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Dive into the research topics where O. Byron Ward is active.

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Featured researches published by O. Byron Ward.


Hormones and Behavior | 2003

Fetal testosterone surge: Specific modulations induced in male rats by maternal stress and/or alcohol consumption

Ingeborg L. Ward; O. Byron Ward; John D Affuso; William Long; Jeffrey A. French; Shelton E. Hendricks

Plasma testosterone (T) was measured in control male and female rats on gestational days 16, 17, 18, 19, and 20 and on days 17-20 in males from dams who were fed ethanol and/or were stressed during pregnancy. Circulating T in control males showed an earlier rise, yielding a longer period of prenatal T elevation, than was reported previously (Endocrinology 106 (1980)306). Compared to control males, exposure to alcohol-alone augmented T on days 18 and 19, stress-alone attenuated prenatal T, and the combination of stress and alcohol completely blocked the normal rise in T between days 17 and 18. When these prenatal alterations in T are viewed along with effects these same treatments have on the postparturient T surge (Horm. Behav. 41 (2002) 229), a possible explanatory mechanism emerges for the uniquely different behavioral patterns of sexual behavior differentiation induced in males by prenatal exposure to alcohol, stress, or both factors. Whereas the potential for feminine behavior is retained to the extent that either the prenatal or the neonatal T surge is attenuated, the male potential is more sensitive to reductions in the fetal surge and is maximally disrupted if both the prenatal and the postparturitional T surges are suppressed.


Pharmacology, Biochemistry and Behavior | 1986

Naltrexone blocks the effects of prenatal stress on sexual behavior differentiation in male rats

O. Byron Ward; Edward P. Monaghan; Ingeborg L. Ward

The male offspring of rats stressed three times daily during days 14-21 of pregnancy were more likely to show lordotic behavior when tested in adulthood than were control males. This feminization of sexual behavior was not observed if the mothers were injected with the opioid antagonist naltrexone before being stressed. These data suggest that endogenous opioids released under conditions of stress can alter the normal process of sexual behavior differentiation in the fetal male rat.


Physiology & Behavior | 1973

From dud to stud: copulatory behavior elicited through conditioned arousal in sexually inactive male rats.

William R. Crowley; Herbert B. Popolow; O. Byron Ward

Abstract Sexually inactive male rats were conditioned to associate tones with electric shock to the flanks. In subsequent tests, when only tones were presented in the presence of an estrous female, these males began to copulate, pacing their behavior to the tone presentations. Only one animal tested for sexual behavior without the tones mated. It is suggested that the momentary augmentation of nonspecific arousal can lead to the initiation and subsequent pacing of mating responses in noncopulators.


Hormones and Behavior | 2002

Postparturitional Testosterone Surge in Male Offspring of Rats Stressed and/or Fed Ethanol during Late Pregnancy

O. Byron Ward; Ingeborg L. Ward; John H. Denning; Jeffrey A. French; Shelton E. Hendricks

Male offspring of rats exposed to restraint stress and/or alcohol during late pregnancy show aberrant patterns of sexual behavior masculinization and defeminization that vary as a function of treatment. The impact of these treatments on the postparturitional testosterone (T) surge that contributes to sexual behavior differentiation was investigated. Plasma T was measured using radioimmunoassay in individual males sampled on day 21 of gestation within 10 min of cesarean delivery or 1, 2, or 4 h thereafter. Neonatal T in the group exposed only to stress did not differ from that in the control group. T was lower than control levels at birth in both alcohol groups. The magnitude of the T surge that occurred during the first hour of birth in the control group was diminished by 50% in both alcohol groups, whose T pattern was very similar. There was no common alteration in postparturitional T associated with the increased lordotic behavior potential that males in all three treatment groups typically share, nor were there idiosyncratic endocrine abnormalities linked to the very different male copulatory pattern each exhibits. Exposure to an abnormal T milieu during fetal as well as neonatal ontogeny may underlie the etiology of the different sexual behavior patterns exhibited by males exposed to stress and/or alcohol. Possible unique effects each treatment exerts on perinatal plasma T and its aromatization to estradiol in hypothalamic targets are discussed.


