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Biomedical subjects

R J Barfield

Publications and source records attributed to R J Barfield.

At least 73 records · Page 4Linked to original sources
PubMed1980

Effects of morphine, beta-endorphin and naloxone on catecholamine levels and sexual behavior in the male rat.

Intraperitoneal administration of the opiate antagonist naloxone hydrochloride (30 mg/kg) to sexually experienced male rats caused a significant reduction in mount and intromission latencies, number of mounts preceding ejaculation and ejaculation latencies. Intraperitoneal adminstration of naloxone (30 mg/kg) also stimulated persistant non-copulators to begin mating and to ejaculate within a twenty minute test period. Conversely, intraperitoneal administration of morphine sulphate (6 mg/kg) as well as intraventricular injection of the endogenous opiate beta-endorphin (6 micrograms) produced a complete loss of copulatory behavior in male rats. The deficit in sexual behavior induced by beta-endorphin was correlated with a significant increase in hypothalamic norepinephrine levels. It is suggested that the endogenous opiates may be involved in the mediation of sexual behavior via an interaction with central catecholaminergic systems.

Animals↗
PubMed1980

Postpartum aggression in rats: II. Dependence on maternal sensitivity to young and effects of experience with pregnancy and parturition.

Two experiments were carried out to explore the relation between postpartum aggressive behavior in rats and other aspects of maternal behavior. In Experiment 1, nulliparous females experimentally induced to behave maternally; i.e., sensitized, failed to show elevations in aggressive responding above levels seen in untreated nulliparous controls; lactating females displayed characteristically high levels of aggression. In Experiment 2, animals in these groups were tested, along with parturient females allowed varying amounts (0 hr, 2 days, or 9 days) of postpartum exposure to young, spanning a period that is sensitive for the induction of maternal behavior. The three parturient groups responded with levels of aggression that were similar to one another and significantly higher than those seen in controls. Sensitized animals in Experiment 2 exhibited high levels of fighting; differences between these animals and those in Experiment 1 may be due to differences in both length of sensitization and ovarian cyclicity. These data indicate that the experiences of pregnancy and/or parturition prime the postparturient female to respond aggressively to an intruder later in lactation and that, unlike the initiation of pup-oriented maternal behaviors, establishment of postpartum aggression is not dependent upon pup exposure during the immediate postpartum period.

Aggression↗
PubMed1980

Postpartum aggression in rats: I. Effects of hypophysectomy.

For the purpose of testing the hypothesis that the high level of aggressive behavior exhibited by postparturient rats is mediated by lactogenic hormones, hypophysectomy was performed on Day 5 postpartum, and fighting against an adult male rat was measured 4 days later. Pups were exchanged daily between hypophysectomized and sham-operated or unoperated controls animals. In Experiment 1, no differences in aggressive behavior were seen between hypophysectomized, sham-hypophysectomized, and untreated lactating animals on Day 9 postpartum. In Experiment 2, the hormonal dependence of the characteristic sensitivity to the presence of the litter in the elicitation of postpartum aggression was investigated. All animals were tested three times, on Day 9, 12, and 15 postpartum; litters were removed 4 hr prior to the second aggression test. For all groups, aggression levels were high on Day 9 with the litter present, dropped on Day 12 after removal of the litter, and showed some increment or stabilization on Day 15 with the litter again present. These experiments demonstrate that neither the expression of postpartum aggression nor the sensitivity to the presence of stimuli from the litter is directly dependent upon the hormonal milieu characteristic of lactation.

Aggression↗
PubMed1980

Priming of estrous responsiveness by implants of 17 beta-estradiol in the ventromedial hypothalamic nucleus of female rats.

In an attempt to obtain a more precise localization of the neural target site(s) of estrogen-priming action in the activation of estrous behavior, 30-gauge cannulae containing a preparation of 17 beta-estradiol diluted 1:250 with cholesterol were implanted bilaterally into the brains of ovariectomized rats. Subjects were tested for sexual behavior with intact males at 4-day intervals for 3 weeks beginning 2-3 days after stereotaxic surgery. Animals received a systemic injection of 0.5 mg progesterone 4-6 h before all but 1 test. After this treatment, estrous behavior was observed in 19 of the 20 animals judged to have both cannulae resting in or within 0.25 mm of the ventromedial nucleus of the hypothalamus (VMN). Virtually no estrous behavior was observed without the administration of progesterone. Behavioral scores decreased as a function of the distance of the cannulae tips from the VMN. Cholesterol implants in the same region (n = 8) were without effect. Implants in other regions of the brain (e.g. preoptic area, diagonal band of Broca, lateral habenula, amygdala, or cortex; n = 52) were ineffective. These results indicate that estrogenic stimulation of the region of the VMN alone is sufficient to prime the activation of estrous behavior in the ovariectomized rat.

Animals↗
PubMed1979

Activation of masculine sexual behavior by intracranial estradiol benzoate implants in male rats.

