Pulsatile Gonadotropin-Releasing Hormone (GnRH) Secretion Is an Inherent Function of GnRH Neurons, as Revealed by the Culture of Medial Olfactory Placode Obtained from Embryonic Rats

2000 ◽  
Vol 71 (2) ◽  
pp. 138-144 ◽  
Author(s):  
Toshiya Funabashi ◽  
Shigeo Daikoku ◽  
Kazuyuki Shinohara ◽  
Fukuko Kimura
Keyword(s):  
Gonadotropin Releasing Hormone ◽  
Releasing Hormone ◽  
Olfactory Placode ◽  
Gnrh Secretion ◽  
Gnrh Neurons

scholarly journals Neonatal Immunization against Gonadotropin-Releasing Hormone (GnRH) Results in Diminished GnRH Secretion in Adulthood

Endocrinology ◽  
1998 ◽  
Vol 139 (4) ◽  
pp. 2007-2014 ◽  
Author(s):  
I. J. Clarke ◽  
B. W. Brown ◽  
V. V. Tran ◽  
C. J. Scott ◽  
R. Fry ◽  
...  
Keyword(s):  
Gonadotropin Releasing Hormone ◽  
Releasing Hormone ◽  
Gnrh Secretion

scholarly journals Effect of Inflammation on Female Gonadotropin-Releasing Hormone (GnRH) Neurons: Mechanisms and Consequences

2020 ◽  
Vol 21 (2) ◽  
pp. 529 ◽  
Author(s):  
Klaudia Barabás ◽  
Edina Szabó-Meleg ◽  
István M. Ábrahám
Keyword(s):  
Suppressive Effect ◽  
Gonadotropin Releasing Hormone ◽  
Releasing Hormone ◽  
Inflammatory Signals ◽  
Cholinergic Pathway ◽  
Gnrh Neurons ◽  
Functional Consequences ◽  
Anti Inflammatory ◽  
The Impact

Inflammation has a well-known suppressive effect on fertility. The function of gonadotropin-releasing hormone (GnRH) neurons, the central regulator of fertility is substantially altered during inflammation in females. In our review we discuss the latest results on how the function of GnRH neurons is modified by inflammation in females. We first address the various effects of inflammation on GnRH neurons and their functional consequences. Second, we survey the possible mechanisms underlying the inflammation-induced actions on GnRH neurons. The role of several factors will be discerned in transmitting inflammatory signals to the GnRH neurons: cytokines, kisspeptin, RFamide-related peptides, estradiol and the anti-inflammatory cholinergic pathway. Since aging and obesity are both characterized by reproductive decline our review also focuses on the mechanisms and pathophysiological consequences of the impact of inflammation on GnRH neurons in aging and obesity.

scholarly journals Firing patterns of gonadotropin-releasing hormone neurons are sculpted by their biologic state

2020 ◽  
Vol 7 (8) ◽  
pp. 201040
Author(s):  
Jonathon Penix ◽  
R. Anthony DeFazio ◽  
Eden A. Dulka ◽  
Santiago Schnell ◽  
Suzanne M. Moenter
Keyword(s):  
Action Potential ◽  
Polycystic Ovary ◽  
Brain Slices ◽  
Gonadotropin Releasing Hormone ◽  
Neuron Activity ◽  
Interval Order ◽  
Short Term ◽  
Firing Patterns ◽  
Releasing Hormone ◽  
Gnrh Neurons

Gonadotropin-releasing hormone (GnRH) neurons form the final pathway for the central neuronal control of fertility. GnRH is released in pulses that vary in frequency in females, helping drive hormonal changes of the reproductive cycle. In the common fertility disorder polycystic ovary syndrome (PCOS), persistent high-frequency hormone release is associated with disrupted cycles. We investigated long- and short-term action potential patterns of GnRH neurons in brain slices before and after puberty in female control and prenatally androgenized (PNA) mice, which mimic aspects of PCOS. A Monte Carlo (MC) approach was used to randomize action potential interval order. Dataset distributions were analysed to assess (i) if organization persists in GnRH neuron activity in vitro , and (ii) to determine if any organization changes with development and/or PNA treatment. GnRH neurons in adult control, but not PNA, mice produce long-term patterns different from MC distributions. Short-term patterns differ from MC distributions before puberty but become absorbed into the distributions with maturation, and the distributions narrow. These maturational changes are blunted by PNA treatment. Firing patterns of GnRH neurons in brain slices thus maintain organization dictated at least in part by the biologic status of the source and are disrupted in models of disease.

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