Neal G Simon
Biographic Data
| ID | 5222874 |
|---|---|
| NAME | Neal G Simon |
| GIVEN NAMES | Neal G |
| FAMILY NAME | Simon |
| SIGNATURE | SIMON N G |
| AFFILIATIONS | Lehigh University |
| VERIFIED | No |
| TOTAL WORKS | 6 |
| TOTAL CITATIONS | 1 |
| AUTHOR COUNT | 6 |
| EDITOR COUNT | 0 |
| FIRST PUBLICATION YEAR | 1983 |
| LATEST PUBLICATION YEAR | 2001 |
| H-INDEX | 1 |
Prenatal testosterone treatment potentiates the aggression‐inhibiting effect of the neurosteroid dehydroepiandrosterone in female mice
The neurosteroid dehydroepiandrosterone (DHEA) is a powerful inhibitor of aggression in murine models when given for 15 days and potentially may be useful in the management of inappropriate human aggression. Although the biosynthesis and metabolism of DHEA have been described, little is known about the potential effect of the steroidal environment during sexual differentiation on the subsequent response to DHEA. Whether prenatal androgen exposure…
XIII World Meeting, International Society for Research on Aggression
Three research programs on the genetics of aggression in mice and one on that for humans concerned with effects of the 5-HT system, especially receptor subtypes, on aggression are presented in this symposium. For mice, inbred strains (Simon), transgenic strains (Hilakivi-Clarke), and knock-out strains (Brunner) have been used in studies of the offense type of aggression. Simon has shown that there is between strain polymorphism for steroid activa…
Activation of intermale aggression by combined estrogen-androgen treatment
Adult CD-1 male mice were gonadectomized and tested for their response to the aggression-promoting property of androgens, estrogens, or combined androgen-estrogen treatment. The results showed that the combined treatment was the most effective, although androgens alone were sufficient for behavioral restoration. These findings suggest that testosterone may activate aggression through both its androgenic and estrogenic metabolites.
Hormonal regulation of aggression: Evidence for a relationship among genotype, receptor binding, and behavioral sensitivity to androgen and estrogen
Gonadectomized male mice from the CF-1, CFW, and CD-1 strains were exposed to different androgens (testosterone, dihydrotestosterone, methyltrienolone) or estrogens (estradiol, diethylstilbestrol) and tested for aggressive behavior. Genetic differences in sensitivity to the aggression-promoting property of the various treatments were found. CF-1 mice responded to either androgenic or estrogenic stimulation, CFW males were most sensitive to the es…
On the expression of H-Y antigen in transsexuals
An empirically derived scoring system for intermale aggression in mice
Scoring systems used to assess intermale aggression have been characterized by arbitrary scales and wide variability in the behaviors selected for measurement. The use of such different systems severely limits the ability of investigators to make meaningful comparisons among studies and indicates that there is a need for a common, statistically derived evaluative system for intermale aggression. We measured the frequency and duration of five majo…
An empirically derived scoring system for intermale aggression in mice
Scoring systems used to assess intermale aggression have been characterized by arbitrary scales and wide variability in the behaviors selected for measurement. The use of such different systems severely limits the ability of investigators to make meaningful comparisons among studies and indicates that there is a need for a common, statistically derived evaluative system for intermale aggression. We measured the frequency and duration of five majo…
Hormonal regulation of aggression: Evidence for a relationship among genotype, receptor binding, and behavioral sensitivity to androgen and estrogen
Gonadectomized male mice from the CF-1, CFW, and CD-1 strains were exposed to different androgens (testosterone, dihydrotestosterone, methyltrienolone) or estrogens (estradiol, diethylstilbestrol) and tested for aggressive behavior. Genetic differences in sensitivity to the aggression-promoting property of the various treatments were found. CF-1 mice responded to either androgenic or estrogenic stimulation, CFW males were most sensitive to the es…
On the expression of H-Y antigen in transsexuals
Activation of intermale aggression by combined estrogen-androgen treatment
Adult CD-1 male mice were gonadectomized and tested for their response to the aggression-promoting property of androgens, estrogens, or combined androgen-estrogen treatment. The results showed that the combined treatment was the most effective, although androgens alone were sufficient for behavioral restoration. These findings suggest that testosterone may activate aggression through both its androgenic and estrogenic metabolites.
XIII World Meeting, International Society for Research on Aggression
Three research programs on the genetics of aggression in mice and one on that for humans concerned with effects of the 5-HT system, especially receptor subtypes, on aggression are presented in this symposium. For mice, inbred strains (Simon), transgenic strains (Hilakivi-Clarke), and knock-out strains (Brunner) have been used in studies of the offense type of aggression. Simon has shown that there is between strain polymorphism for steroid activa…
Prenatal testosterone treatment potentiates the aggression‐inhibiting effect of the neurosteroid dehydroepiandrosterone in female mice
The neurosteroid dehydroepiandrosterone (DHEA) is a powerful inhibitor of aggression in murine models when given for 15 days and potentially may be useful in the management of inappropriate human aggression. Although the biosynthesis and metabolism of DHEA have been described, little is known about the potential effect of the steroidal environment during sexual differentiation on the subsequent response to DHEA. Whether prenatal androgen exposure…
Psychology (6 works) · Aggression (5 works) · Developmental psychology (4 works) · Medicine (4 works) · Androgen (3 works) · Biology (3 works) · Endocrinology (3 works) · Hormone (3 works) · Internal Medicine (3 works) · Stress Responses and Cortisol (3 works)