Seasonal breeder

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Seasonal breeders are animal species that successfully mate only during certain times of the year. These times of year allow for the optimization of survival of young due to factors such as ambient temperature, food and water availability, and changes in the predation behaviors of other species. [1] Related sexual interest and behaviors are expressed and accepted only during this period. Female seasonal breeders will have one or more estrus cycles only when she is "in season" or fertile and receptive to mating. At other times of the year, they will be anestrus, or have a dearth of their sexual cycle. Unlike reproductive cyclicity, seasonality is described in both males and females.[ citation needed ] Male seasonal breeders may exhibit changes in testosterone levels, testes weight, and fertility depending on the time of year. [2]

Contents

Seasonal breeders are distinct from opportunistic breeders, that mate whenever the conditions of their environment become favorable, and continuous breeders that mate year-round.

Timing of seasonal breeding

The breeding season is when seasonal breeders reproduce. Various variables can affect when it occurs. [3] A primary influence on the timing of reproduction is food availability. Organisms generally time especially stressing events of reproduction to occur in sync with increases in food availability. This is not always true, however, both because of the importance of other factors and the invalidation of this generalization. For example, in species reproducing at high latitudes, food availability before breeding is more important than availability during reproduction itself. Other factors can also be responsible. For example, species that are preyed upon frequently may time reproduction to occur out of sync with the peak in density of predators. [4]

Physiology

The hypothalamus is considered to be the central control for reproduction due to its role in hormone regulation. [5] Hence, factors that determine when a seasonal breeder will be ready for mating affect this tissue. This is achieved specifically through changes in the production of the hormone GnRH. GnRH in turn transits to the pituitary where it promotes the secretion of the gonadotropins LH and FSH, both pituitary hormones critical for reproductive function and behavior, into the bloodstream. Changes in gonadotropin secretion initiate the end of anestrus in females.

Day length

Seasonal breeding readiness is strongly regulated by length of day (photoperiod) and thus season. Photoperiod likely affects the seasonal breeder through changes in melatonin secretion by the pineal gland that ultimately alter GnRH release by the hypothalamus. [3]

Hence, seasonal breeders can be divided into groups based on fertility period. "Long day" breeders cycle when days get longer (spring) and are in anestrus in fall and winter. Some animals that are long day breeders include ring-tailed lemurs, horses, hamsters, groundhogs, and mink. "Short day" breeders cycle when the length of daylight shortens (fall) and are in anestrus in spring and summer. The decreased light during the fall decreases the firing of the retinal nerves, in turn decreasing the excitation of the superior cervical ganglion, which then decreases the inhibition of the pineal gland, finally resulting in an increase in melatonin. This increase in melatonin results in an increase in GnRH and subsequently an increase in the hormones LH and FSH, which stimulate cyclicity. [6]

See also

Related Research Articles

Luteinizing hormone is a hormone produced by gonadotropic cells in the anterior pituitary gland. The production of LH is regulated by gonadotropin-releasing hormone (GnRH) from the hypothalamus. In females, an acute rise of LH triggers ovulation and development of the corpus luteum. In males, where LH had also been called interstitial cell–stimulating hormone (ICSH), it stimulates Leydig cell production of testosterone. It acts synergistically with follicle-stimulating hormone (FSH).

Follicle-stimulating hormone

Follicle-stimulating hormone (FSH) is a gonadotropin, a glycoprotein polypeptide hormone. FSH is synthesized and secreted by the gonadotropic cells of the anterior pituitary gland and regulates the development, growth, pubertal maturation, and reproductive processes of the body. FSH and luteinizing hormone (LH) work together in the reproductive system.

Anterior pituitary Anterior lobe of the pituitary gland

A major organ of the endocrine system, the anterior pituitary is the glandular, anterior lobe that together with the posterior lobe makes up the pituitary gland (hypophysis). The anterior pituitary regulates several physiological processes, including stress, growth, reproduction, and lactation. Proper functioning of the anterior pituitary and of the organs it regulates can often be ascertained via blood tests that measure hormone levels.

