Immediate early gene and neuropeptide expression following exposure to the predator odor 2,5-dihydro-2,4,5-trimethylthiazoline (TMT)

Asok, Arun; Ayers, Luke W.; Awoyemi, Bisola; Schulkin, Jay; Rosen, Jeffrey B.

doi:10.1016/j.bbr.2013.03.047

Cited by 56 publications

(63 citation statements)

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“…Similarly, exposure to predator ferret odor dramatically increased the co-expression of c-Fos with CRF in the vBNST compared to control odor and butyric acid-exposed rats. Exposure to 2,5-dihydro-2,4,5-trimethylthiazoline (TMT), a component of fox feces [36–38], as well as exposure to cat urine [39] have both been shown activate vBNST or dlBNST circuits using several immediate early genes, and TMT specifically acts through norepinephrine-dependent mechanisms in the vBNST to modify threat behaviors [40]. Moreover, exposure to TMT increases expression of crh mRNA in the ventral, but not dorsal, BNST [38].…”

Section: Discussionmentioning

confidence: 99%

“…Other studies using dissection of amygdala also demonstrated no increase in c-Fos expression following TMT exposure [53]. In contrast, several studies have demonstrated activation of the CEA using following exposure to TMT [37, 38, 54], as well as an increase in crh mRNA expression in this region [38]. Ferret exposure also increased CRF immunoreactivity in punches of the CEA in a subpopulation of fast-seizing mice [55].…”

Section: Discussionmentioning

confidence: 99%

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Activation of corticotropin releasing factor-containing neurons in the rat central amygdala and bed nucleus of the stria terminalis following exposure to two different anxiogenic stressors

Butler

Oliver

Sharko

et al. 2016

Behavioural Brain Research

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Rats exposed to the odor of a predator or to the elevated plus maze (EPM) express unique unconditioned fear behaviors. The extended amygdala has previously been demonstrated to mediate the response to both predator odor and the EPM. We seek to determine if divergent amygdalar microcircuits are associated with the different behavioral responses. The current experiments compared activation of corticotropin-releasing factor (CRF)-containing neuronal populations in the central amygdala and bed nucleus of the stria terminalis (BNST) of rats exposed to either the EPM (5 minutes) versus home cage controls, or predator ferret odor versus butyric acid, or no odor (30 minutes). Sections of the brains were prepared for dual-labeled immunohistochemistry and counts of c-Fos co-localized with CRF were made in the centrolateral and centromedial amygdala (CLA and CMA) as well as the dorsolateral (dl), dorsomedial (dm), and ventral (v) BNST. Ferret odor-exposed rats displayed an increase in duration and a decrease in latency of defensive burying versus control rats. Exposure to both predator stress and EPM induced neuronal activation in the BNST, but not the central amygdala, and similar levels of neuronal activation were seen in both the high and low anxiety groups in the BNST after EPM exposure. Dual-labeled immunohistochemistry showed a significant increase in the percentage of CRF/c-Fos co-localization in the vBNST of ferret odor-exposed rats compared to control and butyric acid-exposed groups as well as EPM-exposed rats compared to home cage controls. In addition, an increase in the percentage of CRF-containing neurons co-localized with c-Fos was observed in the dmBNST after EPM exposure. No changes in co-localization of CRF with c-Fos was observed with these treatments in either the CLA or CMA. These results suggest that predator odor and EPM exposure activates CRF neurons in the BNST to a much greater extent than CRF neurons of the central amygdala, and indicates unconditioned anxiogenic stimuli may activate unique anatomical circuits in the extended amygdala.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Activation of corticotropin releasing factor-containing neurons in the rat central amygdala and bed nucleus of the stria terminalis following exposure to two different anxiogenic stressors

Butler

Oliver

Sharko

et al. 2016

Behavioural Brain Research

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“…In situ hybridization was conducted as described previously (Asok et al, 2013a; Asok et al, 2013b). An antisense RNA probe (riboprobe) was transcribed from a plasmid containing a sense cDNA sequence coding for a 230 bp sequence of Egr-1 (gift from J. Milbrandt, Washington University, St. Louis, MO).…”

