scholarly journals Interaction of thyroid hormones and gonadotropin inhibitory hormone in the multifactorial control of zebrafish (Danio rerio) spermatogenesis

2021 ◽  
Author(s):  
Maira S. Rodrigues ◽  
Hamideh P. Fallah ◽  
Maya Zanardini ◽  
Hamid R. Habibi ◽  
Rafael H. Nóbrega
Keyword(s):  
Thyroid Hormones ◽  
Sex Steroids ◽  
Ex Vivo ◽  
Model Organism ◽  
Gonadal Hormones ◽  
Adult Males ◽  
Haploid Cell ◽  
Paracrine Factor ◽  
Reproductive Axis ◽  
Gonadotropin Inhibitory Hormone

ABSTRACTReproduction is under multifactorial control of neurohormones, pituitary gonadotropins, as well as a number of gonadal hormones including sex steroids and growth factors. Gonadotropin-inhibitory hormone (Gnih), a novel RFamide neuropeptide, was shown to be involved in the control of pituitary gonadotropin production, as well as being involved as a paracrine factor in the regulation of gonadal function. In this context, recent studies have demonstrated that Gnih inhibited gonadotropin-induced spermatogenesis in the zebrafish testicular explants. Thyroid hormones are known to interact with the reproductive axis, and are, in particular, involved in the regulation of testicular function. Based on this background, we investigated the interaction between Gnih and thyroid hormones in the control of zebrafish spermatogenesis. To this end, zebrafish adult males were treated with the goitrogen methimazole (1mM for 21 days) in order to generate a hypothyroid model organism. Subsequently, a factorial design using an ex vivo testis culture system in combination with histomorphometrical and FACScan cell cycle analyses were adopted. Our results showed that methimazole treatment affected both basal and gonadotropin-induced spermatogenesis, in particular, meiosis and spermiogenesis. Moreover, the goitrogen treatment nullified the inhibitory actions of Gnih on the gonadotropin-induced spermatogenesis, specifically in the haploid cell population. We have demonstrated that thyroid hormones interaction with gonadotropin and Gnih are important components for the regulation of zebrafish spermatogenesis. The results provide a support for the hypothesis that thyroid hormones are important contributors in multifactorial control of spermatogenesis in zebrafish.

scholarly journals Kisspeptin-8 Induces Anxiety-Like Behavior and Hypolocomotion by Activating the HPA Axis and Increasing GABA Release in the Nucleus Accumbens in Rats

Biomedicines ◽  
2021 ◽  
Vol 9 (2) ◽  
pp. 112
Author(s):  
Katalin Eszter Ibos ◽  
Éva Bodnár ◽  
Zsolt Bagosi ◽  
Zsolt Bozsó ◽  
Gábor Tóth ◽  
...  
Keyword(s):  
Nucleus Accumbens ◽  
Ex Vivo ◽  
Gaba Release ◽  
Receptor Activation ◽  
Ambulatory Activity ◽  
Corticosterone Concentration ◽  
Reproductive Axis ◽  
Neuropeptide Ff ◽  
Serum Lh ◽  
Anxiogenic Effect

Kisspeptins (Kp) are RF-amide neuropeptide regulators of the reproductive axis that also influence anxiety, locomotion, and metabolism. We aimed to investigate the effects of intracerebroventricular Kp-8 (an N-terminally truncated octapeptide) treatment in Wistar rats. Elevated plus maze (EPM), computerized open field (OF), and marble burying (MB) tests were performed for the assessment of behavior. Serum LH and corticosterone levels were determined to assess kisspeptin1 receptor (Kiss1r) activation and hypothalamic-pituitary-adrenal axis (HPA) stimulation, respectively. GABA release from the nucleus accumbens (NAc) and dopamine release from the ventral tegmental area (VTA) and NAc were measured via ex vivo superfusion. Kp-8 decreased open arm time and entries in EPM, and also raised corticosterone concentration, pointing to an anxiogenic effect. Moreover, the decrease in arm entries in EPM, the delayed increase in immobility accompanied by reduced ambulatory activity in OF, and the reduction in interactions with marbles show that Kp-8 suppressed exploratory and spontaneous locomotion. The increase in GABA release from the NAc might be in the background of hypolocomotion by inhibiting the VTA-NAc dopaminergic circuitry. As Kp-8 raised LH concentration, it could activate Kiss1r and stimulate the reproductive axis. As Kiss1r is associated with hyperlocomotion, it is more likely that neuropeptide FF receptor activation is involved in the suppression of locomotor activity.

