Figure 4.1

Proposed model for hormonal control of reproduction in anurans. The stimulatory neuropeptide gonadotropin-releasing hormone 1 (GnRH1) and perhaps GnRH2 are released from hypothalamic nerve terminals into the median eminence-portal blood system (not illustrated) and transported to the anterior pituitary, where these decapeptides act on G-protein-coupled GnRH receptor subtypes on gonadotrophs to stimulate the synthesis of luteinizing hormone (LH) and follicle-stimulating hormone (FSH). The release of the gonadotropins is enhanced by prolactin (PRL) secreted from pituitary lactotrophs. Prolactin is stimulated by the tripeptide thyrotropin-releasing hormone (TRH), originally named for that action because of its role in mammals. In anurans it does not effectively stimulate thyrotropin but does stimulate PRL and growth hormone. The RF-amide peptide gonadotropin-inhibitory hormone (GnIH) and the catecholamine dopamine (DA) also play respective stimulatory and inhibitory roles in the regulation of PRL. The effects of the GnRHs on gonadotropins are inhibited by DA in some species, but experimental evidence is lacking for many amphibians. The gonadotropins act on their respective G-protein-coupled receptors in the ovaries and testes to drive steroidogenesis and the release of gametes. In the ovaries, progesterone (P4) is converted through multiple enzymatic steps to testosterone (T), which is aromatised to oestradiol (E2). Oestradiol plays an important role in stimulating the hepatic synthesis of the egg-yolk vitellogenins (VTGs) in females (not shown). The synthesis and release of VTGs from the liver (not shown) is also regulated by LH, FSH, and PRL. Testosterone is converted by 5α-reductase to 5α-dihydrotestosterone (DHT), the main androgen in amphibians. These sex steroids generally play various roles in positive and negative feedback (±) regulation of gonadotropin-release, but direct evidence is lacking in many amphibian species. Steroids are involved in gonadal development, development of secondary sex characters, and can modulate courtship behaviours that are controlled by arginine vasotocin (AVT). Note that AVT neurons project to the posterior pituitary for release into the circulation, and also project widely in the brain. For clarity, this is not depicted in the figure. Intratesticular kisspeptin (KISS-1) and the GnRHs regulate steroidogenesis, proliferation of germ cells, and spermatogenesis. No data for intraovarian KISS and GnRH have yet been reported for amphibians. Kisspeptin is also found in hypothalamic neurons but it is not known if, or how, it may regulate GnRH neurons or gonadotropin-release. Corticotropin-releasing factor (CRF) stimulates the synthesis and release of adrenocorticotropic hormone (ACTH) from the pituitary, which in turn stimulates corticosterone (CORT) from the steroidogenic cells of the interrenal (amphibian equivalent to mammalian adrenal cortex embedded within the kidney complex). Corticosteroids negatively feedback at the level of CRF and ACTH to reduce the synthesis of glucocorticoid. This constitutes the hypothalamo-pituitary-interrenal axis. Accumulating evidence indicates that CORT can modulate reproductive processes at multiple sites (see *). Solid lines indicate functions supported by strong evidence and dashed lines with ? indicate very limited evidence or speculations that will need further investigation. Lines terminating in an arrowhead indicate stimulation whereas lines terminating in an ellipse indicate inhibition. The ± sign indicates a modulatory response since both positive and negative effects have been reported. See text for additional details.