c-Fos Expression In Amygdala Research Articles

Mapping in mice the brain regions involved in the anxiolytic-like properties of α-casozepine, a tryptic peptide derived from bovine αs1-casein

α-Casozepine, a bioactive peptide from milk casein, displays an anxiolytic-like activity in many species. Since its mode of action is still not elucidated, a study was conducted in Swiss mice to investigate c-Fos expression, a marker of neuronal activity, in different brain areas. After an intraperitoneal injection of α-casozepine (1mg/kg), animals were placed either in a non-stressful or in an anxiety-inducing situation triggered with a light/dark box. No effect of α-casozepine on c-Fos expression was observed in the non-stressful situation. In the stressful situation, modulation of neuronal activity by α-casozepine was observed in different brain regions compared to that of vehicle. However, while diazepam, a benzodiazepine, modulated neuronal activity the same way in hippocampus, accumbens nucleus and hypothalamus, differences were observed in c-Fos expression in amygdala and prefrontal cortex compared to α-casozepine. These results strengthen the assumption that the anxiolytic mechanisms of α-casozepine differ partly of those of diazepam.

Anxiety-like behaviour and c-fos expression in rats that inhaled vetiver essential oil

Vetiver essential oil (VEO) has been used in aromatherapy for relaxation. This study aimed to investigate the effects of VEO on an anxiety-related behavioural model (the elevated plus-maze, EPM) and immediate-early gene c-fos in amygdala, known to be involved in anxiety. Male Wistar rats were administered diazepam (1 mg/kg i.p.) for 30 min or inhalated with VEO (1%, 2.5% or 5% w/w) for 7 min prior to exposure to the EPM. Then, the effects of 2.5% VEO, the anxiolytic dose, on c-fos expression in amygdala were investigated. The rats given either 2.5% VEO or diazepam exhibited an anxiolytic-like profile in the EPM. VEO and diazepam significantly increased c-fos expression in the lateral division of the central amygdaloid nucleus (CeL). Therefore, the anxiolytic properties of VEO might be associated with altering neuronal activation in CeL. However, future studies are needed to investigate the precise mechanism of action of VEO.

Region specific galanin receptor/neuropeptide Y Y1 receptor interactions in the tel- and diencephalon of the rat. Relevance for food consumption

The aim of this work was to determine the interactions between NPY and GAL receptor (GALR) subtypes in the hypothalamus and the amygdala using quantitative receptor autoradiography to analyze the binding characteristics of NPY-Y1 and Y2 receptor subtypes in the presence and absence of GAL. Food intake in satiated animals was evaluated after intraventricular coinjections of GAL and NPY-Y1 or Y2 agonists. The expression of c-Fos IR in both regions was also investigated. GAL decreases NPY-Y1 agonist binding in the arcuate nucleus by about 15% ( p < 0.01), but increases NPY-Y1 agonist binding in amygdala (18%) ( p < 0.01). These effects were blocked with the GAL antagonist M35. Y2-agonist binding was not modified by GAL. GAL blocked the food intake induced by the Y1 agonist ( p < 0.01). Coinjections of Y1 agonist and GAL also reduced the c-Fos expression induced by the Y1 agonist in the arcuate nucleus and the dorsomedial hypothalamic nucleus but increased c-Fos expression in amygdala. These results indicate the existence of antagonistic interactions between GALR and NPY-Y1 receptors in the hypothalamus and their functional relevance for food intake. In contrast, a facilitatory interaction between GALR and Y1 receptors exists in the amygdala which may be of relevance for fear related behaviour.

Previous experience of ethanol withdrawal increases withdrawal-induced c-fos expression in limbic areas, but not withdrawal-induced anxiety and prevents withdrawal-induced elevations in plasma corticosterone

Increased anxiety is a characteristic of the acute ethanol withdrawal syndrome. Repeated exposure of rats to withdrawal from chronic ethanol increases sensitivity to seizures. We investigated whether repeated withdrawal experience increases withdrawal-induced anxiety and stress, and if it changes withdrawal-induced activation of related brain areas. Rats were chronically treated with an ethanol-containing liquid diet either for 24 days continuously (single withdrawal, SWD) or interspersed with 2x3-day withdrawal periods (repeated withdrawal, RWD), or with a control diet. Eight hours after ethanol withdrawal, anxiety-like behaviour was tested in the elevated plus-maze, blood corticosterone levels were measured, and expression level of markers of neuronal activity and plasticity, c-fos and zif268, was assessed. Eight hours after ethanol withdrawal, SWD rats showed increased anxiety on the elevated plus-maze relative to control rats. Rats given previous withdrawal experiences did not show further increases in measures of anxiety. Corticosterone levels were elevated during withdrawal in SWD rats but not in RWD rats. RWD resulted in marked increases in c-fos expression in amygdala, hippocampus, nucleus accumbens and dorsolateral periaqueductal grey. In contrast, zif268 expression was not increased after RWD, and in central amygdala the marked increase in zif268 seen after SWD was absent after RWD. The data suggest increased ability of withdrawal to activate neuronal circuits but reduced plasticity after RWD. We suggest parallels between the consequences of repeated ethanol withdrawal and repeated exposure to stress, and discuss implications of withdrawal for brain plasticity.

Conditioned taste aversion memory and c-Fos induction are disrupted in RIIβ-protein kinase A mutant mice

The cAMP-dependent protein kinase (PKA) signaling pathway has been implicated in many forms of learning. The present studies examined conditioned taste aversion (CTA) learning, an amygdala-dependent task, in mice with a targeted disruption of a gene for a specific regulatory subunit of PKA (RIIβ), which is selectively expressed in amygdala. Null mutant (RIIβ−/−) mice and littermate controls (RIIβ+/+) were tested for protein synthesis-independent short-term memory (STM) and protein synthesis-dependent long-term memory (LTM) for CTAs. The ability of the unconditioned stimulus (US) drug, LiCl, to induce c-Fos in regions thought to be important in this learning was also determined. RIIβ−/− mice showed significant impairment in CTA memory when tested 24h after training (LTM). In contrast, STM was normal. With regard to the c-Fos response to LiCl, the US drug, significant elevations were evident in brainstem (nucleus of the solitary tract) and pontine (parabrachial nucleus) regions, in mutants as well as wild-type controls. However, in amygdala, elevations were seen in controls but were absent in the mutants. These findings suggest that disruption of PKA signaling interferes with LTM consolidation of CTA and that a possible mediator of this effect is interference with c-Fos expression in amygdala which may be necessary for CTA memory.