Intracranial implants of estradiol benzoate (EB) were used to explore sites of action for the activation of masculine copulatory behavior in castrated male rats. In experiment 1, 27 or 30 gauge implants were placed unilaterally throughout the hypothalamus and preoptic area. Dihydrotestosterone (DHT) was administered subcutaneously (s.c.) to each male. 25 of 42 males with EB implants located in the medial anterior hypothalamic-preoptic area (AHPOA) exhibited ejaculatory patterns on at least 40% of the post-implantation tests. In contrast, only 4 of 18 of the males with implants located posterior to the anterior hypothalamic area displayed this level of response. This difference in the proportion of animals responding for each implant group was statistically significant. Seminal vesicle weights were not correlated with the occurrence of copulation. In experiment 2, either EB-filled or empty cannulae were placed unilaterally in the AHPOA. Half of the males of each group also received DHT s.c. Intracranial EB in conjunction with DHT s.c. resulted in a significantly greater frequency of ejaculatory response than any other treatment. Despite significant differences among the groups in seminal vesicle weights, there was no correlation with occurrence of ejaculatory behavior. These results are consistent with the hypothesis that testosterone (T) exerts its effects upon masculine sexual behavior via conversion to estradiol (E2); and that the principal neural site of action is the AHPOA.

Animals↗
PubMed1979

Activation of feminine sexual behavior in castrated male rats by intrahypothalamic implants of estradiol benzoate.

The effects of intracerebral estradiol benzoate (EB) implants upon lordosis behavior in castrated male rats were investigated. 27 guage EB-filled or Blank implants were placed unilaterally in either the preoptic area (POA) or the region of the ventromedial hypothalamic nucleus (VMH). When 0.5 microgram of EB was administered subcutaneously for eight days, males with EB implants had significantly higher lordosis quotients (LQ) than males with Blank implants. EB implants located in the region of the VMH were significantly more effective in stimulating lordosis responses than implants in the POA. These results indicate that, in male rats as in females, the VMH region is a primary site for the hormonal activation of lordosis behavior.

Animals↗
PubMed1979

Effects of aromatizable androgens on aggressive behaviour among rats (rattus norvegicus).

Three experiments were used to tests the applicability of the aromatization hypothesis of androgen action to aggressive behaviour among Norway rats. In Expt 1, administration of testosterone propionate was highly effective in restoring aggressive behaviour to castrated rats while 17 beta-hydroxy-5 alpha-androstan-3-one was of intermediate effectiveness. Of the steriods tested in Expt 2, androstenedione and testosterone were highly effective, 17 beta, 19-dihydroxyandrost-4-en-3-one was of intermediate effectiveness and cholesterol was ineffective. The results of Expt 3 indicated that treatment with testosterone or oestradiol both resulted in increased aggression while treatment with (5 alpha,17 beta)-17,19-bis(acetyloxy)-andostan-3-one diacetate (5 alpha-19-hydroxytestosterone) was without effect. Androgens which were aromatizable and could be 5 alpha reduced, i.e. testosterone, testosterone propionate and androstenedione, were highly effective in restoring aggressive behaviour; however, two other steroids, 5 alpha,19-hydroxytestosterone which is 5 alpha reduced, and 19-hydroxytestosterone, which can be aromatized, were respectively of low or medium effectiveness on behaviour. However, oestradiol, which did not maintain sexual development of accessory glands, was highly effective in the restoration of aggressive behaviour. Since the behaviourally active steroids in the present experiments were not only those predicted by the aromatization hypothesis, it is proposed that several steroids are capable of activating aggressive behaviour and that the aromatization hypothesis does not adequately explain the hormonal basis of aggressive behaviour among Norway rats.

Aggression↗
PubMed1978

Influence of gonadal hormones and sexual behavior on ultrasonic vocalization in rats: I. Treatment of females.

Ultrasonic vocalizations were measured when male rats were placed with ovariectomized females that had experienced various hormonal and behavioral treatments. In Experiment 1, 18 males were tested with females in each of the following conditions: nonestrous (OVX), estrogen treated (E), estrogen and progesterone treated (EP), and estrogen and progesterone treated and given two intromissions from a stud male prior to testing (EPI). Control conditions included clean cage (CL) and cage soiled by an estrous female (SOI). The treatments differed in effect on rate and maintenance of vocalization: EP greater than E greater than EPI = OVX greater than SOI greater than CL. In tests in which males produced a high rate of vocalization, some males with short intromission latencies shifted from the normal 50-kHz pulse to a 22-kHz pulse. In Experiment 2, the effect of the female's vocalization and movement on the rate of and latency to vocalization was measured. Twenty-one males were presented with each of the following stimulus conditions: estrous female with red light (EP), estrous female without red light (EP dark), estrous anesthetized female (EP anes), and nonestrous anesthetized female (OVX anes). Effects on vocalization of various treatments were as follows: EP = EP dark greater than EP anes greater than OVX anes. These data suggest that the 50-kHz vocalizations constitute a graded response influenced by the female's hormonal and sexual condition.

Animals↗
PubMed1978

Autoradiographic localization of androgen-concentrating cells in the brain of the male domestic fowl.

Cells in the male fowl brain which accumulate radioactivity following 3H testosterone (T) administration were identified by autoradiography. Labelled cells were found principally in hypothalamic, limbic and midbrain structures. Marked uptake was observed in the preoptic area (POA) and in the anterior and posterior hypothalamus. There was also a significant amount of labelling in the archistriatum (ARCH), particularly in the nucleus taeniae (Tn), and in the lateral septum. In the midbrain, substantial uptake of labelled hormone was found in the nucleus intercollicularis (ICo). The pattern of accumulation of T in the male fowl was comparable to that for sex hormone uptake in vertebrates in general. Furthermore, accumulation was generally found in areas known to be concerned with sex hormone-dependent functions.

Animals↗