Elsevier

Behavioural Brain Research

Volume 240, 1 March 2013, Pages 26-28
Behavioural Brain Research

Short Communication
Selective increase in the association of the β2 adrenergic receptor, β Arrestin-1 and p53 with Mdm2 in the ventral hippocampus one month after underwater trauma

https://doi.org/10.1016/j.bbr.2012.11.009Get rights and content

Abstract

Chronic infusion of mice with a β2 adrenergic receptor (β2AR) analog was shown to cause long-term DNA damage in a pathway which involves β Arresin-1-mediated activation of Mdm2 and subsequent degradation of the tumor suppressor protein p53. The objective of the present study was to test whether a single acute stress, which manifests long lasting changes in behavior, affects the interaction of Mdm2 with p53, β2AR, and β Arrestin-1 in the dorsal and ventral hippocampal CA1. Adult rats were subject to underwater trauma, a brief forceful submersion under water and tested a month later for behavioral and biochemical changes. Elevated plus maze tests confirmed that animals that experienced the threat of drowning present heightened levels of anxiety one month after trauma. An examination of the CA1 hippocampal areas of the same rats showed that underwater trauma caused a significant increase in the association of Mdm2 with β2AR, β Arrestin-1, and p53 in the ventral but not dorsal CA1. Our results provide support for the idea that stress-related events may result in biochemical changes restricted to the ventral ‘emotion-related’ parts of the hippocampus.

Highlights

► Underwater trauma (UWT) causes heightened anxiety one month after trauma. ► UWT increases association of Mdm2 with beta2AR, beat Arrestin-1, and p53 in ventral not dorsal CA1. ► Stress-related events cause changes in ‘emotion-related’ parts of the hippocampus.

References (19)

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Cited by (19)

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    We identified seven genes (Arrb1, Ndn, Dom3z, Rangap1, Spock1, Magel2, Mylk2) with non-synonymous SNPs in our network. One gene of interest is Arrb1 (Arrestin Beta 1), whose protein product has been previously identified as a mediator of DNA damage various brain structures in response to acute stress (Sood et al., 2013), chronic stress (Hara et al., 2011; Hara et al., 2013) and stress-related catecholamines (Jia et al., 2014). Theoretical effects of Arrb1 expression have been proposed to play a role in both general development of neuropsychiatric conditions and plastic changes in the hippocampal ventral CA1 region relating to its connectivity to the amygdala and hypothalamus (so called ‘emotion-related’ connections) (Hara et al., 2011; Hara et al., 2013; Sood et al., 2013).

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    Furthermore, dHC and vHC show opposite electrophysiological responses to the stress hormone corticosterone (17). One month after an acute traumatic stress experience, rats were found to be more anxious and showed increased beta-adrenergic receptor-2 binding to downstream effector proteins in the vHC but not in the dHC (60), and the immediate early gene Fos was primed for activation in the vHC (47). In addition, stress induces different epigenetic changes in dHC and vHC.

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    In parallel to its long-term augmentation of anxious-like behavior [44,45], this procedure induces acute and enduring alterations in cortico-limbic circuits. Recent studies demonstrated that the mere exposure to the UWT induces critical alterations in hippocampal functions, evident after 24 hours [46] and up to 4 weeks [44,45] after exposure. Furthermore, the UWT can be easily paired with contextual stimuli and thus enables to model the cued re-experiencing of the trauma, a core symptom of PTSD, in fear-conditioned rodents [33,46,47].

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    In the current study, we used brief restraint under water (underwater trauma), as the traumatic stressor. This procedure is known to acutely and enduringly increase anxiety-like behavior (Ardi et al., 2014; Richter-Levin, 1998; Sood et al. 2013) without any tissue damage (Moore et al., 2012). We could confirm these results by analyzing activity and anxiety-like behaviors in the EPM and OF four weeks later on the group level, thus further supporting the relevance of UWT as an animal model of trauma-related PTSD.

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    This is supported by a recent study where exposure of animals to high level stressors such as forced swim or to the stress hormone corticosterone, caused a marked reduction of long-term potentiation (LTP) in dorsal CA1 and a parallel increase in the ventral CA1 (Maggio and Segal, 2009). These results are also in accordance with our recent work that showed a significant increase in the association of Mdm2 with the β2-adrenergic receptor, β-Arrestin-1, and p53 in the ventral but not dorsal CA1 of animals that underwent underwater trauma (Sood et al., 2013). We have also recently shown that re-exposure of animals to underwater trauma 24 h following the first event caused a significant increase in activation of the ERK MAP kinase pathway in the ventral hippocampus and the basolateral amygdala, suggesting a specific pattern of neural activation during recollection of a trauma reminder (Ritov et al., 2014).

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Research support: The Israel Science Foundation grant (no. 1403/07) to G.R.-L., by a U.S. Army Medical Research Acquisition Activity (USAMRAA) grant (no. W81XWH-11-20111), and by the Institute for the Study of Affective Neuroscience, University of Haifa, which was endowed by the Hope for Depression Research Foundation.

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