Interaction of naltrexone with postnatal administration of testosterone and estrogen on neurobehavioral sexual differentiation in rats

McGivern, Robert F.

doi:10.1016/0018-506x(90)90024-r

Cited by 10 publications

(2 citation statements)

References 52 publications

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“…However, in our previous study, that EE 2 treatment also decreased postweaning and adult body weights of both sexes, effects not seen here. Saccharin-flavored intake was not altered in either sex, a finding similar to that reported by McGivern and Henschel (1990) for adult male and female rats treated with estradiol benzoate on PNDs 2 and 3. The relatively few significant alterations in EE 2 -treated males suggests that they may be less sensitive to developmental EE 2 treatment than females, a hypothesis that has been presented by Ryan et al (Howdeshell et al, 2008;Ryan et al, 2010 and see Figure 11 in Ryan et al, 2010).…”

Section: Fig 5 (A)supporting

confidence: 87%

Developmental Treatment with Ethinyl Estradiol, but Not Bisphenol A, Causes Alterations in Sexually Dimorphic Behaviors in Male and Female Sprague Dawley Rats

Ferguson

Law

Kissling

2014

Toxicological Sciences

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The developing central nervous system may be particularly sensitive to bisphenol A (BPA)-induced alterations. Here, pregnant Sprague Dawley rats (n = 11-12/group) were gavaged daily with vehicle, 2.5 or 25.0 μg/kg BPA, or 5.0 or 10.0 μg/kg ethinyl estradiol (EE2) on gestational days 6-21. The BPA doses were selected to be below the no-observed-adverse-effect level (NOAEL) of 5 mg/kg/day. On postnatal days 1-21, all offspring/litter were orally treated with the same dose. A naïve control group was not gavaged. Body weight, pubertal age, estrous cyclicity, and adult serum hormone levels were measured. Adolescent play, running wheel activity, flavored solution intake, female sex behavior, and manually elicited lordosis were assessed. No significant differences existed between the vehicle and naïve control groups. Vehicle controls exhibited significant sexual dimorphism for most behaviors, indicating these evaluations were sensitive to sex differences. However, only EE2 treatment caused significant effects. Relative to female controls, EE2-treated females were heavier, exhibited delayed vaginal opening, aberrant estrous cyclicity, increased play behavior, decreased running wheel activity, and increased aggression toward the stimulus male during sexual behavior assessments. Relative to male controls, EE2-treated males were older at testes descent and preputial separation and had lower testosterone levels. These results suggest EE2-induced masculinization/defeminization of females and are consistent with increased volume of the sexually dimorphic nucleus of the preoptic area (SDN-POA) at weaning in female siblings of these subjects (He, Z., Paule, M. G. and Ferguson, S. A. (2012) Low oral doses of bisphenol A increase volume of the sexually dimorphic nucleus of the preoptic area in male, but not female, rats at postnatal day 21. Neurotoxicol. Teratol. 34, 331-337). Although EE2 treatment caused pubertal delays and decreased testosterone levels in males, their behaviors were within the range of control males. Conversely, BPA treatment did not alter any measured endpoint. Similar to our previous reports (Ferguson, S. A., Law, C. D. Jr and Abshire, J. S. (2011) Developmental treatment with bisphenol A or ethinyl estradiol causes few alterations on early preweaning measures. Toxicol. Sci. 124, 149-160; Ferguson, S. A., Law, C. D. and Abshire, J. S. (2012) Developmental treatment with bisphenol A causes few alterations on measures of postweaning activity and learning. Neurotoxicol. Teratol. 34, 598-606), the BPA doses and design used here produced few alterations.

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Section: Fig 5 (A)supporting

confidence: 87%

Developmental Treatment with Ethinyl Estradiol, but Not Bisphenol A, Causes Alterations in Sexually Dimorphic Behaviors in Male and Female Sprague Dawley Rats

Ferguson

Law

Kissling

2014

Toxicological Sciences

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“…Opioid signaling pathways involve the following: (a) inhibition of the adenylate cyclase enzyme (13), (b) inactivation of voltage-dependent calcium channels (14,15), (c) activation of potassium channels (16), (d) mobilization of intracellular Ca 2+ reserves through the activation of phospholipase Cβ (17,18) and (e) stimulation of MAP kinase pathways (19). The most well-known physiological effect associated with EOPs is their efficacy in pain reduction or analgesia, although their effect on a variety of other physiological functions has become apparent in recent years (20).…”

mentioning

confidence: 99%