Disruption of neuroendocrine stress responses to acute ferret odor by medial, but not central amygdala lesions in rats

Abstract

Investigations of the neural pathways associated with responses to predators have implicated the medial amygdala (MeA) as an important region involved in defensive behaviors. To our knowledge, however, the involvement of the MeA in neuroendocrine responses to predator odor exposure has not been investigated. Therefore, the present study examined the effects of MeA disruption in rats exposed to ferret or control odor on hypothalamo-pituitary-adrenocortical (HPA) axis activation. Bilateral lesions of the MeA were made in Sprague-Dawley rats with the neurotoxin ibotenic acid (10 µg/µl; 0.3 µl /side). As a control for regional specificity, additional groups of rats were given lesions in the central amygdala (CeA). One week after recovery, the rats were exposed to ferret or strawberry control towels in small cages to examine HPA axis responses as determined by plasma corticosterone and adrenocorticotropin hormone (ACTH) levels. Rats with complete bilateral MeA but not CeA lesions displayed significantly less corticosterone and ACTH release compared to shamoperated control rats only in the ferret odor conditions. These results suggest that the MeA is an important structure involved in the HPA axis responses to predator odors, in support of previous studies investigating behavioral responses under similar conditions.

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

“…In contrast, our current study showed no increase in c-Fos expression in CRF-containing neurons with EPM exposure. Several prior studies which investigated the effect of lesions to the CEA showed no role in the mediation of unconditioned anxiety to predator odor [50–52]. This supports our own data which demonstrated no activation of CRF-containing neurons in subdivisions of the CEA following predator odor stress.…”

Activation of phenotypically-distinct neuronal subpopulations of the rat amygdala following exposure to predator odor

“…The increase in aversive behaviors in rats upon exposure to a ferret odor corroborates a number of previous studies which showed similar behavioral effects (Masini et al, 2005, Masini et al, 2006, for review see Campeau et al, 2008, Wilson and Junor, 2008, Masini et al, 2009, Weinberg et al, 2009, Masini et al, 2010). Olfactory receptors which are specific to predator threats are processed by unique zones in the olfactory bulb (Kobayakawa et al, 2007), which project to and activate limbic brain regions such as the amygdala following exposure to predator odors (Hebb et al, 2002).…”

“…However, recent studies by Staples et al (2006, 2008b) and others have suggested little to no avoidance behaviors in rats exposed to TMT. The olfactory bulb projects to the amygdala and recent evidence suggests that the MEA plays a prominent role in the expression of aversive behaviors following exposure to ferret odor as lesions to the MEA disrupted hypothalamo-pituitary-adrenocortical axis activation following ferret odor exposure – an effect not observed with CEA lesions (Masini et al, 2009). However, we have previously shown that the CEA can regulate rat aversive behaviors to ferret odor through opioid-dependent mechanisms (Wilson and Junor, 2008).…”

In vivo electrophysiological recordings in amygdala subnuclei reveal selective and distinct responses to a behaviorally identified predator odor

“…B: scatterplot depicting the timing of the peak response to cat urine of all recorded units and the mean Ϯ SE timing of the response peak to cat urine in the MeAV (n ϭ 7), MePV (n ϭ 21), MeAD (n ϭ 16), MePD (n ϭ 28), CoA (n ϭ 7), BLa and BLv (n ϭ 4 each), BMa (n ϭ 6), BMp (n ϭ 10), AHi (n ϭ 13), CeM (n ϭ 3), and BSTIA (n ϭ 8 1995) and is the first site of olfactory convergence (Meredith 1998), it is in an excellent position to integrate olfactory cues signaling predators and engage excitatory or inhibitory events in downstream targets that regulate defensive responses. These findings are consonant with gene activation studies Meredith and Westberry 2004) and converge with lesion studies (Li et al 2004;Masini et al 2009) to highlight the critical involvement of the MeA in predator odor-generated fear.…”