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Short-term adaptation of conditioned fear responses through endocannabinoid signaling in the central amygdala.
Neuropsychopharmacology. 2011 Feb; 36(3):652-63.N

Abstract

The cannabinoid receptor type 1 (CB1) and the central nucleus of the amygdala (CeA) are both known to have crucial roles in the processing of fear and anxiety, whereby they appear to be especially involved in the control of fear states. However, in contrast to many other brain regions including the cortical subregions of the amygdala, the existence of CB1 in the CeA remains enigmatic. In this study we show that CB1 is expressed in the CeA of mice and that CB1 in the CeA mediates short-term synaptic plasticity, namely depolarization-induced suppression of excitation (DSE) and inhibition (DSI). Moreover, the CB1 antagonist AM251 increased both excitatory and inhibitory postsynaptic responses in CeA neurons. Local application of AM251 in the CeA in vivo resulted in an acutely increased fear response in an auditory fear conditioning paradigm. Upon application of AM251 in the basolateral nucleus of the amygdala (BLA) in an otherwise identical protocol, no such acute behavioral effects were detected, but CB1 blockade resulted in increased fear responses during tone exposures on the subsequent days. Moreover, we observed that the efficacy of DSE and DSI in the CeA was increased on the day following fear conditioning, indicating that a single tone-shock pairing resulted in changes in endocannabinoid signaling in the CeA. Taken together, our data show the existence of CB1 proteins in the CeA, and their critical role for ensuring short-term adaptation of responses to fearful events, thereby suggesting a potential therapeutic target to accompany habituation-based therapies of post-traumatic symptoms.

Authors+Show Affiliations

Institute of Physiology I (Neurophysiology), Westfaelische Wilhelms-University, Muenster, Germany.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

20980994

Citation

Kamprath, Kornelia, et al. "Short-term Adaptation of Conditioned Fear Responses Through Endocannabinoid Signaling in the Central Amygdala." Neuropsychopharmacology : Official Publication of the American College of Neuropsychopharmacology, vol. 36, no. 3, 2011, pp. 652-63.
Kamprath K, Romo-Parra H, Häring M, et al. Short-term adaptation of conditioned fear responses through endocannabinoid signaling in the central amygdala. Neuropsychopharmacology. 2011;36(3):652-63.
Kamprath, K., Romo-Parra, H., Häring, M., Gaburro, S., Doengi, M., Lutz, B., & Pape, H. C. (2011). Short-term adaptation of conditioned fear responses through endocannabinoid signaling in the central amygdala. Neuropsychopharmacology : Official Publication of the American College of Neuropsychopharmacology, 36(3), 652-63. https://doi.org/10.1038/npp.2010.196
Kamprath K, et al. Short-term Adaptation of Conditioned Fear Responses Through Endocannabinoid Signaling in the Central Amygdala. Neuropsychopharmacology. 2011;36(3):652-63. PubMed PMID: 20980994.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Short-term adaptation of conditioned fear responses through endocannabinoid signaling in the central amygdala. AU - Kamprath,Kornelia, AU - Romo-Parra,Hector, AU - Häring,Martin, AU - Gaburro,Stefano, AU - Doengi,Michael, AU - Lutz,Beat, AU - Pape,Hans-Christian, Y1 - 2010/10/27/ PY - 2010/10/29/entrez PY - 2010/10/29/pubmed PY - 2011/5/10/medline SP - 652 EP - 63 JF - Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology JO - Neuropsychopharmacology VL - 36 IS - 3 N2 - The cannabinoid receptor type 1 (CB1) and the central nucleus of the amygdala (CeA) are both known to have crucial roles in the processing of fear and anxiety, whereby they appear to be especially involved in the control of fear states. However, in contrast to many other brain regions including the cortical subregions of the amygdala, the existence of CB1 in the CeA remains enigmatic. In this study we show that CB1 is expressed in the CeA of mice and that CB1 in the CeA mediates short-term synaptic plasticity, namely depolarization-induced suppression of excitation (DSE) and inhibition (DSI). Moreover, the CB1 antagonist AM251 increased both excitatory and inhibitory postsynaptic responses in CeA neurons. Local application of AM251 in the CeA in vivo resulted in an acutely increased fear response in an auditory fear conditioning paradigm. Upon application of AM251 in the basolateral nucleus of the amygdala (BLA) in an otherwise identical protocol, no such acute behavioral effects were detected, but CB1 blockade resulted in increased fear responses during tone exposures on the subsequent days. Moreover, we observed that the efficacy of DSE and DSI in the CeA was increased on the day following fear conditioning, indicating that a single tone-shock pairing resulted in changes in endocannabinoid signaling in the CeA. Taken together, our data show the existence of CB1 proteins in the CeA, and their critical role for ensuring short-term adaptation of responses to fearful events, thereby suggesting a potential therapeutic target to accompany habituation-based therapies of post-traumatic symptoms. SN - 1740-634X UR - https://www.unboundmedicine.com/medline/citation/20980994/Short_term_adaptation_of_conditioned_fear_responses_through_endocannabinoid_signaling_in_the_central_amygdala_ L2 - http://dx.doi.org/10.1038/npp.2010.196 DB - PRIME DP - Unbound Medicine ER -