Targeted over-expression of brain-derived neurotrophic factor in the nucleus accumbens increases goal tracking and nicotine locomotor sensitization, but reduces nicotine self-administration in rats

2017 ◽  
Vol 171 ◽  
pp. e28
Author(s):  
Russell W. Brown ◽  
Lauren A. Beuttel ◽  
Sara A. Dean ◽  
Curtis A. Bradley ◽  
James Wherry ◽  
...  
2013 ◽  
Vol 35 (5) ◽  
pp. 384-395 ◽  
Author(s):  
Melissa L. Perreault ◽  
Theresa Fan ◽  
Brian F. O'Dowd ◽  
Susan R. George

2003 ◽  
Vol 18 (7) ◽  
pp. 2093-2098 ◽  
Author(s):  
Tamar Green-Sadan ◽  
Noa Kinor ◽  
Ilana Roth-Deri ◽  
Revital Geffen-Aricha ◽  
Cheryl J. Schindler ◽  
...  

2016 ◽  
Vol 31 (1) ◽  
pp. 75-85
Author(s):  
Elizabeth D Cummins ◽  
Kristen K Leedy ◽  
John M Dose ◽  
Daniel J Peterson ◽  
Seth L Kirby ◽  
...  

This study analyzed the interaction of adolescent methylphenidate on the behavioral response to nicotine and the effects of these drug treatments on brain-derived neurotrophic factor in the nucleus accumbens and hippocampus in male and female Sprague-Dawley rats. Animals were intraperitoneal administered 1 mg/kg methylphenidate or saline using a “school day” regimen (five days on, two days off) beginning on postnatal day (P)28 and throughout behavioral testing. In Experiment 1, animals were intraperitoneal administered 0.5 mg/kg (free base) nicotine or saline every second day for 10 days from P45–P63 and tested after a three-day drug washout on the forced swim stress task on P67–P68. Results revealed that adolescent methylphenidate blunted nicotine behavioral sensitization. However, methylphenidate-treated rats given saline during sensitization demonstrated decreased latency to immobility and increased immobility time on the forced swim stress task in males that was reduced by nicotine. In Experiment 2, a different set of animals were conditioned to nicotine (0.6 mg/kg free base) or saline using the conditioned place preference behavioral paradigm from P44–P51, and given a preference test on P52. On P53, the nucleus accumbens and hippocampus were analyzed for brain-derived neurotrophic factor. Methylphenidate enhanced nicotine-conditioned place preference in females and nicotine produced conditioned place preference in males and females pre-exposed to saline in adolescence. In addition, methylphenidate and nicotine increased nucleus accumbens brain-derived neurotrophic factor in females and methylphenidate enhanced hippocampus brain-derived neurotrophic factor in males and females. Methylphenidate adolescent exposure using a clinically relevant dose and regimen results in changes in the behavioral and brain-derived neurotrophic factor responses to nicotine in adolescence that are sex-dependent.


2021 ◽  
Author(s):  
Jeffrey J. Moffat ◽  
Samuel A. Sakhai ◽  
Yann Ehinger ◽  
Khanhky Phamluong ◽  
Dorit Ron

AbstractBrain-derived neurotrophic factor (BDNF) signaling in the dorsolateral striatum (DLS) gates alcohol self-administration in rodents. The major source of BDNF in the striatum is the cortex, and we recently found that BDNF-expressing neurons in the ventrolateral orbitofrontal cortex (vlOFC) extend axonal projections to the DLS. We therefore hypothesized that BDNF in the vlOFC to DLS circuit moderates alcohol intake. We show that overexpression of BDNF in the vlOFC, which activates BDNF signaling in the DLS, is sufficient to attenuate voluntary consumption and seeking of 20% alcohol in the home cage using a two-bottle choice paradigm. Overexpressing BDNF in the vlOFC had no effect on the consumption of a sweetened saccharin solution. In addition, BDNF overexpression in the neighboring motor cortex did not alter alcohol intake. Finally, pathway-specific overexpression of BDNF in DLS-projecting vlOFC neurons significantly reduced alcohol intake and preference. Overall, BDNF in the vlOFC, and specifically in a vlOFC-DLS pathway, keeps alcohol drinking in moderation.


2013 ◽  
Vol 19 (5) ◽  
pp. 758-769 ◽  
Author(s):  
Jérôme Jeanblanc ◽  
Fabien Coune ◽  
Béatrice Botia ◽  
Mickaël Naassila

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