Expression of c-fos in regions of the basal limbic forebrain following intra-cerebroventricular corticotropin-releasing factor in unstressed or stressed male rats

Arnold, Frederick; Bueno, Mardja; Shiers, H. M.; Hancock, David C.; Evan, Gérard I.; Herbert, J.

doi:10.1016/0306-4522(92)90322-s

Cited by 156 publications

(71 citation statements)

References 44 publications

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“…This pattern of neural activation is consistent with several lines of relevant research. First, several studies have found that a single episode of acute stress produces substantial increases in Fos expression in the PVN, CeA, BNST as well as other areas (2,10). Also, the magnitude of neuronal activation has been shown to be sensitive to briefer periods of maternal separation.…”

Section: Discussionmentioning

confidence: 99%

Maternal separation enhances neuronal activation and cardiovascular responses to acute stress in borderline hypertensive rats

Sanders

Antičević

2007

Behavioural Brain Research

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There is much evidence suggesting early life events, such has handling or repeated separations from the nest, can have a long term effect on the biological and behavioral development of rats. The current study examined the effect of repeated maternal separation (MS) on the behavioral, cardiovascular, and neurobiological responses to stress in subjects vulnerable to environmental stressors as adults. Borderline hypertensive rats (BHR), which are the first generation offspring of spontaneously hyperternsive and Wistar-Kyoto rats, were separated from the dams for 3 hours per day from postnatal day 1 through 14. Non-separated controls remained in the home cage. When allowed to explore the open field chamber for 60 minutes as adults, MS subjects had significantly greater locomotor activity compared to controls. All subjects were exposed to 30 minutes of restraint stress during which time mean arterial pressure (MAP) and heart rate (HR) were measured. Although both groups had comparable increases in MAP, MS animals displayed significantly higher HR throughout the stress period. Finally, MS subjects had significantly more stress-induced Fos positive cells, an estimate of neuronal activation, in the central nucleus of the amygdala (CeA), paraventricular nucleus of the hypothalamus (PVN), and the bed nucleus of the stria terminalis (BNST), each of which plays an important role in organizing the biobehavioral response to stress. These results suggest that maternal separation can further enhance stress reactivity in this model and may represent a useful approach for studying the relationship between early life events and future vulnerability to stressful situations.

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Section: Discussionmentioning

confidence: 99%

Maternal separation enhances neuronal activation and cardiovascular responses to acute stress in borderline hypertensive rats

Sanders

Antičević

2007

Behavioural Brain Research

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“…Davis, 1992). However, several groups have reported differential effects of stress on the induction of c-fos and related fra (fos-related antigen) proteins within individual amygdaloid subnuclei (Arnold et al, 1992;Pezzone et al, 1992), and conflicting effects of stressful stimuli on amygdaloid levels of c-fos mRNA have also been reported (Campeau et al, 1991;Smith et al, 1992). Such variability can be partially explained by qualitative differences between the stressors and techniques employed in these studies, but the contribution of the heterogeneity of the amygdaloid complex to these various findings should also be considered.…”

Section: Discussionmentioning

confidence: 99%

Induction and habituation of immediate early gene expression in rat brain by acute and repeated restraint stress

et al. 1994

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Acute exposure to stress leads to activation of the pituitary-adrenal axis (PA-axis) while repeated exposure to a homotypic stressor generally results in habituation of this response. Previous studies suggested that such habituation is largely due to changes in afferents of the PA-axis. To examine where within these afferents habituation occurs, we studied the effect of acute and repeated exposure to 2 hr restraint stress on expression of c-fos mRNA, as a marker of altered neuronal activity, in brain regions previously shown to influence the activity of the PA-axis. Acute restraint stress increased expression of c-fos mRNA in cortex, hippocampus, hypothalamus, septum, and brainstem. In contrast, the effect of restraint stress on c-fos expression in the aforementioned brain regions was much smaller in animals restrained once daily for 4 d, and nonexistent in animals restrained once daily for 9 d. A similar pattern of induction and habituation of jun-B, but not zif-268, c-jun, or jun-D mRNA expression, was observed in the cortex of animals exposed to acute versus repeated restraint stress. The habituation of c-fos responses was stressor specific: exposure of restraint-adapted animals to a novel (20 min swim) stress produced an increase in levels of c-fos mRNA in every examined brain region comparable to that seen in animals exposed to this stressor for the first time. Adrenalectomy did not alter the pattern of c-fos expression induced by acute and repeated restraint stress. Therefore, activation and habituation of these c-fos responses are independent of changes in circulating levels of corticosterone.