Gonadotropin-releasing hormone

Gonadotropin-releasing hormone (GnRH) is a releasing hormone responsible for the release of follicle-stimulating hormone (FSH) and luteinizing hormone (LH) from the anterior pituitary. GnRH is a tropic peptide hormone synthesized and released from GnRH neurons within the hypothalamus. The peptide belongs to gonadotropin-releasing hormone family. It constitutes the initial step in the hypothalamic–pituitary–gonadal axis.

Gonadotropins are glycoprotein hormones secreted by gonadotropic cells of the anterior pituitary of vertebrates. This family includes the mammalian hormones follicle-stimulating hormone (FSH) and luteinizing hormone (LH), the placental/chorionic gonadotropins, human chorionic gonadotropin (hCG) and equine chorionic gonadotropin (eCG), as well as at least two forms of fish gonadotropins. These hormones are central to the complex endocrine system that regulates normal growth, sexual development, and reproductive function. LH and FSH are secreted by the anterior pituitary gland, while hCG and eCG are secreted by the placenta in pregnant humans and mares, respectively. The gonadotropins act on the gonads, controlling gamete and sex hormone production.

The estrous cycle is the set of recurring physiological changes that are induced by reproductive hormones in most mammalian therian females. Estrous cycles start after sexual maturity in females and are interrupted by anestrous phases, otherwise known as "rest" phases, or by pregnancies. Typically, estrous cycles repeat until death. These cycles are widely variable in duration and frequency depending on the species. Some animals may display bloody vaginal discharge, often mistaken for menstruation. Many mammals used in commercial agriculture, such as cattle and sheep, may have their estrous cycles artificially controlled with hormonal medications for optimum productivity. Naturally, estrous cycles are complemented by a rutting period of male counterparts within a species.

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Hypothalamic–pituitary–gonadal axis

The hypothalamic–pituitary–gonadal axis refers to the hypothalamus, pituitary gland, and gonadal glands as if these individual endocrine glands were a single entity. Because these glands often act in concert, physiologists and endocrinologists find it convenient and descriptive to speak of them as a single system.

Gonadotropin-releasing hormone agonist Drug class affecting sex hormones

A gonadotropin-releasing hormone agonist is a type of medication which affects gonadotropins and sex hormones. They are used for a variety of indications including in fertility medicine and to lower sex hormone levels in the treatment of hormone-sensitive cancers such as prostate cancer and breast cancer, certain gynecological disorders like heavy periods and endometriosis, high testosterone levels in women, early puberty in children, as a part of transgender hormone therapy, and to delay puberty in transgender youth among other uses. GnRH agonists are given by injections into fat, as implants placed into fat, and as nasal sprays.

The gonadotropin-releasing hormone receptor (GnRHR), also known as the luteinizing hormone releasing hormone receptor (LHRHR), is a member of the seven-transmembrane, G-protein coupled receptor (GPCR) family. It is the receptor of gonadotropin-releasing hormone (GnRH). The GnRHR is expressed on the surface of pituitary gonadotrope cells as well as lymphocytes, breast, ovary, and prostate.

Kisspeptin

Kisspeptins are proteins encoded by the KISS1 gene in humans. Kisspeptins are ligands of the G-protein coupled receptor, GPR54. Kiss1 was originally identified as a human metastasis suppressor gene that has the ability to suppress melanoma and breast cancer metastasis. Kisspeptin-GPR54 signaling has an important role in initiating secretion of gonadotropin-releasing hormone (GnRH) at puberty, the extent of which is an area of ongoing research. Gonadotropin-releasing hormone is released from the hypothalamus to act on the anterior pituitary triggering the release of luteinizing hormone (LH), and follicle stimulating hormone (FSH). These gonadotropic hormones lead to sexual maturation and gametogenesis. Disrupting GPR54 signaling can cause hypogonadotrophic hypogonadism in rodents and humans. The Kiss1 gene is located on chromosome 1. It is transcribed in the brain, adrenal gland, and pancreas.

Controlled ovarian hyperstimulation is a technique used in assisted reproduction involving the use of fertility medications to induce ovulation by multiple ovarian follicles. These multiple follicles can be taken out by oocyte retrieval for use in in vitro fertilisation (IVF), or be given time to ovulate, resulting in superovulation which is the ovulation of a larger-than-normal number of eggs, generally in the sense of at least two. When ovulated follicles are fertilised in vivo, whether by natural or artificial insemination, there is a very high risk of a multiple pregnancy.