Section: Methodsmentioning

confidence: 99%

Egr-1 mRNA expression patterns in the prefrontal cortex, hippocampus, and amygdala during variants of contextual fear conditioning in adolescent rats

et al. 2014

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We report activation of the immediate-early gene Egr-1 in the lateral amygdala (LA), hippocampus (CA1), and medial prefrontal cortex (mPFC) 30-min following the training phase in the context pre-exposure facilitation effect (CPFE) and standard context fear conditioning (180 sec context exposure → shock). On day one of the CPFE paradigm, postnatal day (PD) 31 rats (±1) were pre-exposed to Context A (Pre) or Context B (Alt-Pre) for 5 min followed by five additional 1-minute exposures. A day later, Pre and Alt-Pre rats received a 2-sec, 1.5 mA footshock immediately upon placement in Context A. Animals included in in situ hybridization were then sacrificed 30 (±3) min later. On day three, the behaviorally-tested Pre rats showed significantly more fear-conditioned freezing in Context A than Alt-Pre rats. Standard context fear conditioning groups showed much greater freezing than the Pre group, as well as no shock and immediate-shock controls. Thirty minutes after immediate shock training, Pre rats showed increased Egr-1 mRNA in the prelimbic mPFC relative to Alt-Pre rats. Standard context conditioning selectively increased Egr-1 in CA1. In the LA and mPFC, Egr-1 increased to a similar extent in no shock, immediate shock, and standard context conditioning relative to homecage controls. The present study demonstrates that Egr-1 mRNA expression has a complex relationship to fear learning in different brain regions and variants of context conditioning.

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“…Asok et al also showed that exposure to a component of fox odor, 2,5-dihydro-2,4,5-trimethylthiazoline (TMT), which triggers innate fear in rats, increases ENK mRNA levels in the paraventricular nucleus (PVN) of the HPT [43]. An increased expression of ENK mRNA levels is similarly observed after repeated footshocks, in the AMG of SWR/J mice, an inbred strain showing a reduced fear response, while this expression was unchanged in C57Bl/6J mice, an inbred strain showing a high fear response [44].…”

Section: Enkephalins and Their Opioid Receptorsmentioning

confidence: 99%

Enkephalins: Endogenous Analgesics with an Emerging Role in Stress Resilience

et al. 2017

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Psychological stress is a state of mental or emotional strain or tension that results from adverse or demanding circumstances. Chronic stress is well known to induce anxiety disorders and major depression; it is also considered a risk factor for Alzheimer's disease. Stress resilience is a positive outcome that is associated with preserved cognition and healthy aging. Resilience presents psychological and biological characteristics intrinsic to an individual conferring protection against the development of psychopathologies in the face of adversity. How can we promote or improve resilience to chronic stress? Numerous studies have proposed mechanisms that could trigger this desirable process. The roles of enkephalin transmission in the control of pain, physiological functions, like respiration, and affective disorders have been studied for more than 30 years. However, their role in the resilience to chronic stress has received much less attention. This review presents the evidence for an emerging involvement of enkephalin signaling through its two associated opioid receptors, μ opioid peptide receptor and δ opioid peptide receptor, in the natural adaptation to stressful lifestyles.

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Immediate early gene and neuropeptide expression following exposure to the predator odor 2,5-dihydro-2,4,5-trimethylthiazoline (TMT)

Cited by 56 publications

References 50 publications

Activation of corticotropin releasing factor-containing neurons in the rat central amygdala and bed nucleus of the stria terminalis following exposure to two different anxiogenic stressors

Activation of corticotropin releasing factor-containing neurons in the rat central amygdala and bed nucleus of the stria terminalis following exposure to two different anxiogenic stressors

Egr-1 mRNA expression patterns in the prefrontal cortex, hippocampus, and amygdala during variants of contextual fear conditioning in adolescent rats

Enkephalins: Endogenous Analgesics with an Emerging Role in Stress Resilience

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