scholarly journals Influence of Acetylcholine Esterase Inhibitors and Memantine, Clinically Approved for Alzheimer’s Dementia Treatment, on Intestinal Properties of the Mouse

2021 ◽  
Vol 22 (3) ◽  
pp. 1015
Author(s):  
Vu Thu Thuy Nguyen ◽  
Jason Sallbach ◽  
Malena dos Santos Guilherme ◽  
Kristina Endres
Keyword(s):  
Calcium Influx ◽  
Ex Vivo ◽  
Model Organism ◽  
Nmda Receptor Antagonist ◽  
Acetylcholine Esterase ◽  
Enteric Neurons ◽  
Acetylcholine Esterase Inhibitors ◽  
E Coli ◽  
Esterase Inhibitors ◽  
Intestinal Functions

Four drugs are currently approved for the treatment of Alzheimer’s disease (AD) by the FDA. Three of these drugs—donepezil, rivastigmine, and galantamine—belong to the class of acetylcholine esterase inhibitors. Memantine, a NMDA receptor antagonist, represents the fourth and a combination of donepezil and memantine the fifth treatment option. Recently, the gut and its habitants, its microbiome, came into focus of AD research and added another important factor to therapeutic considerations. While the first data provide evidence that AD patients might carry an altered microbiome, the influence of administered drugs on gut properties and commensals have been largely ignored so far. However, the occurrence of digestive side effects with these drugs and the knowledge that cholinergic transmission is crucial for several gut functions enforces the question if, and how, this medication influences the gastrointestinal system and its microbial stocking. Here, we investigated aspects such as microbial viability, colonic propulsion, and properties of enteric neurons, affected by assumed intestinal concentration of the four drugs using the mouse as a model organism. All ex vivo administered drugs revealed no direct effect on fecal bacteria viability and only a high dosage of memantine resulted in reduced biofilm formation of E. coli. Memantine was additionally the only compound that elevated calcium influx in enteric neurons, while all acetylcholine esterase inhibitors significantly reduced esterase activity in colonic tissue specimen and prolonged propulsion time. Both, acetylcholine esterase inhibitors and memantine, had no effect on general viability and neurite outgrowth of enteric neurons. In sum, our findings indicate that all AD symptomatic drugs have the potential to affect distinct intestinal functions and with this—directly or indirectly—microbial commensals.

scholarly journals Nonhuman primates’ tissue banks: resources for all model organism research

2021 ◽  
Author(s):  
Claire Witham ◽  
Sara Wells
Keyword(s):  
Nonhuman Primates ◽  
Ex Vivo ◽  
Model Organism ◽  
Translation Studies ◽  
Model Organisms ◽  
Laboratory Animals ◽  
Tissue Banks ◽  
Post Mortem ◽  
Wide Range ◽  
Research Programmes

AbstractBiobanks containing tissue and other biological samples from many model organisms provide easy and faster access to ex vivo resources for a wide-range of research programmes. For all laboratory animals, collecting and preserving tissue at post-mortem is an effective way of maximising the benefits of individual animals and potentially reducing the numbers required for experimentation in the future. For primate tissues, biobanks represent the scarcest of these resources but quite possibly those most valuable for preclinical and translation studies.

scholarly journals Ex vivo antibacterial properties of rufloxacin compared with those of norfloxacin in a study with healthy volunteers.

1996 ◽  
Vol 40 (1) ◽  
pp. 17-21 ◽  
Author(s):  
L Aguilar ◽  
I P Balcabao ◽  
P Salvá ◽  
M Martín ◽  
J Costa ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Clinical Trial ◽  
Ex Vivo ◽  
Antibacterial Properties ◽  
Adult Males ◽  
E Coli ◽  
Crossover Phase ◽  
Uncomplicated Cystitis ◽  
And Staphylococcus Aureus ◽  
Early Sample

