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Involvement of plastic mechanisms associated to fluoxetine-induced neuronal turnover on the fear extinction in the cued conditioned model

Grant number: 13/02549-0
Support type:Scholarships in Brazil - Doctorate
Effective date (Start): June 01, 2013
Effective date (End): August 31, 2016
Field of knowledge:Biological Sciences - Pharmacology - Neuropsychopharmacology
Principal researcher:Sâmia Regiane Lourenço Joca
Grantee:Cassiano Ricardo Alves Faria Diniz
Home Institution: Faculdade de Ciências Farmacêuticas de Ribeirão Preto (FCFRP). Universidade de São Paulo (USP). Ribeirão Preto , SP, Brazil


Cued fear conditioning is a form of learning in which an association is made between stimuli and their aversive consequences. Fear conditioning has been used in preclinical research to study the neurobiology of post-traumatic stress disorder (PTSD), since it is characterized by exaggerated conditioned emotional responses to fear and a deficit in their extinction. The chronic treatment with fluoxetine, a selective serotonin reuptake inhibitor (SSRI) clinically used to treat PTSD, facilitates the extinction of conditioned fear to context, an effect that is dependent on BDNF levels in the hippocampus. SSRIs also increase hippocampal proliferation and survival of newborn neurons, in a BDNF-dependent way. There is evidence that the survival and integration of the newborn neurons to the adjacent neuronal network seem to influence tasks related to hippocampal function, including conditioning and extinction process. In addition, SSRIs not only increase hippocampal neurogenesis, but also increase the programmed hippocampal neuronal death, facilitating cell turnover. Therefore, we hypothesized that fluoxetine would facilitate the extinction process by promoting cell turnover in the hippocampus. This facilitation would require a greater newborn neurons integration to the neuronal network responsible for extinction process (which would be BDNF dependent), while there would be also a greater death of newborn neurons related to conditioning process. Therefore, we intend to evaluate hippocampal cell turnover, in response to chronic fluoxetine treatment in animals submitted to sound fear conditioning and extinction. (AU)

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Scientific publications
(References retrieved automatically from Web of Science and SciELO through information on FAPESP grants and their corresponding numbers as mentioned in the publications by the authors)
DINIZ, CASSIANO R. A. F.; BIOJONE, CAROLINE; JOCA, SARNIA R. L.; RANTAMAKI, TOMI; CASTREN, EERO; GUIMARAES, FRANCISCO S.; CASAROTTO, PLINIO C.. Dual mechanism of TRKB activation by anandamide through CB1 and TRPV1 receptors. PeerJ, v. 7, . (13/02549-0, 18/04250-5, 11/02746-4, 13/01029-2)
ALVES FARIA DINIZ, CASSIANO RICARDO; DA SILVA, LEANDRO ANTERO; DOMINGOS, LUANA BARRETO; SONEGO, ANDREZA BUZOLIN; BARBOSA MORAES, LEONARDO RESSTEL; JOCA, SAMIA. Fluoxetine acts concomitantly on dorsal and ventral hippocampus to Trk-dependently modulate the extinction of fear memory. PROGRESS IN NEURO-PSYCHOPHARMACOLOGY & BIOLOGICAL PSYCHIATRY, v. 113, . (13/02549-0)

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