Stress-induced c-fos expression in the rat brain: activation mechanism of sympathetic pathway

Senba, Emiko; Matsunaga, Keiji; Tohyama, Masaya; Noguchi, Koichi

doi:10.1016/0361-9230(93)90225-z

Cited by 223 publications

(103 citation statements)

References 38 publications

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“…The c-Fos expression seen in the control group (animals submitted to saline and restraint) was similar to that previously reported for stress-induced c-Fos expression (Senba et al, 1993;Chen and Herbert, 1995). It was widely distributed in the brain, with moderate to intense staining in areas involved with the stress response, such as limbic structures and cell groups involved in neuroendocrine and autonomic control (Table 1).…”

Section: Resultssupporting

confidence: 86%

Stress-Induced c-Fos Expression is Differentially Modulated by Dexamethasone, Diazepam and Imipramine

Medeiros

Reis

Mello

2005

Neuropsychopharmacol

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Immobilization stress upregulates c-Fos expression in several CNS areas. Repeated stress or the use of drugs can modulate stressinduced c-Fos expression. Here, we investigated in 40 different areas of the rat brain the effects of dexamethasone (SDX, a synthetic glucocorticoid), diazepam (SBDZ, a benzodiazepine), and imipramine (IMI, an antidepressant) on the c-Fos expression induced by restraint stress. Wistar rats were divided into four groups and submitted to 20 days of daily injection of saline (three first groups) or imipramine, 15 mg/kg, i.p. On day 21, animals were submitted to injections of saline (somatosensory, SS), SDX (1 mg/kg, i.p.), SBDZ (5 mg/kg, i.p.), or IMI (15 mg/kg, i.p.) before being submitted to restraint. Immediately after stress, the animals were perfused and their brains processed with immunohistochemistry for c-Fos (Ab-5 Oncogene Science). Dexamethasone reduced stress-induced c-Fos expression in SS cortex, hippocampus, paraventricular nucleus of the hypothalamus (PVH), and locus coeruleus (LC), whereas diazepam reduced c-Fos staining in the SS cortex, hippocampus, bed nucleus of stria terminalis, septal area, and hypothalamus (preoptic area and supramammillary nucleus). Chronic administration of imipramine decreased staining in the hippocampus, PVH, and LC, while increasing it in the nucleus raphe pallidus. We conclude that dexamethasone, diazepam and imipramine differentially modulate stress-induced Fos expression. The present study provides an important comparative background that may help in the further understanding of the effects of these compounds and on the brain activation as well as on the behavioral, neuroendocrine, and autonomic responses to stress.

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Section: Resultssupporting

confidence: 86%

Stress-Induced c-Fos Expression is Differentially Modulated by Dexamethasone, Diazepam and Imipramine

Medeiros

Reis

Mello

2005

Neuropsychopharmacol

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“…As previously reported (59,70), following AS, increased number of neurons expressing c-Fos immunoreactivity was observed in hypothalamic PVN. Apelin immunostaining was detected in cytoplasm of some neurons in PVN, and c-Fos protein expression was observed as nuclear immunoreactivity in a group of PVN neurons.…”

Section: Resultssupporting

confidence: 86%

Central apelin mediates stress-induced gastrointestinal motor dysfunction in rats

