دانلود مقاله ISI انگلیسی شماره 37048
ترجمه فارسی عنوان مقاله

استروئید آنابولیک آندروژنی مجموعه تغییر و آموزش معکوس در موش صحرایی نر را با اختلال مواجه می کند

عنوان انگلیسی
Anabolic–androgenic steroids impair set-shifting and reversal learning in male rats
کد مقاله سال انتشار تعداد صفحات مقاله انگلیسی
37048 2015 8 صفحه PDF
منبع

Publisher : Elsevier - Science Direct (الزویر - ساینس دایرکت)

Journal : European Neuropsychopharmacology, Volume 25, Issue 4, April 2015, Pages 583–590

ترجمه کلمات کلیدی
عوامل آنابولیک - شناخت - رفتار فعالیت کننده - پاداش غذایی - تستوسترون
کلمات کلیدی انگلیسی
Anabolic agents; Cognition; Operant behavior; Food reward; Testosterone
پیش نمایش مقاله
پیش نمایش مقاله  استروئید آنابولیک آندروژنی مجموعه تغییر و آموزش معکوس در موش صحرایی نر را با اختلال مواجه می کند

چکیده انگلیسی

Anabolic–androgenic steroid (AAS) abuse is prevalent not only among elite athletes, but is increasingly common in high school and collegiate sports. AAS are implicated in maladaptive behaviors such as increased aggression and risk taking, which may result from impaired cognition. Because they affect dopamine function in prefrontal cortical (PFC)-striatal circuitry, AAS may disrupt PFC-dependent processes such as behavioral flexibility. This was the focus of the present study. Adolescent male Long-Evans rats were treated chronically with high-dose testosterone (7.5 mg/kg in water with 13% cyclodextrin) or vehicle sc, and tested for set-shifting and reversal-learning. For set-shifting, rats were trained on a visual cue task (VCT), then were shifted to a direction cue task (DCT), or vice-versa. For reversal learning, rats were first trained on VCT and were then required to press the opposite lever. 2-cue set-shifting introduced a novel paradigm in which rats shifted from a 1-Light Visual Task (1LVT) to a tone cue task (TCT). Testosterone-treated rats were significantly impaired on the set-shift from DCT to VCT compared to vehicle-treated controls (trials to criterion: vehicle 240.9±29.9, testosterone 388.3±59.3, p<0.05). However, on the set-shift from VCT to DCT, testosterone did not affect performance. During reversal-learning, testosterone significantly increased trials to criterion (vehicle: 495.9±91.8 trials, testosterone: 793.7±96.7 trials, p<0.05). In 2-cue set-shifting, testosterone diminished performance and the difference showed borderline significance (vehicle: 443.2±84.4 trials, testosterone: 800.4±178.2 trials, p=0.09). Our results show that testosterone impairs behavioral flexibility and have implications for understanding cognitive and behavioral changes in human AAS users.

مقدمه انگلیسی

Anabolic–androgenic steroids (AAS) are drugs of abuse used to increase muscle mass and enhance athletic performance. Once restricted to elite athletes, AAS abuse is now present in high school and college athletics. In fact, 4–6% of high school males admit using AAS (Yesalis and Bahrke, 2005). Health risks of AAS include cardiovascular, hepatic and reproductive dysfunction (Pope et al., 2013). AAS may also cause maladaptive behavioral changes, including increased impulsivity and aggression (Wood et al., 2013). Recent human studies further suggest that AAS induce cognitive impairments. AAS users exhibited diminished visuospatial memory compared to non-users, and the level of impairment was correlated with lifetime AAS use (Kanayama et al., 2012). However, little is known about the effects of AAS on other aspects of cognition, including behavioral flexibility. Behavioral flexibility allows appropriate adaptations in dynamic environments. The present study determined if AAS impair behavioral flexibility. AAS have been implicated in changes to dopamine function in the prefrontal cortical–striatal circuitry on which behavioral flexibility depends (Wood et al., 2013 and Kurling-Kailanto et al., 2010). In particular, because prefrontal cortex (PFC) circuitry is still developing during adolescence (Blakemore and Choudhury, 2006), it is important to understand how adolescent steroid use may impair behavioral flexibility and its underlying neurobiological mechanisms.