Contrasting Fos expression induced by acute reboxetine and fluoxetine in the rat forebrain: neuroanatomical substrates for the antidepressant effect

Miyata, Shinji; Hamamura, Takashi; Lee, Youmei; Miki, Masahito; Habara, Toshiyuki; Oka, Takuro; Endo, Shiro; Taoka, Hideki; Kuroda, Shigetoshi

doi:10.1007/s00213-004-2072-7

Cited by 22 publications

(12 citation statements)

References 43 publications

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“…In all, 5 mg/kg reboxetine induced expression of c-Fos in the NAc to a similar extent as that seen following administration of 3 mg/kg AMPH, 10 mg/kg GBR12909, and 10 mg/kg citalopram. Hence, the doses of reboxetine used in this study are able to induce a transcriptional response in neurons of the NAc (Figure 1b) (Miyata et al, 2005). Together, these data show that selective activation of either DA or 5-HT but not NE signaling is sufficient to drive induction of pMeCP2 in the NAc.…”

Section: Selective Blockade Of the Dat Or Sert Is Sufficient To Inducsupporting

confidence: 58%

Differential Regulation of MeCP2 Phosphorylation in the CNS by Dopamine and Serotonin

Hutchinson

Deng

Aryal

et al. 2011

Neuropsychopharmacol

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Systemic administration of amphetamine (AMPH) induces phosphorylation of MeCP2 at Ser421 (pMeCP2) in select populations of neurons in the mesolimbocortical brain regions. Because AMPH simultaneously activates multiple monoamine neurotransmitter systems, here we examined the ability of dopamine (DA), serotonin (5-HT), and norepinephrine (NE) to induce pMeCP2. Selective blockade of the DA transporter (DAT) or the 5-HT transporter (SERT), but not the NE transporter (NET), was sufficient to induce pMeCP2 in the CNS. DAT blockade induced pMeCP2 in the prelimbic cortex (PLC) and nucleus accumbens (NAc), whereas SERT blockade induced pMeCP2 only in the NAc. Administration of selective DA and 5-HT receptor agonists was also sufficient to induce pMeCP2; however, the specific combination of DA and 5-HT receptors activated determined the regional-and cell-type specificity of pMeCP2 induction. The D 1 -class DA receptor agonist SKF81297 induced pMeCP2 widely; however, coadministration of the D 2 -class agonist quinpirole restricted the induction of pMeCP2 to GABAergic interneurons of the NAc. Intra-striatal injection of the adenylate cyclase activator forskolin was sufficient to induce pMeCP2 in medium-spiny neurons, suggesting that the combinatorial regulation of cAMP by different classes of DA and 5-HT receptors may contribute to the cell-type specificity of pMeCP2 induction. Consistent with the regulation of pMeCP2 by multiple monoamine neurotransmitters, genetic disruption of any single monoamine transporter in DAT-, SERT-, and NETknockout mice failed to eliminate AMPH-induced pMeCP2 in the NAc. Together, these studies indicate that combinatorial signaling through DA and 5-HT receptors can regulate the brain region-and cell-type specific pMeCP2 in the CNS.

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Section: Selective Blockade Of the Dat Or Sert Is Sufficient To Inducsupporting

confidence: 58%

Differential Regulation of MeCP2 Phosphorylation in the CNS by Dopamine and Serotonin

Hutchinson

Deng

Aryal

et al. 2011

Neuropsychopharmacol

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“…Essentially all studies were conducted after acute (30 min-2 h) administration of antidepressants. A reasonably consistent observation is that administration of pharmacologically diverse antidepressants (SSRIs, selective NRIs, MAOIs, mirtazapine) increase c-fos or c-Fos in the central nucleus of the amygdala (CeA) and BNST (Beck, 1995;Duncan et al, 1996;Fraga et al, 2005;Miyata et al, 2005;Morelli et al, 1999;Slattery et al, 2005;Sumner et al, 2004;Thomsen and Helboe, 2003). This increase was also seen in female rats treated acutely with fluoxetine (Torres et al, 1998).…”

Section: Discussionmentioning

confidence: 83%

Induction of c-Fos and ΔFosB Immunoreactivity in Rat Brain by Vagal Nerve Stimulation

Cunningham

Mifflin

Gould

et al. 2007

Neuropsychopharmacol

149

123

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Vagus nerve stimulation (VNS) is used as therapy for treatment-resistant depression or epilepsy. This study used immunohistochemistry for biomarkers of short-term (c-Fos) and long-term (DFosB) neuronal activation to map regions in brain that are activated by acute (2 h) or chronic (3 weeks) VNS in conscious Sprague-Dawley rats. Electrodes (Cyberonics Inc.) were implanted on the left vagus nerve and 1 week after surgery, stimulation began using parameters employed clinically (one burst of 20 Hz, 250 ms pulse width, 0.25 mA stimulation for 30 s every 5 min). Radio telemetry transmitters were used for monitoring blood pressure, heart rate, activity, and respiratory rate during VNS; neither acute nor chronic VNS significantly affected these parameters. Acute VNS significantly increased c-Fos staining in the nucleus of the solitary tract, paraventricular nucleus of the hypothalamus, parabrachial nucleus, ventral bed nucleus of the stria terminalis, and locus coeruleus but not in the cingulate cortex or dorsal raphe nucleus (DRN). Acute VNS did not affect DFosB staining in any region. Chronic VNS significantly increased DFosB and c-Fos staining bilaterally in each region affected by acute VNS as well as in the cingulate cortex and DRN. Using these stimulation parameters, VNS was tested for antidepressant-like activity using the forced swim test (FST). Both VNS and desipramine significantly decreased immobility in the FST; whereas desipramine decreased immobility by increasing climbing behavior, VNS did so by increasing swimming behavior. This study, then, identified potential sites in brain where VNS may produce its clinical effects.

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“…Reboxetine has been studied in rat models using invasive and highly focal intra-cerebral microdialysis techniques (Sacchetti et al 1999) and also by Fos-immunoreactivity (Miyata et al 2005). Clinical studies have also examined the effects of reboxetine administration on cognitive processing using fMRI methods (Norbury et al , 2008Miskowiak et al 2007;McCabe et al 2010).…”

Section: Introductionmentioning

confidence: 99%

Neuroanatomical targets of reboxetine and bupropion as revealed by pharmacological magnetic resonance imaging

et al. 2011

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Contrasting Fos expression induced by acute reboxetine and fluoxetine in the rat forebrain: neuroanatomical substrates for the antidepressant effect

Abstract: These results suggest that the shell region may be one possible target for the antidepressant effects of fluoxetine and reboxetine. Furthermore, the difference in their clinical effects may depend on their different target sites of action.

Cited by 22 publications

References 43 publications

Differential Regulation of MeCP2 Phosphorylation in the CNS by Dopamine and Serotonin

Differential Regulation of MeCP2 Phosphorylation in the CNS by Dopamine and Serotonin

Induction of c-Fos and ΔFosB Immunoreactivity in Rat Brain by Vagal Nerve Stimulation

Neuroanatomical targets of reboxetine and bupropion as revealed by pharmacological magnetic resonance imaging

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