Membrane androgen receptors may mediate androgen reinforcement

Sato, Satoru M.; Johansen, Jamie A.; Jordan, Cynthia L.; Wood, Ruth I.

doi:10.1016/j.psyneuen.2010.01.007

Cited by 36 publications

(31 citation statements)

References 67 publications

(114 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In adult male Tfm rats, which express a defective androgen receptor and therefore have greatly reduced sensitivity to testosterone in peripheral tissues, the effects of DHT and hydroxyflutamide on CA1 dendritic spine synapse density are indistinguishable from those observed in wild-type normal males (MacLusky and others 2006a). That the mutated androgen receptor found in Tfm rats remains capable of supporting some central androgen responses has also been demonstrated with respect to reinforcement behavior induced by anabolic-androgens (Sato and others 2010). …”

Section: Mechanisms Of Androgen Actionmentioning

confidence: 88%

Androgen Modulation of Hippocampal Structure and Function

et al. 2014

View full text Add to dashboard Cite

Androgens have profound effects on hippocampal structure and function, including induction of spines and spine synapses on the dendrites of CA1 pyramidal neurons, as well as alterations in long-term synaptic plasticity (LTP) and hippocampally dependent cognitive behaviors. How these effects occur remains largely unknown. Emerging evidence, however, suggests that one of the key elements in the response mechanism may be modulation of brain-derived neurotrophic factor (BDNF) in the mossy fiber (MF) system. In male rats, orchidectomy increases synaptic transmission and excitability in the MF pathway. Testosterone reverses these effects, suggesting that testosterone exerts tonic suppression on MF BDNF levels. These findings suggest that changes in hippocampal function resulting from declining androgen levels may reflect the outcome of responses mediated through normally balanced, but opposing, mechanisms: loss of androgen effects on the hippocampal circuitry may be compensated, at least in part, by an increase in BDNF-dependent MF plasticity.

show abstract

Section: Mechanisms Of Androgen Actionmentioning

confidence: 88%

Androgen Modulation of Hippocampal Structure and Function

et al. 2014

View full text Add to dashboard Cite

show abstract

“…However, gonadal hormones can modulate behavior without binding classical receptors. For instance, the reinforcing effects of AAS do not require classical androgen receptors (Sato et al 2010). Furthermore, some behavioral effects of androgens occur too quickly to be mediated by gene transcription, suggesting AAS may act on non-genomic receptors in Acb (Foradori et al 2008).…”

Section: Discussionmentioning

confidence: 99%

Anabolic-androgenic steroids decrease dendritic spine density in the nucleus accumbens of male rats

Wallin-Miller

Kelishani

et al. 2016

Neuroscience

Self Cite

View full text Add to dashboard Cite

Recent studies have demonstrated that anabolic-androgenic steroids (AAS) modify cognitive processes such as decision making and behavioral flexibility. However, the neural mechanisms underlying these AAS-induced cognitive changes remain poorly understood. The mesocorticolimbic dopamine (DA) system, particularly the nucleus accumbens (Acb), is important for reward, motivated behavior, and higher cognitive processes such as decision making. Therefore, AAS-induced plasticity in the DA system is a potential structural substrate for the observed cognitive alterations. High doses of testosterone (the most commonly-used AAS) increase dendritic spine density in limbic regions including the amygdala and hippocampus. However, effects on Acb are unknown. This was the focus of the present study. Adolescent male Long-Evans rats were treated chronically for 8 weeks with high-dose testosterone (7.5 mg/kg in water with 13% cyclodextrin) or vehicle sc. Brains were stained by Golgi-Cox to analyze neuronal morphology in medium spiny neurons of the shell region of Acb (AcbSh). 8 weeks of testosterone treatment significantly decreased spine density in AcbSh compared to brains of vehicle-treated rats (F1,14 = 5.455, p<0.05). Testosterone did not significantly affect total spine number, dendritic length, or arborization measured by Sholl analysis. These results show that AAS alter neuronal morphology in AcbSh by decreasing spine density throughout the dendritic tree, and provides a potential mechanism for AAS to modify cognition and decision-making behavior.

show abstract

“…Although testosterone is classically thought to act over a relatively slow time-course (days to weeks), the rewarding effects of high-dose androgens can be rapid (minutes to hours) and do not require classical genomic androgen receptors (Sato et al, 2010). In this regard, brain circuits for reward and executive function, including the ventral striatum and frontal cortex, have relatively few androgen receptors.…”

Section: Discussionmentioning

confidence: 99%

Testosterone enhances risk tolerance without altering motor impulsivity in male rats

Cooper

Goings

Kim

et al. 2014

Psychoneuroendocrinology

Self Cite

View full text Add to dashboard Cite

Summary Anabolic-androgenic steroids (AAS) increase impulsive and uncontrolled aggressive (‘roid rage) in humans and enhance agonistic behavior in animals. However, the underlying mechanisms for AAS-induced aggression remain unclear. Potential contributing elements include an increase risk-taking and/or motor impulsivity due to AAS. This study addressed the effects of chronic high-dose testosterone on risk tolerance using a risky decision-making task (RDT) and motor impulsivity with a go/no-go task in operant chambers. Male Long-Evans rats were treated for at least 4 weeks with testosterone (7.5mg/kg) or vehicle beginning in late adolescence. Testosterone was used because it is popular among human AAS users. In RDT testing, one lever was paired with delivery of a small “safe” food reward, while the other was paired with a large “risky” reward associated with an increasing risk of footshock (0, 25, 50, 75, 100%) in successive test blocks. Three shock intensities were used: 1.0, 1.2, and 1.4 mA/kg. As shock intensity and risk of shock increased, preference for the lever signifying a large reward significantly declined for both vehicle- and testosterone-treated rats (p<0.05). There was also a significant effect of drug (p<0.05), where testosterone-treated rats showed greater preference for the large reward, compared to vehicle- treated controls. Increased preference for the large reward, despite risk of footshock, is consistent with increased risk tolerance. In go/no-go testing, rats were trained to press a single lever if the go cue was presented (stimulus light) or to refrain from pressing during the no-go cue (tone). There was no effect of testosterone on pre-cue responses, or performance in go and no-go trials. These results suggest that AAS may increase risk-tolerance without altering motor impulsivity.

show abstract

Membrane androgen receptors may mediate androgen reinforcement

Cited by 36 publications

References 67 publications

Androgen Modulation of Hippocampal Structure and Function

Androgen Modulation of Hippocampal Structure and Function

Anabolic-androgenic steroids decrease dendritic spine density in the nucleus accumbens of male rats

Testosterone enhances risk tolerance without altering motor impulsivity in male rats

Contact Info

Product

Resources

About