Brain Research | 1995

Sexually dimorphic areas in the rat medial amygdala: resistance to the demasculinizing effect of prenatal stress.

Michael Kerchner; Charles W. Malsbury; O. Byron Ward; Ingeborg L. Ward

Exposure to prenatal stress blocks full masculinization of several sexually dimorphic nuclei in the brain and spinal cord of male rats. We now compare the adult volume of the medical amygdala (MA) and two of its component cell groups, posterodorsal (MePD) and posteroventral (MePV), in prenatally stressed male rats and nonstressed males and females. Previous reports of sex differences (male > female) in the overall size of the MA and the MePD component were confirmed, and we identified a previously unreported sex difference (male > female) in MePV. Prenatal stress had no effect on the size of the total MA, or of the MePD or MePV in males. Maternal stress attenuates the surge in plasma testosterone (T) which normally occurs on days 18 and 19 of gestation in male rats. This brief suppression of T during prenatal development leads to incomplete masculinization of some sexually dimorphic features of the CNS (i.e. the SDN-MPOA of the hypothalamus, and SNB and DLN of the spinal cord) but not others (i.e. the MA, MePD, and MePV). The selective effects of prenatal stress on neural differentiation may be due to differences in the onset and duration of the periods when each of these structures in most sensitive to T and/or its metabolites.


Behavioral Neuroscience | 1992

Prenatal beta-endorphin can modulate some aspects of sexual differentiation in rats.

Michael L. Kashon; O. Byron Ward; William Grisham; Ingeborg L. Ward

Sexually dimorphic traits were studied in offspring of rats injected with 33 micrograms rat beta-endorphin (beta-END) three times daily from Day 14 to Day 21 of pregnancy. beta-END males had shorter neonatal anogenital distances than did controls and were more likely to show the female lordosis pattern as adults, but they did not differ in male copulatory behavior. When given a choice between spending time with an estrous female or a male, beta-END males showed a lower preference for the female than did control males. The number and somal size of neurons in the bulbocavernosus and dorsolateral nucleus of the lumbar spinal cord were unaffected by drug exposure. Elevated beta-END during fetal ontogeny apparently alters the differentiation of some, but not all, sexually dimorphic traits. The data suggest that endogenous opioids may contribute to the etiology of the prenatal stress syndrome.


Behavioral Neuroscience | 1996

Prenatal Alcohol and Stress Interact to Attenuate Ejaculatory Behavior, but Not Serum Testosterone or LH in Adult Male Rats

Ingeborg L. Ward; O. Byron Ward; Daniel Mehan; Robert J. Winn; Jeffrey A. French; Shelton E. Hendricks

Restraint stress reduced blood alcohol levels in pregnant rats given a liquid alcohol diet. The male offspring prenatally exposed to both stress and alcohol failed to ejaculate spontaneously, although they copulated normally following exogenous testosterone (T) administration. Males prenatally exposed only to alcohol or only to stress showed no behavioral deficits. Adult serum T and luteinizing hormone levels were normal in both of the fetal alcohol exposed male groups. It appears that the androgen threshold for ejaculatory behavior is elevated in males prenatally exposed to alcohol plus stress and cannot be realized with normal testosterone titers, but it can be attained with exogenous hormone administration. Presumably the alcohol and stress combination interfered with ontogenetic patterns of T needed to fully masculinize the fetal nervous system.


Archives of Sexual Behavior | 2002

Hormonal mechanisms underlying aberrant sexual differentiation in male rats prenatally exposed to alcohol, stress, or both