Functional hypothalamic amenorrhea (FHA) is a form of amenorrhea and chronic anovulation and is one of the most common types of secondary amenorrhea. It is classified as hypogonadotropic hypogonadism. It was previously known as "juvenile hypothalamosis syndrome," prior to the discovery that sexually mature females are equally affected. FHA has multiple risk factors, with links to stress-related, weight-related, and exercise-related factors. FHA is caused by stress-induced suppression of the hypothalamic-pituitary-ovarian (HPO) axis, which results in inhibition of gonadotropin-releasing hormone (GnRH) secretion, and gonadotropins, follicle-stimulating hormone (FSH) and luteinizing hormone (LH). Severe and potentially prolonged hypoestrogenism is perhaps the most dangerous hormonal pathology associated with the disease, because consequences of this disturbance can influence bone health, cardiovascular health, mental health, and metabolic functioning in both the short and long-term. Because many of the symptoms overlap with those of organic hypothalamic, pituitary, or gonadal disease and therefore must be ruled out, FHA is a diagnosis of exclusion; "functional" is used to indicate a behavioral cause, in which no anatomical or organic disease is identified, and is reversible with correction of the underlying cause. Diagnostic workup includes a detailed history and physical, laboratory studies, such as a pregnancy test, and serum levels of FSH and LH, prolactin, and thyroid-stimulating hormone (TSH), and imaging. Additional tests may be indicated in order to distinguish FHA from organic hypothalamic or pituitary disorders. Patients present with a broad range of symptoms related to severe hypoestrogenism as well as hypercortisolemia, low serum insulin levels, low serum insulin-like growth factor 1 (IGF-1), and low total triiodothyronine (T3). Treatment is primarily managing the primary cause of the FHA with behavioral modifications. While hormonal-based therapies are potential treatment to restore menses, weight gain and behavioral modifications can have an even more potent impact on reversing neuroendocrine abnormalities, preventing further bone loss, and re-establishing menses, making this the recommended line of treatment. If this fails to work, secondary treatment is aimed at treating the effects of hypoestrogenism, hypercortisolism, and hypothyroidism.

Gonadotropin-releasing hormone (GnRH) insensitivity also known as Isolated gonadotropin-releasing hormone (GnRH)deficiency (IGD) is a rare autosomal recessive genetic and endocrine syndrome which is characterized by inactivating mutations of the gonadotropin-releasing hormone receptor (GnRHR) and thus an insensitivity of the receptor to gonadotropin-releasing hormone (GnRH), resulting in a partial or complete loss of the ability of the gonads to synthesize the sex hormones. The condition manifests itself as isolated hypogonadotropic hypogonadism (IHH), presenting with symptoms such as delayed, reduced, or absent puberty, low or complete lack of libido, and infertility, and is the predominant cause of IHH when it does not present alongside anosmia.

Hypogonadotropic hypogonadism (HH), is due to problems with either the hypothalamus or pituitary gland affecting the hypothalamic-pituitary-gonadal axis. Hypothalamic disorders result from a deficiency in the release of gonadotropic releasing hormone (GnRH), while pituitary gland disorders are due to a deficiency in the release of gonadotropins from the anterior pituitary. GnRH is the central regulator in reproductive function and sexual development via the HPG axis. GnRH is released by GnRH neurons, which are hypothalamic neuroendocrine cells, into the hypophyseal portal system acting on gonadotrophs in the anterior pituitary. The release of gonadotropins, LH and FSH, act on the gonads for the development and maintenance of proper adult reproductive physiology. LH acts on Leydig cells in the male testes and theca cells in the female. FSH acts on Sertoli cells in the male and follicular cells in the female. Combined this causes the secretion of gonadal sex steroids and the initiation of folliculogenesis and spermatogenesis. The production of sex steroids forms a negative feedback loop acting on both the anterior pituitary and hypothalamus causing a pulsatile secretion of GnRH. GnRH neurons lack sex steroid receptors and mediators such as kisspeptin stimulate GnRH neurons for pulsatile secretion of GnRH.

