the two endocannabinoids anandamide (AEA) and 2-arachidonoylglycerol (2-AG) are poorly understood.

Aims: We assessed the specific effects of AEA and 2-AG on acute responses to a traumatic event and consolidation and extinction of traumatic memories.

Methods: Fear conditioning employing electric foot-shock was followed by seven consecutive daily contextual reminders and a reminder 28 days after conditioning. AEA and 2-AG signalling was enhanced in Wistar rats by the blockade of their respective degrading enzymes fatty acid amid hydrolase and monoacylglycerol lipase. Systemic treatments were administered before fear conditioning or before the first contextual reminder. Site-specific treatments were administered before fear conditioning to the ventral hippocampus (vHC), prelimbic cortex (PrL), basolateral amygdala (BLA).

Results: Acute fear responses were decreased by local enhancement of AEA signalling in the vHC but not in the PrL or BLA and 2-AG inhibited the effect of AEA. Interestingly, systemic enhancement of 2-AG signalling before fear conditioning decreased acute fear responses and AEA supressed the effects of 2-AG. Local enhancement of AEA in the vHC and PrL led to strong memory consolidation and this effect was inhibited by 2-AG. In contrast, enhanced AEA signalling in the BLA prevented traumatic memory formation. Enhancement of 2-AG or AEA signalling before the first contextual reminder accelerated traumatic memory extinction.

Conclusion: Taken together, endocannabinoids differentially, interactively regulate behavioural responses to trauma. Acute fear responses are regulated predominantly by 2-AG but under the influence of AEA. In the PrL and vHC AEA enhances traumatic memory consolidation under the control of 2-AG but in the BLA AEA inhibits traumatic memory formation. In traumatic memory extinction endocannabinoids have a synergistic role and promote fear relief.

Kind

Meghívott

Előadás fájl jóváhagyás

nem rendelkezett róla

Előadó

1001

Authors (legacy)

Zoltán Balogh1, 2; László Szente1; Zoltán Kristóf Varga1, 2; László Biró1, 2; József Haller1; Manó Aliczki1
1 Laboratory of Behavioural and Stress Studies, Department of Behavioural Neurobiology, Institute of Experimental Medicine, Hungarian Academy of Sciences, Budapest, Hungary
2 Janos Szentagothai Doctoral School of Neurosciences, Semmelweis University, Budapest, Hungary