Cloning of corticotropin-releasing hormone (CRH) precursor cDNA and immunohistochemical detection of CRH peptide in the brain of the Japanese eel, paying special attention to gonadotropin-releasing hormone

2014 ◽  
Vol 356 (1) ◽  
pp. 243-251 ◽  
Author(s):  
Masafumi Amano ◽  
Nanami Mizusawa ◽  
Kataaki Okubo ◽  
Noriko Amiya ◽  
Kanta Mizusawa ◽  
...  
2016 ◽  
Vol 236 ◽  
pp. 174-180 ◽  
Author(s):  
Masafumi Amano ◽  
Noriko Amiya ◽  
Takehiko Yokoyama ◽  
Kengo Onikubo ◽  
Naoyuki Yamamoto ◽  
...  

1994 ◽  
Vol 72 (1) ◽  
pp. 48-53 ◽  
Author(s):  
Glenda M. Wright ◽  
Kim M. McBurney ◽  
John H. Youson ◽  
Stacia A. Sower

Lamprey gonadotropin-releasing hormone was demonstrated in the brains of larval, metamorphic, and adult sea lampreys, Petromyzon marinus, using an immunoperoxidase technique. Gonadotropin-releasing hormone was observed in the neurohypophysis and preoptic area of the brain of larval, metamorphic, juvenile, and prespawning adults. The occurrence of immunoreactive cells and the intensity of the immunostaining was lowest in larvae, but by stage 5 of metamorphosis there was a marked increase in the prevalence and staining of these cells, which continued into adults. In larvae and lampreys in metamorphic stages 1–4, most immunoreactive fibres were confined to the dorsal region of the neurohypophysis. During stage 5 there was an expansion of immunopositive fibres into the ventral portion of the neurohypophysis. Prominent immunoreactivity was observed throughout the neurohypophysis from stage 5 onward through the adult stages. Changes in immunoreactivity of these cells and fibres in the brain and neurohypophysis correlate well with increased concentrations of hormone in the brain during development and with the timing of presumed changes in activity of cells in the adenohypophysis during metamorphosis.


2020 ◽  
Author(s):  
Aaron Lanz ◽  
Grant Gordon ◽  
Jaideep Bains

AbstractChloride (Cl-) dynamics shape inhibitory neurotransmission in the brain. In the hypothalamus, GABA signalling onto corticotropin-releasing hormone (CRHPVN) neurons can switch from inhibitory to excitatory during stress. Although Cl- fluctuations mediate this stress-dependent shift in GABA signalling, the underlying Cl- dynamics are poorly understood. Here, using a novel optogenetic strategy to load intracellular Cl- using halorhodopsin, we demonstrate that KCC2 rapidly restores Cl- setpoints in CRHPVN neurons from naïve animals, but that this process is slowed following stress. Further, we report that somatic Cl- homeostasis remains intact after stress. Our results strongly support the idea that KCC2 functions primarily to maintain Cl- setpoints and that inhibitory synapses onto dendritic and somatic compartments of CRHPVN neurons are differentially regulated during stress.


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