Annual variation in reproductive behavior, testosterone, and plasma FSH levels in the Rouen duck, Anas platyrhynchos.
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The present study sought to determine (1) whether estrogen by itself can defeminize the behavior of pigs during the late juvenile-early pubertal period, and (2) whether the progressive late defeminization reported for pigs is a true organizational effect, as opposed to an artifact of the time between castration and testing. Male pigs were castrated at 19-22 days or left intact and females were ovariectomized at 3 months. Additional males castrated at 19-22 days and females ovariectomized at 3 months were implanted with estradiol benzoate (EB) from 3 to 5.5 months. After castration of the previously intact males at the age of 5.5 months, all subjects were tested beginning at 6.5 months for proceptivity (choice of a male versus a female in a T-maze) and receptivity (immobilization to a mounting male) following an injection of EB. EB administered during development significantly defeminized proceptivity and receptivity in both sexes. The decrease in proceptivity was more pronounced in males than in females and was more pronounced than the decrease in receptivity, as if differentiation ends earlier for proceptivity than for receptivity; the decrease in receptivity was more pronounced in females. To see whether the capacity to display female-typical behavior is a function of time since castration, we castrated additional males at 4 months and tested for receptivity 9 days later following an injection of EB, then tested again with the other subjects at 6.5 months. The proceptivity and receptivity scores for males castrated at 4 months fell between those for intact males and males castrated at 3 weeks, and thus these animals were not completely defeminized. They were more receptive at 6.5 months than at 4 months, but the difference was not significant. These results indicate that in pigs estradiol defeminizes both receptive and proceptive behavior and that this defeminization can occur relatively late in development.
To determine the relative contribution of mate access and environmental cues in stimulating egg-laying and plasma luteinizing hormone (LH) secretion in cockatiels (Nymphicus hollandicus), and of mate access on nest-inspection and bowl-formation, mated pairs were permitted different degrees of mate access (full contact, auditory plus visual contact, auditory contact only, or no contact) and sequentially exposed to three environmental conditions (8L:16D without nest-box access for 6 weeks; 15L:9D without nest-box access for 3 weeks; 15L:9D with nest-box access for 3 weeks). The results indicate that a high degree of mate access is essential for the performance of nesting behaviors, since birds allowed no mate access or only auditory mate access were significantly less likely to inspect the nest or form a nest-bowl. Furthermore, pairs permitted no contact, auditory contact only, or auditory and visual contact delayed nest-inspection and bowl-formation and were significantly less likely to lay eggs than pairs with total mate contact. LH levels were significantly elevated only in photostimulated females of pairs of permitted full mate and nest-box access. These results suggest that maximal sexual activity in cockatiels requires an array of behavioral and environmental cues and that a linear relationship exists between extent of social cues and sexual activity.
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Eighteen ovariectomized ring doves (Streptopelia risoria) received subcutaneous silastic implants of either testosterone propionate (TP), 5 alpha-dihydrotestosterone propionate (DHTP) or cholesterol. Birds were paired daily for 1-hr with intact males. Eleven days after implantation the pairs were observed. Both TP and DHTP activated wingflipping behavior in the females. None of the females showed receptive crouching. Aromatization of testosterone to estrogen does not appear to be involved in wingflipping in female doves. The results suggest that wingflipping in females is not as hormone specific as it appears to be in male doves.
Castrated DBA/2J male mice emitted 70 kHz vocalizations to female stimuli in response to 10 days of treatment with either testosterone (T, 300 micrograms/day), diethylstilbestrol (DES, 1 or 3 micrograms/day) or methyltrienolone (R1881, 900 micrograms/day). Lower dosages of R1881 (300 and 600 micrograms/day) and the oil vehicle were relatively ineffective in restoring vocalizations. The effects of these hormones on restoring seminal vesicle weight did not always parallel their effects upon behavior. In general T and R1881 (600 and 900 micrograms/day) were effective in restoring seminal vesicles while DES, the lowest dose of R1881 (300 micrograms/day), and the oil vehicle were ineffective. In receptor competition studies, R1881 pretreatment significantly reduced estrogen binding in hypothalamic-preoptic cytosol. In fact the most effective dose for restoring vocalizations (900 micrograms/day) reduced available estrogen binding sites by 91%. We propose that the male-typical vocalizations of mice may normally be stimulated through the activation of estrogen receptors following androgen aromatization and that the ability of a pharmacological dosage of R1881 (900 micrograms/day) to restore behavior may be due to interaction with estrogen receptors in the brain.
Analogs of LH-RH were studied for their effect on lordosis in ovariectomized rats primed with estrogen. Classified by their gonadotropin-releasing activity, representatives of three types of analogs were tested for facilitation of lordotic (L) responses of preselected females to mounting (M) by male studs. Positive responses (L/M greater than 0.5) were found after SC administration of LH-RH peptides modified so as to be inhibitory, stimulatory, or inactive in releasing LH and FSH. The results further support the concept of a dissociation between the endocrine and extra-endocrine effects of peripherally injected hypothalamic peptides.
The adult male accessory glands of D. melanogaster synthesize and secrete a peptide that represses female sexual receptivity and stimulates oviposition. Normally, this peptide is transferred to females during copulation; however, the peptide shows the same biological activity after purification and subsequent injection into the abdominal cavity of female virgins. Amino acid sequencing of the purified peptide and oligonucleotide-directed cDNA cloning established that the peptide consists of 36 amino acids. It appears to be synthesized as a precursor with a hydrophobic signal sequence of 19 residues at its N-terminal end. The precursor peptide is encoded by a short mRNA that accumulates exclusively in the male accessory gland. The gene has been localized by in situ hybridization to polytene chromosomes at 70A.
The present experiment was performed to examine the role of serotonergic mechanisms in the control of copulation and the post-ejaculatory refractory period in the male rat. Disruption of central serotonergic systems in two separate groups of animals was achieved by: (1) selective electrolytic lesions of the midbrain raphe nuclei, or (2) localized intraventricular or intracerebral injection of a specific serotonergic neurotoxin, 5,7-dihydroxytryptamine (5,7-DHT). A third group of animals was tested for sexual behavior following intraperitoneal injection of p-chlorophenylalanine (PCPA), an inhibitor of serotonin synthesis. Both electrolytic and neurochemical lesions localized in the dorsal raphe nucleus produced a highly significant shortening of the ejaculatory latency, and the post-ejaculatory refractory period. Disruption of serotonergic mechanisms following intraventricular injection of 5,7-DHT or systemic administration of PCPA also caused a significant reduction in the length of the refractory period. These results support the hypothesis that central serotonergic systems are normally inhibitory to certain facets of male copulatory behavior and suggest the existence of a serotonergic control system which normally exerts an inhibitory influence over the resumption of mating following ejaculation.
This study was designed to examine the role of central dopaminergic mechanisms in the control of copulation and the subsequent post-ejaculatory refractory period in the male rat. Disruption of central dopaminergic pathways was achieved in two separate groups of animals by: (1) selective electrolytic lesions of the substantia nigra (the major locus for dopamine cell bodies in the brain); or (2) localized intracerebral injection of 6-hydroxydopamine, a specific neurotoxin for catecholaminergic pathways. A third group of animals was tested for sexual behavior following administration of the dopamine receptor blocker pimozide. Both electrolytic and neurochemical lesions localized in the substantia nigra produced a significant increase in the length of the post-ejaculatory refractory period. Dopamine receptor blockade following administration of pimozide also caused a significant increase in refractory period duration. These results support the hypothesis that central dopaminergic pathways are involved in the motivational or arousal component of copulation and may be integral to the maintenance of a normal post-ejaculatory refractory period.