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Regulation of Reproduction by Dopamine
Published in Nira Ben-Jonathan, Dopamine, 2020
The hypothalamus is a key player in the sex-specific control of reproductive hormone secretion and sexual behaviors. It is also a brain structure that contains nuclei with prominent gender-dependent differences in volume and morphology. As shown in Figure 10.2, notable examples are the sexually dimorphic nucleus of the preoptic area (SDN-POA), which is several times larger in males than in females, and the anteroventral periventricular nucleus (AVPN) which is larger in females [3]. In addition, the principle bed nucleus of the stria terminalis (PBNST), a part of the limbic system that is involved in stress-related behaviors, is denser in male brains. A list of neuroanatomical sex differences in the rat brain is presented in Table 10.1.
Problems with puberty and its onset
Published in David J Cahill, Practical Patient Management in Reproductive Medicine, 2019
While the trigger for the onset of puberty is still unclear, there is increasing knowledge about the peptides that control the secretion of GnRH by the arcuate nucleus (12). A group of neurones, the anteroventral periventricular nucleus – sited close to the lateral walls of the third ventricle in the preoptic area – and neurones in the arcuate nucleus release kisspeptin, a neuropeptide hormone, so named because it was first identified in Hershey, Pennsylvania, USA, the home of Hershey's Kisses (14). Receptors for kisspeptin (KISS1R), found in the anteroventral periventricular nucleus, seem to be as important as the hormone itself. Absence of the gene for the receptor has been linked with idiopathic hypogonadotrophic hypogonadism (15). Gamma-aminobutyric acid (GABA – suppressive) and glutamate (stimulatory) are also active at the anteroventral periventricular nucleus level, while at the arcuate nucleus, kisspeptin neurones also secrete neurokinin B and dynorphin A (Figure 1.4). Before puberty starts, dynorphin A has a dominant inhibitory influence. As puberty starts, neurokinin B increases in its stimulatory drive overcoming dynorphin A, allowing kisspeptin to become active and stimulatory as well (12). From this, it seems reasonable to speculate that whatever increases neurokinin B is the responsible factor for the initiation of the GnRH pulses.
Sexual Differentiation of Neuronal Circuitry in the Hypothalamus
Published in Akira Matsumoto, Sexual Differentiation of the Brain, 2017
Akira Matsumoto, Yoshie Sekine, Shizuko Murakami, Yasumasa Arai
Gorski et al.11 found an intensely staining neuron group with a striking sex difference in the rat medial preoptic area (POA) that is called the sexually dimorphic nucleus of the POA (SDN-POA). The sex difference in nuclear volume is due to the presence of a greater number of neurons in the SDN-POA of males than in that of females.13 Neonatal castration of males reduces the volume of the SDN-POA to a level comparable with that of females. Conversely, the nuclear volume of females is increased by exposure to androgen in the early postnatal period. The functional significance of the SDN-POA still remains unclear, but it is presumably concerned with the regulation of male sexual behavior.38 On the other hand, a sexually dimorphic cell group which is larger and more densely cellular in females than in males is identified in the periventricular gray of the POA just caudal to the Organum vasculosum of the lamina terminalis.39 This neuron group is called the anteroventral periventricular nucleus of the POA (AVPvN-POA). This structure is thought to play a critical role in regulating the cyclic release of pituitary gonadotropins in female rats.40 Its volume in female rats41 and guinea pigs42 is decreased by perinatal exposure to androgen. According to Weisz and Ward,43 plasma androgen titers are much higher in males than in females during the perinatal period. These results suggest that the sexual dimorphism in these nuclei is not determined genetically at birth, but rather is dependent on the perinatal sex steroid environment.
Systematic review of sex-based differences in opioid-based effects
Published in International Review of Psychiatry, 2018
Andrew S. Huhn, Meredith S. Berry, Kelly E. Dunn
A second study explored whether sex hormones influenced the expression of endogenous opioids. More specifically, in situ hybridization was utilized to examine whether gonadal hormone administration modified the number of proenkephalin and prodynorphin mRNA-containing neurons in the anteroventral periventricular nucleus (AVPv) of both developing and adult male and female rats (Simerly, 1991). Data suggested testosterone produced divergent effects in developing females; indeed, testosterone-treated females expressed more proenkephalin but fewer prodynorphin mRNA-containing neurons in the AVPv, relative to untreated females. Within the adult cohort, male rats expressed twice the amount of proenkephalin mRNA containing neurons in the AVPv than female mature rats at baseline. Administering oestradiol significantly increased prodynorphin mRNA levels in adult ovariectomized female rats, but no changes in prodynorphin or proenkephalin mRNA expression were observed in male rats that had been orchidectomized or administered testosterone.
The neuro control of the ovarain cycle – a hypothesis
Published in Gynecological Endocrinology, 2018
Besides the increasing E2 levels, the anteroventral periventricular nucleus receives afferent fibers from the suprachiasmatic nucleus, the location of circadian clock, which coordinates and provides precise timing for the LH surge (demonstrated in animals). With the beginning of the LH surge, the dominant follicle undergoes Meiosis 1, 36 h later it ruptures and releases the secondary oocyte.
Effects of dihydrotestosterone administration on the expression of reproductive and body weight regulatory factors in ovariectomized and estradiol-treated female rats
Published in Gynecological Endocrinology, 2018
Takeshi Iwasa, Toshiya Matsuzaki, Kiyohito Yano, Yiliyasi Mayila, Minoru Irahara
Whole hypothalamic explants were dissected from the frozen brains, as described previously [15]. Briefly, the target region of the brain was dissected out via an anterior coronal cut at the posterior border of the mammillary bodies, parasagittal cuts along the hypothalamic fissures, and a dorsal cut 2.5 mm from the ventral surface. Subsequently, the obtained brain tissue was divided into two blocks using coronal cuts at the posterior border of the optic chiasm. The anterior hypothalamic block contained the anteroventral periventricular nucleus (AVPV), and the posterior hypothalamic block contained the arcuate nucleus (ARC) [18]. Kisspeptin in the AVPV and ARC receives positive and negative feedback signals from estrogen, respectively [2]. Total RNA was isolated from the hypothalamic explants and visceral fat using a TRIzol® reagent kit (Invitrogen Co., Carlsbad, CA) and an RNeasy® mini kit (Qiagen Gmbh, Hilden, Germany). cDNA was synthesized with oligo (deoxythymidine) primers at 50 °C using the SuperScript III first-strand synthesis system for the real-time polymerase chain reaction (PCR; Invitrogen Co.). The PCR analysis was performed using the StepOnePlusTM real-time PCR system (PE Applied Biosystems, Foster City, CA) and FAST SYBR® green. The mRNA levels of neuropeptide Y (NPY), proopiomelanocortin (POMC), prepro-orexin (pporexin), Kiss1 (the gene encoding kisspeptin), Kiss1r, RFRP/GnIH (the gene encoding the kisspeptin receptor), and GPR147 in the posterior hypothalamus, and the Kiss1 mRNA levels of the anterior hypothalamus were measured. The mRNA expression level of each molecule was normalized to that of GAPDH. Dissociation curve analysis was also performed for each gene at the end of the PCR. Each amplicon generated a single peak. The primer sequences, product sizes, and annealing temperatures are shown in Table 1. The PCR conditions were as follows: initial denaturation and enzyme activation at 95 °C for 20 s, followed by 45 cycles of denaturation at 95 °C for 3 s, and annealing and extension for 30 s.