Marcos Santibañez

Pontifical Catholic University of Chile, CiudadSantiago, Santiago, Chile

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Publications (4)13.82 Total impact

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    ABSTRACT: The present report provides evidence that repeated immobilization stress (RIS) induced a noradrenergic-dependent depressive-like behaviour and an augmented behavioural response to desipramine (DMI), a noradrenaline reuptake inhibitor (NRI), in the forced swimming test (FST). The present results show that RIS decreased the baseline of climbing behaviour in the FST. Whereas subchronic administration of DMI (10mg/kg, three times in a 24h period) induced a significantly higher increase in climbing behaviour on repeatedly stressed rats compared to controls. The results also show that the concomitant administration of the low dose of DMI (3mg/Kg) during the RIS fully prevented the decrease of climbing behaviour induced by RIS, without exerting behavioural effects in control rats, further supporting an augmented response to the DMI antidepressant effects in the repeatedly stressed rats. In conclusion, our data indicate that RIS not only changes the behavioural responses in the FST but also increases the antidepressant effects of DMI.
    Behavioural brain research 12/2010; 214(2):285-9. · 3.22 Impact Factor
  • Marcos Santibañez, Katia Gysling, María Inés Forray
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    ABSTRACT: Clinical and experimental studies have shown that the activation of corticotropin-releasing hormone (CRH) and noradrenergic systems mediate stress-induced anxiety. Repeated immobilization stress (RIS) has been shown to induce long-lasting anxiety behavior and changes in noradrenaline turnover. The present work was aimed at studying the effect of RIS on the in situ expression of CRH-LI in the central extended amygdala and paraventricular nucleus of the hypothalamus (PVN). Our results showed that RIS for 15 days induces a significant increase of CRH-LI expression in the central extended amygdala. The increase in CRH-LI expression in the central extended amygdala was sustained even after a 25-day stress-free period. The concomitant administration of desipramine (DMI), a specific noradrenaline uptake inhibitor, fully prevented the RIS-induced increase in CRH expression. RIS also induced an increase of CRH-LI expression in the PVN that was prevented by the concomitant DMI administration. In contrast to the sustained effect observed in the central extended amygdala, the RIS-induced increase of CRH-LI expression in the PVN was nonlasting. DMI administration also prevented the RIS-induced increase of adrenal gland weight. The present findings showing that RIS induces a sustained increase of CRH expression in the central extended amygdala suggest that the repeated activation of CRH neurons and CRH receptors in the central extended amygdala may underlie the long-lasting anxiety behavior induced by RIS. Further studies should address the mechanisms involved in the effect of DMI and its eventual relevance in the therapeutic actions of DMI.
    Journal of Neuroscience Research 12/2006; 84(6):1270-81. · 2.97 Impact Factor
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    ABSTRACT: Astrocytes and microglia associate to amyloid plaques, a pathological hallmark of Alzheimer disease. Microglia are activated by and can phagocytose beta-amyloid (Abeta). Scavenger receptors (SRs) are among the receptors mediating the uptake of fibrillar Abeta in vitro. However, little is known about the function of the astrocytes surrounding the plaques or the nature of their interaction with Abeta. It is unknown whether glial cells bind to nonfibrillar Abeta and if binding of astrocytes to Abeta depends on the same Scavenger receptors described for microglia. We determined the binding of glia to Abeta by an adhesion assay and evaluated the presence of scavenger receptors in glial cells by immunocytochemistry, immunohistochemistry of brain sections, and immunoblot. We found that astrocytes and microglia from neonatal rats adhered in a concentration-dependent manner to surfaces coated with fibrillar Abeta or nonfibrillar Abeta. Fucoidan and poly(I), known ligands for SR-type A, inhibited adhesion of microglia and astrocytes to Abeta and also inhibited Abeta phagocytosis. In contrast, a ligand for SR-type B like low density lipoprotein, did not compete glial adhesion to Abeta. Microglia presented immunodetectable SR-BI, SR-AI/AII, RAGE, and SR-MARCO (macrophage receptor with collagenous structure, a member of the SR-A family). Astrocytes presented SR-BI and SR-MARCO. To our knowledge, this is the first description of the presence of SR-MARCO in astrocytes. Our results indicate that both microglia and astrocytes adhere to fibrillar and nonfibrillar Abeta. Adhesion was mediated by a fucoidan-sensitive receptor. We propose that SR-MARCO could be the Scavenger receptor responsible for the adhesion of astrocytes and microglia to Abeta.
    Journal of Biological Chemistry 09/2005; 280(34):30406-15. · 4.65 Impact Factor
  • Marcos Santibañez, Katia Gysling, María Inés Forray
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    ABSTRACT: The bed nucleus of the stria terminalis (BNST) has a high density of corticotropin-releasing hormone (CRH)-containing neurons that are significantly innervated by noradrenergic and dopaminergic nerve terminals. This limbic structure is involved in the extrahypothalamic response to stress. The purpose of the present work is to study whether the absence of glucocorticoids, induced by a long-term adrenalectomy, regulates CRH gene expression and noradrenaline and dopamine extracellular levels in the rat BNST. The results showed that adrenalectomy decreases CRH mRNA in the dorsal lateral BNST but not in the ventral lateral BNST. Adrenalectomy also decreases CRH-like immunoreactivity both in BNST subnuclei and in the central nucleus of the amygdala. In addition, adrenalectomy significantly increases noradrenaline and dopamine extracellular levels in the lateral BNST. The present results suggest that adrenalectomy regulates CRH gene expression and noradrenaline and dopamine extracellular levels in the BNST in an opposite way. Thus, the present study adds novel evidence further supporting that the BNST and the central nucleus of the amygdala form part of an adrenal steroid-sensitive extrahypothalamic circuit that has been involved in fear and anxiety responses and in clinical syndromes such as melancholic depression, posttraumatic stress disorders, and addiction.
    Journal of Neuroscience Research 08/2005; 81(1):140-52. · 2.97 Impact Factor