The possible role of 2-hydroxyestradiol in the development of estrogen-induced striatal dopamine receptor hypersensitivity

Clopton, J. Kirk; Gordon, John H.

doi:10.1016/0006-8993(85)90117-9

Cited by 47 publications

(19 citation statements)

References 48 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…These findings may be mediated by the metabolite 2-hydroxyestradiol. Administration of 2-hydroxyestradiol has been shown to increase dopamine 2-type receptor binding capacity in the striatum in OVX rats, a result consistent with an increase in receptor number (Clopton and Gordon 1985; but see also Fernandez-Ruiz et al 1987). An increase in the number of pre-synaptic dopamine 2-type receptors (the autoreceptor) would likely decrease dopamine efflux, such as is reported here.…”

Section: Discussion-studymentioning

confidence: 75%

“…Others have shown that 2-hydroxyestradiol and estradiol can have opposing effects on behavior mediated by dopamine in female rats, with 2-hydroxyestradiol stimulating the behavior and estradiol reducing it. Furthermore, the behavioral effects of 2-hydroxyestradiol may be mediated by changes in dopamine 2-type receptors that have been shown to occur even 72 hours after the last injection (Clopton and Gordon 1985). This supports the idea that 2-hydroxyestradiol can induce delayed changes in dopamine signaling, which are particularly impressive given its short half-life.…”

Section: Discussion-studymentioning

confidence: 99%

See 1 more Smart Citation

2-Hydroxyestradiol enhances binge onset in female rats and reduces prefrontal cortical dopamine in male rats

Babbs

Unger

Corwin

2013

Hormones and Behavior

View full text Add to dashboard Cite

Women are more likely to suffer from a bingeing-related eating disorder, which is surprising, since estradiol reduces meal size and is associated with reduced binge frequency. This apparent contradiction may involve the estradiol metabolite, 2-hydroxyestradiol. We previously reported that female rats had faster escalations in shortening intake during the development of bingeing than did males, but acute administration of 2-hydroxyestradiol increased the intake of vegetable shortening to a greater extent in male rats once bingeing was established. Here, we report two separate studies that follow up these previous findings. In the first, we hypothesized that chronic exposure to 2-hydroxyestradiol would promote escalation of bingeing during binge development in ovariectomized female rats. In the second, we hypothesized that acute exposure to 2-hydroxyestradiol would enhance dopamine signaling in the prefrontal cortex after bingeing was established in male rats. In study 1, non-food-deprived female rats were separated into 3 groups: ovariectomized (OVX) with chronic 2-hydroxyestradiol supplementation (E), OVX with vehicle supplementation (O), and intact with vehicle (I). Each group was given access to an optional source of dietary fat (shortening) on Mon, Wed, and Fri for four weeks. 2-hydroxyestradiol supplementation prevented OVX-induced weight gain and enhanced escalation of shortening intake over the four-week period (ps < 0.05). Additionally, in week 4, rats in the E group ate significantly more shortening than I controls, less chow than either the O or I group, and had a higher shortening to chow ratio than O or I (ps < 0.05). Study 2 indicated that acute injection of 2-hydroxyestradiol abolished shortening-evoked dopamine efflux in the prefrontal cortex of bingeing male rats (p < 0.05). Together, these studies indicate that 2-hydroxyestradiol can exacerbate bingeing as it develops and can suppress dopamine signaling in the prefrontal cortex once bingeing is established.

show abstract

Section: Discussion-studymentioning

confidence: 75%

Section: Discussion-studymentioning

confidence: 99%

2-Hydroxyestradiol enhances binge onset in female rats and reduces prefrontal cortical dopamine in male rats

Babbs

Unger

Corwin

2013

Hormones and Behavior

View full text Add to dashboard Cite

show abstract

“…However, this literature is complex for three main reasons. First, reports on the direction of these effects diverge, a fact attributed to a number of factors, including within-studies differences in hormone levels (Becker, 1990; Clopton and Gordon, 1985), selected striatal sub-regions (Bazzett and Becker, 1994), behavioral contexts (Davis et al, 2005; Galea et al, 2001), and gender (e.g., Becker, 1990; Yoest et al, 2014). For example, estradiol in the striatum is able to acutely enhance DA signaling in females but not males.…”

Section: Effects Of Sex Hormonesmentioning

confidence: 99%

Striatum on the anxiety map: Small detours into adolescence

et al. 2017

View full text Add to dashboard Cite

Adolescence is the most sensitive period for the development of pathological anxiety. Moreover, specific neural changes associated with the striatum might be related to adolescent vulnerability to anxiety. Up to now, the study of anxiety has primarily focused on the amygdala, bed nucleus of the stria terminalis (BNST), hippocampus and ventromedial prefrontal cortex (vmPFC), while the striatum has typically not been considered as part of the anxiety system. This review proposes the addition of the striatum, a complex, multi-component structure, to the anxiety network by underscoring two lines of research. First, the co-occurrence of the adolescent striatal development with the peak vulnerability of adolescents to anxiety disorders might potentially reflect a causal relationship. Second, the recognition of the role of the striatum in fundamental behavioral processes that do affect anxiety supports the putative importance of the striatum in anxiety. These behavioral processes include (1) attention, (2) conditioning/prediction error, and (3) motivation. This review proposes a simplistic schematic representation of the anxiety circuitry that includes the striatum, and aims to promote further work in this direction, as the role of the striatum in shaping an anxiety phenotype during adolescence could have critical implications for understanding and preventing the peak onset of anxiety disorders during this period.

show abstract

“…However, the presence of E2, as well as PRL derivatives within the CNS might support hyper-PRL effects on VIP binding sites (Clapp et al, 1989;Weisz and Crowley, 1986). On the one hand, estrogen-%-hydroxylase, which converts E2 in its derivatives, has been demonstrated in the CNS (Weisz and Crowley, 1986) and influenced the effect of E2 on dopamine receptor hypersensitivity in the striatum (Clopton and Gordon, 1985). Thus, it cannot be excluded that the effects observed here depend on such E2 derivatives.…”

mentioning

confidence: 83%