During the last few years several studies have highlighted the possibility that major depression can be characterized by a general redn. in brain plasticity and an increased vulnerability under challenging situations. Such dysfunction may be the consequence of reduced expression and function of proteins important for neuroplasticity such as brain-derived neurotrophic factor (BDNF). On this basis, by using a sensitive non-radioactive in-situ hybridization, we evaluated the effects of a chronic treatment with fluoxetine on BDNF expression within rat dopaminergic regions. In fact, besides the well-established role of the hippocampus, increasing evidence indicates that other brain regions may be involved in the pathophysiol. of depression and consequently be relevant for the therapeutic action of antidepressant drugs. Our results indicate that 3 wk of fluoxetine administration up-regulates BDNF mRNA levels selectively within structures belonging to the meso-cortico-limbic pathway. The expression of the neurotrophin is significantly increased in the ventral tegmental area, prefrontal cortex, and shell region of the nucleus accumbens, whereas no changes were detected in the substantia nigra and striatum. Moreover, in agreement with previous studies, fluoxetine increased BDNF mRNA levels in the hippocampus, an effect that was limited to the cell bodies without any change in its dendritic targeting. These data show that chronic treatment with fluoxetine increases BDNF gene expression not only in limbic areas but also in dopaminergic regions, suggesting that such an effect may contribute to improve the function of the dopaminergic system in depressed subjects

Chronic treatment with fluoxetine up-regulates cellular BDNF mRNA expression in rat dopaminergic regions / R. Molteni, F. Calabrese, F. Bedogni, E. Tongiorgi, F. Fumagalli, G. Racagni, M.A. Riva. - In: INTERNATIONAL JOURNAL OF NEUROPSYCHOPHARMACOLOGY. - ISSN 1461-1457. - 9:3(2006), pp. 307-317.

Chronic treatment with fluoxetine up-regulates cellular BDNF mRNA expression in rat dopaminergic regions

R. Molteni;F. Calabrese;F. Bedogni;F. Fumagalli;G. Racagni;M.A. Riva
2006

Abstract

During the last few years several studies have highlighted the possibility that major depression can be characterized by a general redn. in brain plasticity and an increased vulnerability under challenging situations. Such dysfunction may be the consequence of reduced expression and function of proteins important for neuroplasticity such as brain-derived neurotrophic factor (BDNF). On this basis, by using a sensitive non-radioactive in-situ hybridization, we evaluated the effects of a chronic treatment with fluoxetine on BDNF expression within rat dopaminergic regions. In fact, besides the well-established role of the hippocampus, increasing evidence indicates that other brain regions may be involved in the pathophysiol. of depression and consequently be relevant for the therapeutic action of antidepressant drugs. Our results indicate that 3 wk of fluoxetine administration up-regulates BDNF mRNA levels selectively within structures belonging to the meso-cortico-limbic pathway. The expression of the neurotrophin is significantly increased in the ventral tegmental area, prefrontal cortex, and shell region of the nucleus accumbens, whereas no changes were detected in the substantia nigra and striatum. Moreover, in agreement with previous studies, fluoxetine increased BDNF mRNA levels in the hippocampus, an effect that was limited to the cell bodies without any change in its dendritic targeting. These data show that chronic treatment with fluoxetine increases BDNF gene expression not only in limbic areas but also in dopaminergic regions, suggesting that such an effect may contribute to improve the function of the dopaminergic system in depressed subjects
Neurotrophic factors Role: BSU (Biological study, unclassified), BIOL (Biological study) (brain-derived; fluoxetine increased brain-derived neurotrophic factor mRNA expression not only in limbic areas but also within dopaminergic regions of rat); Brain (corpus striatum; fluoxetine showed no changes in brain-derived neurotrophic factor mRNA level in striatum of rat brain); Brain (dentate gyrus; fluoxetine increased brain-derived neurotrophic factor mRNA expression in dentate gyrus granule cells of rat brain); Nervous system (dopaminergic; fluoxetine increased brain-derived neurotrophic factor mRNA expression not only in meso-cortico-limbic pathway related areas but also within dopaminergic regions like ventral tegmental area, prefrontal cortex and nucleus accumbens of rat); mRNA Role: BSU (Biological study, unclassified), BIOL (Biological study) (fluoxetine increased brain-derived neurotrophic factor mRNA expression not only in limbic areas but also within dopaminergic regions of rat); Brain (fluoxetine increased brain-derived neurotrophic factor mRNA expression not only in limbic areas but also within dopaminergic regions of rat brain); Neurotrophic factors Role: BSU (Biological study, unclassified), BIOL (Biological study) (fluoxetine increased brain-derived neurotrophic factor mRNA expression not only in meso-cortico-limbic pathway related areas but also within dopaminergic regions like ventral tegmental area, prefrontal cortex and nucleus accumbens of rat); Brain (hippocampus; fluoxetine increased brain-derived neurotrophic factor mRNA expression in hippocampus of rat brain); Brain (mesocorticolimbic dopaminergic system; fluoxetine increased brain-derived neurotrophic factor mRNA expression not only in meso-cortico-limbic pathway related areas but also within dopaminergic regions like ventral tegmental area, prefrontal cortex and nucleus accumbens of rat); Mental and behavioral disorders (mood-affecting; fluoxetine increased brain-derived neurotrophic factor mRNA expression within dopaminergic pathways which play vital role in mood disorder in rat); Brain (nucleus accumbens; fluoxetine increased brain-derived neurotrophic factor mRNA expression in shell region of nucleus accumbens of rat brain); Brain (prefrontal cortex; fluoxetine increased brain-derived neurotrophic factor mRNA expression in prefrontal cortex of rat brain); 5-HT reuptake inhibitors; Antidepressants; Drug targets (selective serotonin reuptake inhibitor fluoxetine increased brain-derived neurotrophic factor mRNA expression not only in limbic areas but also within dopaminergic regions of rat); Brain (substantia nigra; fluoxetine showed no changes in brain-derived neurotrophic factor mRNA level in substantia nigra of rat brain); Brain (ventral tegmental area; fluoxetine increased brain-derived neurotrophic factor mRNA expression in ventral tegmental area of rat brain)
Settore BIO/14 - Farmacologia
INTERNATIONAL JOURNAL OF NEUROPSYCHOPHARMACOLOGY
http://journals.cambridge.org/action/displayAbstract?fromPage=online&aid=323200
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Utilizza questo identificativo per citare o creare un link a questo documento: http://hdl.handle.net/2434/24076
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