P.4.C.009 Fluoxetine modulating dorsal and ventral hippocampal BDNF as responsible for facilitating extinction memory retention

Diniz, Cassiano Ricardo Alves Faria; Antero, Leandro S.; Resstel, Leonardo Barbosa Moraes; Joca, Sâmia Regiane Lourenço

doi:10.1016/s0924-977x(14)70979-4

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“…Finally, we found no effect of treatment on BDNF levels within the VH. These data are similar to a conference report also showing increased DH BDNF, but no change in VH BDNF after chronic FLX (Diniz et al, 2014). Therefore, FLX dependent changes in hippocampal BDNF protein may be primarily the result of changes in DH BDNF expression patterns.…”

Section: Discussionsupporting

confidence: 91%

Chronic fluoxetine ameliorates adolescent chronic nicotine exposure-induced long-term adult deficits in trace conditioning

Connor

Gould

2017

Neuropharmacology

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Development of the brain, including the prefrontal cortex and hippocampus, continues through adolescence. Chronic nicotine exposure during adolescence may contribute to long-term deficits in forebrain-dependent learning. It is unclear if these deficits emerge immediately after exposure and if they can be ameliorated. In this study, C57BL/6J mice were treated with chronic nicotine (6.3 or 12.6 mg/kg/day) over 12 days beginning at adolescence, postnatal day (PND) 38, or adulthood, PND 56–63±3. We investigated the effects of short-term (24 hr) abstinence on trace fear conditioning and found that adult treatment resulted in deficits (6.3 and 12.6 mg/kg/day), but adolescent chronic nicotine treatment had no effect. In contrast, adolescent treatment with chronic nicotine (12.6 mg/kg/day) elicited a long-term (30 days) learning deficit, but adult chronic nicotine treatment did not. Using the elevated plus maze (EPM) we found no long-term changes in anxiety-related behavior after chronic nicotine exposure at either time-point. We investigated if chronic fluoxetine (FLX) could ameliorate adolescent chronic nicotine-associated long-term deficits in trace conditioning. We found that chronic FLX (160 mg/L) in drinking water ameliorated the long-term deficit in trace fear conditioning associated with nicotine exposure during adolescence. Additionally, in the same animals, we examined changes in total BDNF protein in the dorsal hippocampus (DH), ventral hippocampus (VH), and prefrontal cortex (PFC). Chronic FLX increased DH BDNF. Our data indicate nicotine administration during adolescence leads to late onset, long-lasting deficits in hippocampus-dependent learning that chronic FLX treatment ameliorate.

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Section: Discussionsupporting

confidence: 91%