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Behavioral Neuroendocrinology |
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Emilio Dominguez-Salazar |
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Dept. of Biochemistry and Molec. Genetics 1229 Jordan Hall 1300 Jefferson Park Ave Charlottesville, VA 22908 Phone Number: 434-982-4742 Fax Number: 434-243-8433 Email: ed4n@virginia.edu Download my CV here. |
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Research Description: From my final year of high school until I finished my bachelors, I worked in the psychoneuroendocrinology laboratory of Javier Velazquez-Moctezuma (and for Maria L. Rueda for a year) at the Autonomous Metropolitan University (UAM) in Mexico City. During my early training at UAM, I worked with prenatal stress. We assessed the effect of different stressors on sexual behavior in adulthood and observed the dependence of the nature of the stressor on its effect on masculine sexual behavior. Also we gave evidence that acetylcholine facilitates the expression of male sexual behavior. I worked in the same lab during my first year of master studies. During the final year of my Masters and during my PhD, I worked in the laboratory of neuronal plasticity and behavior with Raul G. Paredes on kindling (master) and sexual differentiation (PhD) at the Neurobiology Institute, UNAM at Queretaro, Mexico. With
my Masters I demonstrated that
little electric brain stimulations (kindling) in the most important area
that regulates masculine sexual behaviour, the medial preoptica area, are
enough to increase the masculine behavioral patterns in female rats. In my PhD dissertation I had some interesting results. I worked with female and male rats perinatally treated with an anti-androgen (ATD) or with an inhibitor of aromatization (the conversion of androgen to estrogen) and described that the “feminine” behavior observed in males treated with the inhibitor of aromatization is only an increase of the lordosis reflex and is not a preference of male, this increase of lordosis was also observed in females. The olfactory preference of ATD treated males was blocked and I postulated that estrogens are important for sexual differentiation of the accessory olfactory pathway. The males perinatally treated with the ATD showed a decrease of male sexual behavior more than ATD-treated males and I postulated that the androgens, not only the estrogens, are important for the sexual differentiation of male, that is true also for females. Some of these results are not yet published. I
have been a postdoctoral fellow in Emilie’s laboratory as for a
year and have initiated a series of projects. A)
Conditioned Place Preference First
I modified the conditioned place preference paradigm I had used in rats to
use in male mice. I used this to test WT and dopamine receptor D5 knockout
males. Even though alll males are fertile and mate, we found that while
both intromission alone and those including ejaculations were rewarding
for WT males, the KO mice required ejaculation to form a place preference.
These data are interesting since the D5 had not been previously associated
with male sexual behavior. B)
Genetic Background Increases Sexual Behavior in ERaKO male
mice. We also
have intriguing results of crossing the ERaKO into strain of mice, other
than C57BL/6J. Differences between mouse strains in aspects of their
sexual behavior is well know, but no one had tried to cross the ERaKO into any strain other than C57. We found that crossing ERaKO into either BALB/c or DBA/2J produces a marked increase (from 0 to 40%)
in the number of ERaKO mice that perform complete sexual behavior including ejaculations.
This interesting result lead us to wonder about the hybrid mouse first
characterized by McGill in the 1960’s, the B6D2F1. C)
Masculine Sexual Behavior in B6D2F1 is Independent of Gonads. McGill showed that males produced by this cross (C57BL/6J moms and DBA/2J sires) were able to perform sexual behavior for up to two years after castration. The reciprocal cross does not have this ability. Lynn Clemens and his students conducted a few studies on this mouse in the 1980s and concluded that the testosterone concentration in plasma and the aromatase activity in their brains were reduced, but that the estrogen receptor binding and estradiol concentrations in plasma were not affected by castration. Based on these data and others we are examining the mechanisms underlying this behavior. First we are asking if the androgen receptor, perhaps activated by another ligand, is essential for the continued behavior after castration. We are repeating the original McGill effect and then treated males with flutamide (antagonist of androgen receptor). Flutaminde treated animals are slower but are able to show ejaculatory behavior. We also are also evaluating the role of estrogen receptor and dopamine in this behavior. This behavior is only present in the hybrids from dad DBA, then it is possible that Y chromosome is involved. We are reducing the genetic background from DBA mice crossing the original hybrid with C57 females. We have now the 7th generation that is 98% C57, the Y chromosome is practically from the DBA strain. If this generation presents behavior after gonadectomy, we could explain that sexual behavior without gonads is an interaction between a gene from C57 mom and a gene from Y chromosome of DBA sire.
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