Twelve adult males participated in a randomized crossover phase I clinical trial comparing serum bactericidal titers (SBTs), urine bactericidal titers (UBTs), and urine killing rates (UKRs) against Escherichia coli ATCC 25922 and Staphylococcus aureus ATCC 29213, after the administration of single 400-mg doses of rufloxacin and norfloxacin at different times up to 72 h postdose. SBTs were significantly higher (P < 0.05) against E. coli from 8 to 48 h and against S. aureus from 4 to 24 h with rufloxacin. UBTs for E. coli were higher (P < 0.05) for norfloxacin at early sample times (0 to 8 h) but higher for rufloxacin (P < 0.05) at sample times from 16 h on for both E. coli and S. aureus. Similar UKRs were obtained for both quinolones for 0 to 2 h and 8 to 12 h, but the UKR was maintained for 72 h with rufloxacin. The high and sustained mean levels of rufloxacin in urine (> 35 micrograms/ml), median UBTs (> 32 for E. coli and 16 for S. aureus) and UKRs for E. coli suggest prolonged urine antibacterial activity (for at least 72 h) and its use as a single 400-mg dose in the treatment of uncomplicated cystitis.

scholarly journals Zebrafish as a model to study autophagy and its role in skeletal development and disease

2020 ◽  
Author(s):  
Joanna J. Moss ◽  
Chrissy L. Hammond ◽  
Jon D. Lane
Keyword(s):  
Protein Degradation ◽  
Ex Vivo ◽  
Skeletal Development ◽  
Model Organism ◽  
Degradation Pathway ◽  
Tissue Homeostasis ◽  
Genetic Mutations ◽  
High Fecundity ◽  
Skeletal Disorders ◽  
The Many

Abstract In the last twenty years, research using zebrafish as a model organism has increased immensely. With the many advantages that zebrafish offer such as high fecundity, optical transparency, ex vivo development, and genetic tractability, they are well suited to studying developmental processes and the effect of genetic mutations. More recently, zebrafish models have been used to study autophagy. This important protein degradation pathway is needed for cell and tissue homeostasis in a variety of contexts. Correspondingly, its dysregulation has been implicated in multiple diseases including skeletal disorders. In this review, we explore how zebrafish are being used to study autophagy in the context of skeletal development and disease, and the ways these areas are intersecting to help identify potential therapeutic targets for skeletal disorders.

scholarly journals Neurokinin B and the Control of the Gonadotropic Axis in the Rat: Developmental Changes, Sexual Dimorphism, and Regulation by Gonadal Steroids

Endocrinology ◽  
2012 ◽  
Vol 153 (10) ◽  
pp. 4818-4829 ◽  
Author(s):  
F. Ruiz-Pino ◽  
V. M. Navarro ◽  
A. H. Bentsen ◽  
D. Garcia-Galiano ◽  
M. A. Sanchez-Garrido ◽  
...  
Keyword(s):  
Sexual Dimorphism ◽  
Sex Steroids ◽  
Developmental Stages ◽  
Female Rats ◽  
Sex Steroid ◽  
Adult Males ◽  
Neurokinin B ◽  
Male And Female Rats ◽  
Gonadotropic Axis ◽  
Key Aspects

Abstract Neurokinin B (NKB), encoded by Tac2 in rodents, and its receptor, NK3R, have recently emerged as important regulators of reproduction; NKB has been proposed to stimulate kisspeptin output onto GnRH neurons. Accordingly, NKB has been shown to induce gonadotropin release in several species; yet, null or even inhibitory effects of NKB have been also reported. The basis for these discrepant findings, as well as other key aspects of NKB function, remains unknown. We report here that in the rat, LH responses to the NK3R agonist, senktide, display a salient sexual dimorphism, with persistent stimulation in females, regardless of the stage of postnatal development, and lack of LH responses in males from puberty onward. Such dimorphism was independent of the predominant sex steroid after puberty, because testosterone administration to adult females failed to prevent LH responses to senktide, and LH responsiveness was not restored in adult males treated with estradiol or the nonaromatizable androgen, dihydrotestosterone. Yet, removal of sex steroids by gonadectomy switched senktide effects to inhibitory, both in adult male and female rats. Sexual dimorphism was also evident in the numbers of NKB-positive neurons in the arcuate nucleus (ARC), which were higher in adult female rats. This is likely the result of differences in sex steroid milieu during early periods of brain differentiation, because neonatal exposures to high doses of estrogen decreased ARC NKB neurons at later developmental stages. Likewise, neonatal estrogenization resulted in lower serum LH levels that were normalized by senktide administration. Finally, we document that the ability of estrogen to inhibit hypothalamic Tac2 expression seems region specific, because estrogen administration decreased Tac2 levels in the ARC but increased them in the lateral hypothalamus. Altogether, our data provide a deeper insight into relevant aspects of NKB function as major regulator of the gonadotropic axis in the rat, including maturational changes, sexual dimorphism, and differential regulation by sex steroids.

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