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“…Stress, including intracerebroventricular inf usion of CRH, induces strong c-fos activation within the amygdala (Arnold et al, 1992;Honkaniemi, 1992;Honkaniemi et al, 1992;Imaki et al, 1993), along with increased CRH mRNA (Swanson and Simmons, 1989;Mamalaki et al, 1992;Makino et al, 1994aMakino et al, ,b, 1995. Furthermore, CRH is released in the amygdala after restraint stress (Pich et al, 1995).…”

Section: Implications For a Possible Distinction Between Fear And Anxmentioning

confidence: 99%

Role of the Hippocampus, the Bed Nucleus of the Stria Terminalis, and the Amygdala in the Excitatory Effect of Corticotropin-Releasing Hormone on the Acoustic Startle Reflex

1997

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Previously, we demonstrated that transection of the fimbria/ fornix blocked the excitatory effect of corticotropin-releasing hormone (CRH) on startle (CRH-enhanced startle), suggesting that the hippocampus and its efferent target areas that communicate via the fimbria may be critically involved in CRHenhanced startle. The bed nucleus of the stria terminalis (BNST) receives direct projections from the ventral hippocampus via the fimbria/fornix. Therefore, the role of the ventral hippocampus, the BNST, and the amygdala in CRH-enhanced startle was investigated. NMDA lesions of the BNST completely blocked CRH-enhanced startle, whereas chemical lesions of the ventral hippocampus and the amygdala failed to block CRH-enhanced startle. However, the same amygdala-lesioned animals showed a complete blockade of fear-potentiated startle, a conditioned fear response sensitive to manipulations of the amygdala. In contrast, BNST-lesioned rats had normal fear-potentiated startle. This indicates a double dissociation between the BNST and the amygdala in two different paradigms that enhance startle amplitude. Microinfusions of CRH into the BNST, but not into the ventral hippocampus, mimicked intracerebroventricular CRH effects. Furthermore, infusion of a CRH antagonist into the BNST blocked CRH-enhanced startle in a dose-dependent manner. Control studies showed that this blockade did not result from either leakage of the antagonist into the ventricular system or a local anesthetic effect caused by infusion of the antagonist into the BNST. The present studies strongly suggest that CRH in the CSF can activate the BNST, which could lead to activation of brainstem and hypothalamic BNST target areas involved in anxiety and stress responses. Key words: bed nucleus of the stria terminalis (BNST ); amygdala; hippocampus; corticotropin-releasing hormone (CRH); startle; anxiety; fearIntracerebroventricular inf usion of corticotropin-releasing hormone (CRH) elicits a constellation of behavioral, physiological, and endocrinological changes similar to those produced by natural stressors (cf. Dunn and Berridge, 1990). Thus far, however, the exact anatomical sites responsible for these behavioral and physiological actions of CRH after intracerebroventricular administration have not been identified. As part of an effort to delineate the neural circuitry underlying intracerebroventricular CRH effects, recently we investigated a possible involvement of the septum, using increased acoustic startle amplitude after CRH (CRH-enhanced startle) as a behavioral measure (Lee and Davis, 1997). Electrolytic lesions of the whole septum and the medial septum, but not the lateral septum, blocked CRH-enhanced startle. However, fiber-sparing chemical lesions of the medial septum failed to block CRH-enhanced startle, suggesting that the blockade seen with electrolytic lesions was probably caused by damage to fibers of passage, presumably the fornix. Supporting this conclusion, f unctional lesions of the fornix induced by knife cuts of the fimbria /fornix complete...

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Expression of c-fos in regions of the basal limbic forebrain following intra-cerebroventricular corticotropin-releasing factor in unstressed or stressed male rats

Cited by 156 publications

References 44 publications

Maternal separation enhances neuronal activation and cardiovascular responses to acute stress in borderline hypertensive rats

Maternal separation enhances neuronal activation and cardiovascular responses to acute stress in borderline hypertensive rats

Induction and habituation of immediate early gene expression in rat brain by acute and repeated restraint stress

Role of the Hippocampus, the Bed Nucleus of the Stria Terminalis, and the Amygdala in the Excitatory Effect of Corticotropin-Releasing Hormone on the Acoustic Startle Reflex

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