Differential responses to anxiogenic drugs in a mouse model of panic disorder as revealed by Fos immunocytochemistry in specific areas of the fear circuitry
| Autor: | Xavier Estivill, Mara Dierssen, Xavier Gallego, Patricia Murtra, Ramon Trullas, Rafael Maldonado, Mònica Gratacòs, Ignasi Sahún |
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| Jazyk: | angličtina |
| Rok vydání: | 2007 |
| Předmět: |
Male
Fos immunohistochemistry medicine.medical_specialty NT-3 Clinical Biochemistry Mice Transgenic Anxiety Biochemistry Tropomyosin receptor kinase C Amygdala Sodium Lactate Mice Random Allocation Internal medicine Caffeine medicine Animals Panic disorder business.industry Organic Chemistry TrkC Antagonist Brain Yohimbine Fear medicine.disease Adenosine receptor Disease Models Animal Oncogene Proteins v-fos medicine.anatomical_structure Endocrinology Anxiogenic Locus ceruleus medicine.symptom business medicine.drug |
| Zdroj: | Digital.CSIC. Repositorio Institucional del CSIC instname |
| ISSN: | 1438-2199 0939-4451 |
| Popis: | Sensitivity to pharmacological challenges has been reported in patients with panic disorder. We have previously validated transgenic mice overexpressing the neurotrophin-3 (NT-3) receptor, TrkC (TgNTRK3), as an engineered murine model of panic disorder. We could determine that TgNTRK3 mice presented increased cellularity in brain regions, such as the locus ceruleus, that are important neural substrates for the expression of anxiety in severe anxiety states. Here, we investigated the sensitivity to induce anxiety and panic-related symptoms by sodium lactate and the effects of various drugs (the α2-adrenoceptor antagonist, yohimbine and the adenosine antagonist, caffeine), in TgNTRK3 mice. We found enhanced panicogenic sensitivity to sodium lactate and an increased intensity and a differential pattern of Fos expression after the administration of yohimbine or caffeine in TgNTRK3. Our findings validate the relevance of the NT-3/TrkC system to pathological anxiety and raise the possibility that a specific set of fear-related pathways involved in the processing of anxiety-related information may be differentially activated in panic disorder. © 2006 Springer-Verlag. This work was funded by the Spanish Ministry of Education and Sciences SAF2001-1231, SAF-2004-02808 and GEN2003-20651-C06-03. DURSISGR0500008, CIBER-CB06/07/0089. P.M. is a scientific researcher supported by the Juan de la Cierva program of Ministerio de Ciencia y Tecnología. |
| Databáze: | OpenAIRE |
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