@article{MTMT:1637689,
	title = {Estrogen-induced hypothalamic synaptic plasticity and pituitary sensitization in the control of the estrogen-induced gonadotrophin surge},
	url = {https://m2.mtmt.hu/api/publication/1637689},
	author = {Naftolin, F and Garcia-Segura, LM and Horvath, TL and Zsarnovszky, Attila and Demir, N and Fadiel, A and Leranth, C and Vondracek-Klepper, S and Lewis, C and Chang, A and Párducz, Árpád},
	doi = {10.1177/1933719107301059},
	journal-iso = {REPROD SCI},
	journal = {REPRODUCTIVE SCIENCES},
	volume = {14},
	unique-id = {1637689},
	issn = {1933-7191},
	abstract = {Proper gonadal function requires coordinated (feedback) interactions between the gonads, adenohypophysis, and brain: the gonads elaborate sex steroids (progestins, androgens, and estrogens) and proteins (inhibin-activin family) during gamete development. In both sexes, the brain-pituitary gonadotrophin-regulating interaction is coordinated by estradiol through its opposing actions on pituitary gonadotrophs (sensitization of the response to gonadotrophin-releasing hormone [GnRH]) versus hypothalamic neurons (inhibition of GnRH secretion). This dynamic tension between the gonadotrophs and the GnRH cells in the brain regulates the circulating gonadotrophins and is termed reciprocal/negative feedback. In females, reciprocal/negative feedback dominates similar to 90% of the ovarian cycle. In a spectacular exception, the dynamic tension is broken during the surge of circulating estrogen that marks follicle and oocyte(s) maturation. The cause is an estradiol-induced disinhibition of the GnRH neurons that releases GnRH secretion to the highly sensitized pituitary gonadotrophs that in turn release the gonadotrophin surge (the estrogen-induced gonadotrophin surge [EIGS], also known as positive feedback). Studies during the past 4 decades have shown this disinhibition to result from estrogen-induced synaptic plasticity (EISP), including a reversible similar to 50% loss in arcuate nucleus synapses. The disinhibited GnRH secretion occurs during maximal gonadotroph sensitization and results in the EIGS. Specific immunoneutralization of estradiol blocks the EISP and EIGS. The EISP is accompanied by increases in insulinlike growth factor 1, polysialylated neural cell adhesion molecule, and ezrin, 3 proteins that the authors believe are the links between estrogen-induced astroglial extension. and the EISP that releases GnRH secretion at the moment Of maximal sensitization of the pituitary gonadotrophs. The result is the paradoxical surge of gonadotrophins at the peak of ovarian estrogen secretion and the triggering of ovulation. This enhanced understanding of the mechanics of gonadotrophin control clarifies elements of the involved feedback loops and opens the way to a better understanding of the neurobiology of reproduction.},
	year = {2007},
	eissn = {1933-7205},
	pages = {101-116}
}

@article{MTMT:154106,
	title = {Neuroendocrine Asymmetry},
	url = {https://m2.mtmt.hu/api/publication/154106},
	author = {Gerendai, Ida and Halász, Béla},
	doi = {10.1006/frne.1997.0154},
	journal-iso = {FRONT NEUROENDOCRIN},
	journal = {FRONTIERS IN NEUROENDOCRINOLOGY},
	volume = {18},
	unique-id = {154106},
	issn = {0091-3022},
	abstract = {The information available at present clearly indicates that 
		asymmetry exists from the level of elementary particles to the 
		human cerebral cortex, the latest stage of evolution. Cerebral 
		lateralization is one of the well-known asymmetries. This paper 
		summarizes the data published in the past decades on the 
		asymmetry of the neuroendocrine system. The information on the 
		sided-differences between the gonads, adrenals, and thyroid 
		lobes and that on the lateralization of hypothalamic, limbic, 
		and other brain structures participating in the control of the 
		endocrine glands as well as relevant clinical observations are 
		reviewed here. The innervation of the peripheral endocrine 
		glands is also briefly summarized because the afferent and 
		efferent fibers of these glands may represent one part of the 
		pathway involved in neuroendocrine asymmetry. The data reviewed 
		clearly indicate that some kind of asymmetry (morphological, 
		biochemical, physiological, pathological) is evident at 
		different levels of the neuroendocrine system (at limbic, 
		hypothalamic, peripheral endocrine glands and their innervation) 
		and there are species, sex, and age differences. Most of the 
		information accumulated deals with the CNS-gonadal system. A 
		majority of the observations suggest that in both male and 
		female rats there is a predominance of the right half of brain 
		structures controlling gonadal function. The asymmetry, however, 
		is not restricted to CNS structures: it also exists at the level 
		of the gonads, including their innervation. It appears that the 
		characteristic pattern of the CNS-gonadal system becomes fixed 
		only after sexual maturation. Very few reports are available 
		suggesting some kind of asymmetry of the CNS-adrenal cortex and 
		the CNS-thyroid system. There are convincing findings consistent 
		with the view that in addition to the hypothalamo-
		adenohypophyseal system acting via the general circulation on 
		the peripheral endocrine glands, there is also a pure neural 
		link between the CNS and the gonads, the CNS and the adrenal 
		gland, and also between the CNS and the thyroid. This link 
		contains afferent and efferent pathways and is able to modulate 
		the functional activity or the responsiveness of the gland. It 
		may also serve as a neural reflex arc. It is assumed that the 
		neuroendocrine asymmetry expresses itself through (i) 
		hypophysiotrophic neurohormones and hormones of the peripheral 
		endocrine glands, (ii) neural pathways, or (iii) a combination 
		of (i) and (ii). The authors hope that this publication, in 
		addition to providing an overview, will also stimulate 
		research, both basic and clinical, in this exciting area of 
		neuroendocrinology.},
	year = {1997},
	eissn = {1095-6808},
	pages = {354-381}
}