O. Byron Ward; Ingeborg L. Ward; John H. Denning; Shelton E. Hendricks; Jeffrey A. French

The male offspring of rats exposed to restraint stress, alcohol, or both during late pregnancy show normally masculinized genitalia; however, sexual differentiation of behavior is dissociated from the external morphology. In contrast to controls, males exposed prenatally to stress, alcohol, or a combination of these factors exhibited the female lordotic pattern. Thus, all 3 prenatal treatments led to incomplete behavioral defeminization. Behavioral masculinization was not altered by fetal alcohol exposure alone, but a significant number of males that experienced prenatal stress alone failed to copulate. A more severe disruption of behavioral masculinization occurred when stress and alcohol were combined. Very few males exposed to the combination treatment mated with females. This study attempted to relate the effects of these treatments on sexual behavior to the postparturitional surge in plasma testosterone (T) that is known to influence the process of sexual differentiation. Prenatally stressed males, like control males showed a large, brief surge in plasma T that peaked 1 hr after delivery. Altered defeminization and masculinization were seen in prenatally stressed males, despite a normal postparturitional T surge. Fetal alcohol exposure, with or without concomitant stress, depressed T to the same extent right after birth and led to a similarly blunted T surge 1 hr later. Thus, equal disruption of the neonatal T pattern occurred in alcohol-alone males, who showed normal male copulatory behavior, and in alcohol-plus-stress males, whose behavior was severely attenuated. The results suggest that consideration of abnormal exposure to T during prenatal ontogeny may be required to understand the atypical sexual behaviors associated with these treatments.


Hormones and Behavior | 1999

Androgen Threshold to Activate Copulation Differs in Male Rats Prenatally Exposed to Alcohol, Stress, or Both Factors

Ingeborg L. Ward; Amy L. Bennett; O. Byron Ward; Shelton E. Hendricks; Jeffrey A. French

Few male rats prenatally exposed to a combination of alcohol and stress copulate spontaneously. This study determined adult sensitivity to testosterone (T) in males prenatally exposed to alcohol, to stress, or to both factors. Sexually naive males were tested with receptive females following castration and implantation of 20-, 30-, or 45-mm Silastic T-filled capsules. Serum T levels provided by these implants were measured. The behavior shown by males exposed only to prenatal alcohol did not differ from untreated control animals at any T dosage. Prenatal stress alone diminished the copulatory potential below control levels only when the intermediate T dosage was provided. Few males exposed to both alcohol and stress copulated under the lowest or the intermediate dose of adult T replacement, but most ejaculated normally when the largest capsule was implanted. The threshold to the sexual behavior-activating-properties of adult T exposure was moderately raised by prenatal stress but was severely affected when prenatal stress was combined with alcohol. We conclude that a diminished sensitivity to androgen in adulthood underlies some copulatory deficits resulting from treatments that alter fetal T levels. Such deficits may be concealed when behavior is evaluated in gonadally intact animals.


Hormones and Behavior | 1996

Critical Periods of Sensitivity of Sexually Dimorphic Spinal Nuclei to Prenatal Testosterone Exposure in Female Rats

O. Byron Ward; Ann M. Wexler; Joseph R. Carlucci; Mark A. Eckert; Ingeborg L. Ward

Male rats normally have more neurons than do females in two nuclei of the lumbar spinal cord, the spinal nucleus of the bulbocavernosus (SNB) and the dorsolateral nucleus (DLN). Female rats exposed to testosterone propionate (TP) on the 2 days of gestation (Days 18 and 19) when males normally experience a surge in plasma testosterone showed a maximal increase in both SNB and DLN neuronal number. TP exposure just prior to, or following, Days 18 and 19 led to smaller increments. Administration of a small (5 microg) dose of TP after birth, while having no effect by itself, synergized with prenatal TP to enhance the number of SNB neurons. DLN neurons were less responsive to postnatal TP. The somal and nuclear size of SNB, but not DLN, neurons was increased by perinatal TP. Paradoxically, the number of DLN neurons with large somas (1358 microm2 or larger) was reduced by perinatal TP, a finding congruent with a previous report that females and feminized males have more of these large DLN neurons than control males. Our data suggest an exquisite sensitivity of the developing spinal nuclei to the timing of hormonal surges normally found in fetal males. Exposure to androgens during a brief prenatal period is needed to assure responsiveness to the low amounts of androgen circulating during neonatal ontogeny, when the process of sexual differentiation is completed.

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Jeffrey A. French

University of Nebraska Omaha

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Shelton E. Hendricks

University of Nebraska Omaha

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Andrzej Bartke

Southern Illinois University School of Medicine

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Dudley F. Peeler

University of Mississippi Medical Center

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