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

Medeiros, Magda Alves de; Reis, L. C.; Mello, Luiz E.

doi:10.1038/sj.npp.1300694

Cited by 57 publications

(27 citation statements)

References 34 publications

(47 reference statements)

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“…The latter results are supported by former studies which investigated the effects of the treatment with diazepam on c-Fos expression in the amygdala of stressed rats, also reporting increased c-Fos expression in the central amygdala by diazepam (Beck and Fibiger 1995;de Medeiros et al 2005). Additionally, another study showed that diazepam increased c-Fos expression also in the central amygdala of habituated rats without any behavioral task (Salminen et al 1996).…”

Section: Discussionsupporting

confidence: 73%

Examining face and construct validity of a noninvasive model of panic disorder in Lister-hooded rats

et al. 2010

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Similar to human panic attacks, ultrasound application to LH rats activated the autonomic, but not the neuroendocrine, stress system. Also, like in humans, the current data confirm and extend that the dPAG/dlPAG plays a key role in ultrasound-induced escape behavior. These observations suggest that ultrasound-induced escape behaviors in LH rats have face and construct validity for panic disorders.

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Section: Discussionsupporting

confidence: 73%

Examining face and construct validity of a noninvasive model of panic disorder in Lister-hooded rats

et al. 2010

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“…This study suggests that GBP might differentially modulate c-Fos expression in surgical paw incision (de Medeiros et al 2005).…”

Section: Discussionmentioning

confidence: 92%

Effect of Gabapentin on c-Fos Expression in the CNS after Paw Surgery in Rats

Kazi

Gee

2007

J Mol Neurosci

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Gabapentin (neurontin), a GABA analogue anticonvulsant has proven to be effective in anti-nociceptive activity as well as for the treatment of anxiety. Gabapentin (GBP) is well tolerated and shows very favorable side effects profile: The exact molecular mechanism of action of GBP to block postoperative pain and stress is not known. Therefore, to identify the functional neuroanatomical target sites of GBP in post-surgery as well as its effect on postsurgical process, we examined the effects of GBP on c-Fos expression in the supraspinal part of the central nervous system in rats. Using a well-validated rat model of surgical pain, we studied the neuroanatomical functional target sites of gabapentin after paw surgery. The effect of GBP was examined by means of c-Fos immunohistochemistry. A single intraperitoneal injection (i.p.) of GBP (150 mg/kg) or saline (control) was administered 20 min before surgical incision in the paw under anesthesia. Ninety minutes after surgical incision, the deeply anesthetized rats were perfused transcardially with 4% paraformaldehyde. Serial 40-microm-thick sections of whole brain (except spinal cord) were cut and processed by immunohistochemistry to locate and quantify the sites and number of neurons with c-Fos immunoreactivity. Detection of c-Fos protein was performed using the peroxidase-antiperoxidase detection protocol. Our present study demonstrated that compared to control, administration of GBP (150 mg/kg, i.p.) before paw surgery significantly (p < 0.01) attenuated the incision-induced c-Fos expression only in the paraventricular nucleus of the hypothalamus. In addition, GBP-induced increase in c-Fos expression was observed in the dorsal raphe (DRN) and in the nucleus raphe magnus. Present results indicate that GBP may differentially modulate c-Fos expression in surgical paw incision. Moreover, this study provides some clue to examine whether GBP exerts its action simultaneously through two separate pathways in post-surgery.

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“…One common functional response to chronic antidepressant treatment, especially tricyclic antidepressants, is an attenuation of stress-induced activation of the HPA axis (Duncan et al, 1996;Connor et al, 2000;de Medeiros et al, 2005;Butterweck et al, 2001). To explore the functional relevance of the changes in the endocannabinoid system induced by chronic desipramine treatment, we examined the effects of acute blockade of the CB 1 receptor with AM251 on the peak hormonal and cellular responses to stress following this antidepressant regimen.…”

Section: Discussionmentioning

confidence: 99%

“…Furthermore, the ability of glucocorticoid hormones to exert negative feedback on HPA axis activity appears to be deficient in depression, resulting in a feed-forward hyperactivation of this system (Parker et al, 2003;Holsboer, 2000). This enhanced output of the HPA axis appears functionally relevant to depression, as long-term antidepressant treatment attenuates this phenomenon in humans (De Bellis et al, 1993;Pariante et al, 2004;Greden et al, 1983;Michelson et al, 1997), and suppresses stress-induced activation of the HPA axis in other species (Reul et al, 1993;Connor et al, 2000;Holsboer and Barden, 1996;de Medeiros et al, 2005;Butterweck et al, 2001;Stout et al, 2002). The ability of antidepressants to suppress HPA axis hyperactivity has been shown to be coupled to their clinical efficacy (Appelhof et al, 2006;Young et al, 2004).…”

Section: Introductionmentioning

confidence: 99%

Involvement of the Endocannabinoid System in the Ability of Long-Term Tricyclic Antidepressant Treatment to Suppress Stress-Induced Activation of the Hypothalamic–Pituitary–Adrenal Axis

Hill

Sinopoli

et al. 2006

Neuropsychopharmacol

109

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The efficacy of antidepressants has been linked in part to their ability to reduce activity of the hypothalamic-pituitary-adrenal (HPA) axis; however, the mechanism by which antidepressants regulate the HPA axis is largely unknown. Given that recent research has demonstrated that endocannabinoids can regulate the HPA axis and exhibit antidepressant potential, we examined the hypothesis that the endocannabinoid system is regulated by long-term antidepressant treatment. Three-week administration of the tricyclic antidepressant desipramine (10 mg/kg/day) resulted in a significant increase in the density of the cannabinoid CB 1 receptor in the hippocampus and hypothalamus, without significantly altering endocannabinoid content in any brain structure examined. Furthermore, chronic desipramine treatment resulted in a reduction in both secretion of corticosterone and the induction of the immediate early gene c-fos in the medial dorsal parvocellular region of the paraventricular nucleus of the hypothalamus (PVN) following a 5 min exposure to swim stress. Acute treatment with the CB 1 receptor antagonist, AM251 (1 mg/kg), before exposure to swim stress, completely occluded the ability of desipramine to reduce both corticosterone secretion and induction of c-fos expression in the PVN. Collectively, these data demonstrate that CB 1 receptor density in the hippocampus and hypothalamus is increased by chronic tricyclic antidepressant treatment, and suggest that this upregulation could contribute to the ability of tricyclic antidepressants to suppress stress-induced activation of the HPA axis.

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

Cited by 57 publications

References 34 publications

Examining face and construct validity of a noninvasive model of panic disorder in Lister-hooded rats

Examining face and construct validity of a noninvasive model of panic disorder in Lister-hooded rats

Effect of Gabapentin on c-Fos Expression in the CNS after Paw Surgery in Rats

Involvement of the Endocannabinoid System in the Ability of Long-Term Tricyclic Antidepressant Treatment to Suppress Stress-Induced Activation of the Hypothalamic–Pituitary–Adrenal Axis

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