Bülbül

İzgüt‐Uysal

Sinen

et al. 2016

American Journal of Physiology-Gastrointestinal and Liver Physi

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Apelin, an endogenous ligand for APJ receptor, has been reported to be upregulated in paraventricular nucleus (PVN) following stress. Central apelin is known to stimulate release of corticotropin-releasing factor (CRF) via APJ receptor. We tested the hypothesis that stress-induced gastrointestinal (GI) dysfunction is mediated by central apelin. We also assessed the effect of exogenous apelin on GI motility under nonstressed (NS) conditions in conscious rats. Prior to solid gastric emptying (GE) and colon transit (CT) measurements, APJ receptor antagonist F13A was centrally administered under NS conditions and following acute stress (AS), chronic homotypic stress (CHS), and chronic heterotypic stress (CHeS). Plasma corticosterone was assayed. Strain gage transducers were implanted on serosal surfaces of antrum and distal colon to record postprandial motility. Stress exposure induced coexpression of c-Fos and apelin in hypothalamic PVN. Enhanced hypothalamic apelin and CRF levels in microdialysates were detected following AS and CHeS, which were negatively and positively correlated with GE and CT, respectively. Central F13A administration abolished delayed GE and accelerated CT induced by AS and CHeS. Central apelin-13 administration increased the plasma corticosterone and inhibited GE and CT by attenuating antral and colonic contractions. The inhibitory effect elicited by apelin-13 was abolished by central pretreatment of CRF antagonist CRF9-41 in antrum, but not in distal colon. Central endogenous apelin mediates stressinduced changes in gastric and colonic motor functions through APJ receptor. The inhibitory effects of central exogenous apelin-13 on GI motility appear to be partly CRF dependent. Apelin-13 inhibits colon motor functions through a CRF-independent pathway.

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“…The amygdala is considered an essential link between sensory and limbic areas of the cerebral cortex and subcortical brain regions, and amygdaloid subnuclei participate in the modulation of fear, memory, and attention (for review, see McDonald, 1998;Rasia-Filho et al, 2000). The PVN also contributes to learning, memory, as well as having a role in stress, pain, and immune responses (Bodnar et al, 1986;Senba et al, 1993;Smith and Day, 1994;Matsumoto et al, 1997;Marquez et al, 2004;see Doris (1984) for review). The greater baseline activity in the SII, AD, BLA, and PVN of the LE may explain, in part, published reports that LE rats perform better in cognitive tasks (Lindner and Schallert, 1988;Tonkiss et al, 1992;Andrews et al, 1995;Harker and Whishaw, 2002), have higher baseline levels of locomotor activity (Aulakh et al, 1988;Onaivi et al, 1992;van Lier et al, 2003), and show less reactivity to external stimuli (Glowa and Hanson, 1994;Acri et al, 1995;Faraday, 2002).…”

Section: Discussionmentioning

confidence: 99%

Differences in forebrain activation in two strains of rat at rest and after spinal cord injury

Paulson

Gorman²,

Yezierski

et al. 2005

Experimental Neurology

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Forebrain activation patterns in normal and spinal-injured Sprague-Dawley (SD) rats were determined by measuring regional cerebral blood flow as an indicator of neuronal activity. Data are compared to our previously published findings from normal and spinal-injured Long-Evans (LE) rats and reveal a striking degree of overlap, as well as differences, between strains in the basal (unstimulated) forebrain activation in normal animals. Specifically, 81% of the structures sampled showed similar activation in both strains, suggesting a consistent and identifiable pattern of basal cerebral activation in the rat. LE controls showed significantly greater basal activation in the remaining structures compared to SD control group, including the anterior dorsal thalamus, basolateral amygdala, SII cortex, and the hypothalamic paraventricular nucleus. In contrast, spinal cord injury (SCI) resulted in strain-specific changes in forebrain activation categorized by structures that showed significant increases in: (1) only LE SCI rats (posterior, ventrolateral, and ventroposterolateral thalamic nuclei); (2) only SD SCI rats (anterior-dorsal and medial thalamus, basolateral amygdala, cingulate and retrosplenial cortex, habenula, interpeduncular nucleus, hypothalamic paraventricular nucleus, periaqueductal gray); or (3) both strains (arcuate nucleus, ventroposteromedial thalamus, SI and SII somatosensory cortex). These results provide information related to the remote, i.e. supraspinal, effects of spinal cord injury and suggest that genetic differences play an important part in the forebrain response to such injury. Brain activation studies therefore provide a useful tool in understanding the full extent of secondary consequences following spinal injury and for identifying potential central mechanism responsible for the development of pain.

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Stress-induced c-fos expression in the rat brain: activation mechanism of sympathetic pathway

Cited by 223 publications

References 38 publications

Stress-Induced c-Fos Expression is Differentially Modulated by Dexamethasone, Diazepam and Imipramine

Stress-Induced c-Fos Expression is Differentially Modulated by Dexamethasone, Diazepam and Imipramine

Central apelin mediates stress-induced gastrointestinal motor dysfunction in rats

Differences in forebrain activation in two strains of rat at rest and after spinal cord injury

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