Pulsatile secretion is a biochemical phenomenon observed in a wide variety of cell and tissue types, in which chemical products are secreted in a regular temporal pattern. The most common cellular products observed to be released in this manner are intercellular signaling molecules such as hormones or neurotransmitters. Examples of hormones that are secreted pulsatilely include insulin, thyrotropin, TRH, gonadotropin-releasing hormone (GnRH) and growth hormone (GH). In the nervous system, pulsatility is observed in oscillatory activity from central pattern generators. In the heart, pacemakers are able to work and secrete in a pulsatile manner. A pulsatile secretion pattern is critical to the function of many hormones in order to maintain the delicate homeostatic balance necessary for essential life processes, such as development and reproduction. Variations of the concentration in a certain frequency can be critical to hormone function, as evidenced by the case of GnRH agonists, which cause functional inhibition of the receptor for GnRH due to profound downregulation in response to constant (tonic) stimulation. Pulsatility may function to sensitize target tissues to the hormone of interest and upregulate receptors, leading to improved responses. This heightened response may have served to improve the animal's fitness in its environment and promote its evolutionary retention.

Gonadotropin-releasing hormone modulator

A GnRH modulator, or GnRH receptor modulator, also known as an LHRH modulator or LHRH receptor modulator, is a type of medication which modulates the GnRH receptor, the biological target of the hypothalamic hormone gonadotropin-releasing hormone. They include GnRH agonists and GnRH antagonists. These medications may be GnRH analogues like leuprorelin and cetrorelix – peptides that are structurally related to GnRH – or small-molecules like elagolix and relugolix, which are structurally distinct from and unrelated to GnRH analogues.

Gonadotropin surge-attenuating factor (GnSAF) is a nonsteroidal ovarian hormone produced by the granulosa cells of small antral ovarian follicles in females. GnSAF is involved in regulating the secretion of luteinizing hormone (LH) from the anterior pituitary and the ovarian cycle. During the early to mid-follicular phase of the ovarian cycle, GnSAF acts on the anterior pituitary to attenuate LH release, limiting the secretion of LH to only basal levels. At the transition between follicular and luteal phase, GnSAF bioactivity declines sufficiently to permit LH secretion above basal levels, resulting in the mid-cycle LH surge that initiates ovulation. In normally ovulating women, the LH surge only occurs when the oocyte is mature and ready for extrusion. GnSAF bioactivity is responsible for the synchronised, biphasic nature of LH secretion.

Kisspeptin, neurokinin B, and dynorphin (KNDy) neurons are neurons in the hypothalamus of the brain that are central to the hormonal control of reproduction.

Gonadotropin-inhibitory hormone (GnIH) is a RFamide-related peptide coded by the NPVF gene in mammals.

References

  1. ↑ Prendergast BJ (2005). "Internalization of seasonal time". Horm. Behav. 48 (5): 503–11. doi:10.1016/j.yhbeh.2005.05.013. PMID   16026787. S2CID   24785237.
  2. ↑ Johnson, A.D. (1970). Development, Anatomy, and Physiology. Academic Press. ISBN   0-12-386601-4.
  3. 1 2 M. N. Lehman; R. L. Goodman; F. J. Karsch; G. L. Jackson; S. J. Berriman; H. T. Jansen (1997). "The GnRH System of Seasonal Breeders: Anatomy and Plasticity". Brain Res. Bull. 44 (4): 445–57. doi:10.1016/S0361-9230(97)00225-6. PMID   9370210. S2CID   29049687.
  4. ↑ Williams, Cory T.; Klaassen, Marcel; Barnes, Brian M.; Buck, C. Loren; Arnold, Walter; Giroud, Sylvain; Vetter, Sebastian G.; Ruf, Thomas (2017). "Seasonal reproductive tactics: annual timing and the capital-to-income breeder continuum". Philosophical Transactions of the Royal Society B: Biological Sciences. 372 (1734): 20160250. doi:10.1098/rstb.2016.0250. ISSN   0962-8436. PMC   5647277 . PMID   28993494.
  5. ↑ "An Overview of the Hypothalamus". EndocrineWeb. Retrieved 2017-01-26.
  6. ↑ L. Senger, Phillip (2005). Pathways to Pregnancy and Parturition (2nd Revised ed.). p.  154.
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