Acute corticosterone treatment is sufficient to induce anxiety and amygdaloid dendritic hypertrophy

Abstract

Stress is known to induce dendritic hypertrophy in the basolateral amygdala (BLA) and to enhance anxiety. Stress also leads to secretion of glucocorticoids (GC), and the BLA has a high concentration of glucocorticoid receptors. This raises the possibility that stress-induced elevation in GC secretion might directly affect amygdaloid neurons. To address the possible effects of GC on neurons of amygdala and on anxiety, we used rats treated either acutely with a single dose or chronically with 10 daily doses of high physiological levels of corticosterone (the rat-specific glucocorticoid). Behavior and morphological changes in neurons of BLA were measured 12 days after the initiation of treatment in both groups. A single acute dose of corticosterone was sufficient to induce dendritic hypertrophy in the BLA and heightened anxiety, as measured on an elevated plus maze. Moreover, this form of dendritic hypertrophy after acute treatment was of a magnitude similar to that caused by chronic treatment. Thus, plasticity of BLA neurons is sufficiently sensitive so as to be saturated by a single day of stress. The effects of corticosterone were specific to anxiety, as neither acute nor chronic treatment caused any change in conditioned fear or in general locomotor activity in these animals.amygdala ͉ glucocorticoid ͉ neuron S tress is known to cause structural alterations in neurons of the central nervous system including changes in dendritic architecture and density of spines. For example, chronic restraint stress reduces dendritic length and number of branch points of hippocampal neurons (1-3). This atrophy of hippocampal neurons is known to be correlated with behavioral deficits in hippocampal-dependent spatial memory tasks, such as the Morris water maze (2-7). In contrast, chronic immobilization stress enhances dendritic length, branch points, and spines in neurons of basolateral amygdala (BLA) (8,9). In addition to such dendritic hypertrophy in the amygdala, animals treated with chronic immobilization stress show enhanced anxiety (8-10). Thus, structural alterations in the hippocampus and amygdala are associated with concomitant behavioral alterations.Stressful stimuli activate the hypothalamus-pituitary-adrenal (HPA) axis, leading to secretion of stress hormones, including glucocorticoids (GCs) (11-13). GCs play important roles in organizing the stress response by binding to glucocorticoid receptors in peripheral tissue and in brain. Both the hippocampus (14) and the BLA (15) have high concentration of GC receptors. Chronic GC treatment is known to cause the neuronal atrophy in the hippocampus and spatial memory deficits (16-18) similar to that seen in stress, leading to suggestions that GC secretion is critical in stressinduced hippocampal damage (5). However, the effects of GC on amygdaloid neurons remain unknown. Specifically it is not known whether high GC concentrations alone are sufficient to induce dendritic hypertrophy of BLA neurons and accompanying anxiety. Interactions between GC and the BLA might be importan...

Effects of 900MHz radiofrequency on corticosterone, emotional memory and neuroinflammation in middle-aged rats

“…Our data appears to contradict the acute anxiogenic effect of CORT in the fear response (Mitra and Sapolsky, 2008) as increased CORT level was not linked to an increased fear response in GSM-exposed young adults. Indeed, this group rather displayed a tendency toward a decrease in response to the sound, which may be underlined by the fear-reducing effects of CORT, linked to its ability to inhibit the recall of previously acquired, emotionally arousing information (Roozendaal et al, 2009;Sartori et al, 2011).…”

Personality traits in rats predict vulnerability and resilience to developing stress-induced depression-like behaviors, HPA axis hyper-reactivity and brain changes in pERK1/2 activity

“…Additionally, it is interesting to note that individual differences in coping with predator stress -as manifested by post-stress anxiety responses in the elevated plus maze -were previously found in the literature to correlate with differences in the structure of the dendritic trees in the basolateral amygdala; thus, maladapted (extremely anxious) rats showed larger dendrites than welladapted (less anxious) animals (Mitra et al, 2009). Corticosterone treatment was found to mimic dendritic hypertrophy in the BLA and the enhanced anxiety observed after chronic stress (Mitra and Sapolsky, 2008). Differences in corticosterone responses and in neural activity in the amygdala were also previously found to be associated with coping responses to stress, with active coping leading to lower activation on those parameters (Walker et al, 2009).…”

Chronobiology by moonlight

“…Light pulses, constant light or dim light during the night may cause elevated GC levels in laboratory rats and mice, and in Nile grass rats [118][119][120][121][122][123], although in some cases, it was reported to have no effect or even decrease GC release [124,125]. It was recently reported that aberrant light may directly affect mood and cognitive functions in mice [123]; GC treatment was shown to increase anxiety and conditioned fear [126][127][128][129], and acute corticosterone elevation enhanced anti-predator behaviours in tree lizard species [130].…”

“…For example, in a light dark box test, GC treatment resulted in increased latency to leave the dark compartment, and in the elevated plus maze, it increased time spent in the sheltered arms [126][127][128][129]. Tree lizards treated with GC responded more quickly to predators and hid longer [130], and in the Adelie penguin (Pygoscelis adeliae) individuals with high pre-foraging corticosterone levels spent less time foraging, and stayed closed to the colony [131].…”