Early postnatal development of electrophysiological and histological properties of sensory sural nerves in male rats that were maternally deprived and artificially reared: Role of tactile stimulation

2017 ◽  
Vol 78 (4) ◽  
pp. 351-362 ◽  
Author(s):  
Rene Zempoalteca ◽  
Mercedes G. Porras ◽  
Suelem Moreno-Pérez ◽  
Gabriela Ramirez-Funez ◽  
Elsa L. Aguirre-Benítez ◽  
...  
2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Hee Sook Bae ◽  
Yun-Kyeong Jin ◽  
Sangwoo Ham ◽  
Hee Kyoung Kim ◽  
Hyejung Shin ◽  
...  

AbstractThyroid hormone (TH) has long been believed to play a minor role in male reproduction. However, evidences from experimental model of thyrotoxicosis or hypothyroidism suggests its role in spermatogenesis. Cellular action of TH requires membrane transport via specific transporters such as monocarboxylate transporter 8 (MCT8). SLC16A2 (encodes for MCT8) inactivating mutation in humans can lead to Allan-Herndon Dudley-syndrome, a X-linked psychomotor and growth retardation. These patients present cryptorchidism which suggests a role of MCT8 during spermatogenesis. In this study, we found that Mct8 is highly expressed during early postnatal development and decreases its expression in the adulthood of testis of wild-type male rats. Histological analysis revealed that spermatogonia largely lacks MCT8 expression while spermatocytes and maturing spermatids highly express MCT8. To further understand the role of Mct8 during spermatogenesis, we generated Slc16a2 (encodes MCT8) knockout rats using CRISPR/Cas9. Serum THs (T3 and T4) level were significantly altered in Slc16a2 knockout rats when compared to wild-type littermates during early to late postnatal development. Unlike Slc16a2 knockout mice, Slc16a2 knockout rats showed growth delay during early to late postnatal development. In adult Slc16a2 knockout rats, we observed reduced sperm motility and viability. Collectively, our data unveil a functional involvement of MCT8 in spermatogenesis, underscoring the importance of TH signaling and action during spermatogenesis.


2019 ◽  
Vol 63 (2) ◽  
Author(s):  
Shule Hou ◽  
Jiarui Chen ◽  
Jun Yang

The Kölliker’s organ is a transient epithelial structure during cochlea development that gradually degenerates and disappears at postnatal 12-14 days (P12-14). While apoptosis has been shown to play an essential role in the degeneration of the Kölliker’s organ, the role of another programmed cell death, autophagy, remains unclear. In our study, autophagy markers including microtubule associated protein light chain 3-II (LC3-II), sequestosome 1 (SQSTM1/p62) and Beclin1 were detected in the supporting cells of the Kölliker’s organ through immunohistochemistry staining. In addition, Western blot and real-time PCR revealed a gradually decreased expression of LC3-II and an increased expression of p62 during early postnatal development. Compared to apoptosis markers that peaks between P7 and P10, autophagy flux peaked earlier at P1 and decreased from P1 to P14. By transmission electron microscopy, we observed representative autophagosome and autolysosome that packaged various organelles in the supporting cells of the Kölliker’s organ. During the degeneration, these organelles were digested via autophagy well ahead of the cellular apoptosis. These results suggest that autophagy plays an important role in transition and degeneration of the Kölliker’s organ prior to apoptosis during the early postnatal development.


2013 ◽  
Vol 218 (1) ◽  
pp. 117-124 ◽  
Author(s):  
Hiroto Kobayashi ◽  
Saori Yoshida ◽  
Ying-Jie Sun ◽  
Nobuyuki Shirasawa ◽  
Akira Naito

Gastric parietal cells synthesize and secrete estradiol-17β (E2) into gastric veins joining the portal vein, and a large amount of gastric E2first binds to its receptors in the liver. However, the role of the gastric E2is not entirely clear during postnatal development. The objective of this study was to reveal the onset of aromatase and other steroid-synthesizing enzymes in the gastric mucosa; to determine the period of rising E2levels in the portal vein; and to further understand the relationship between gastric E2and liver estrogen receptor α (ERα). The immunoblot bands and the immunohistochemistry of gastric mucosa revealed that aromatase protein began to express itself at 20 days and then increased in the levels of aromatase protein from 20 days onward. Expression of mRNAs for gastric aromatase (Cyp19a1) and other steroid-synthesizing enzymes, 17α-Hydroxylase (Cyp17a1) and 17β-hydroxysteroid dehydrogenase (HSD17b3), also increased similar to the increment of aromatase protein. Portal venous E2levels were elevated after 20 days and increased remarkably between 23 and 30 days, similar to gastric aromatase mRNA levels. The E2level was approximately three times higher at 40 days than that at 20 days. The liver weight andEsr1levels began to increase after 20 days and the increment was positively correlated with the change of portal venous E2levels. These findings suggest that some changes may occur around 20 days to regulate the gastric E2synthesis and secretion.


Haematologica ◽  
2016 ◽  
Vol 101 (4) ◽  
pp. e126-e128 ◽  
Author(s):  
Luigia De Falco ◽  
Mariasole Bruno ◽  
Ebru Yilmaz-Keskin ◽  
Ertan Sal ◽  
Mustafa Büyükavci ◽  
...  

Author(s):  
Karine Roversi ◽  
Carolina Buizza ◽  
Paola Brivio ◽  
Francesca Calabrese ◽  
Michel M. M. Verheij ◽  
...  

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Daria S. Kostyunina ◽  
Lin Zhang ◽  
Anastasia A. Shvetsova ◽  
Ekaterina K. Selivanova ◽  
Olga S. Tarasova ◽  
...  

AbstractMembrane transporters and their functional contribution in vasculature change during early postnatal development. Here we tested the hypothesis that the contribution of Cl− channels to arterial contraction declines during early postnatal development and this decline is associated with the trophic sympathetic influence. Endothelium‐denuded saphenous arteries from 1- to 2-week-old and 2- to 3-month-old male rats were used. Arterial contraction was assessed in the isometric myograph, in some experiments combined with measurements of membrane potential. mRNA and protein levels were determined by qPCR and Western blot. Sympathectomy was performed by treatment with guanethidine from the first postnatal day until 8–9-week age. Cl− substitution in the solution as well as Cl−-channel blockers (MONNA, DIDS) had larger suppressive effect on the methoxamine-induced arterial contraction and methoxamine-induced depolarization of smooth muscle cells in 1- to 2-week-old compared to 2- to 3-month-old rats. Vasculature of younger group demonstrated elevated expression levels of TMEM16A and bestrophin 3. Chronic sympathectomy increased Cl− contribution to arterial contraction in 2-month-old rats that was associated with an increased TMEM16A expression level. Our study demonstrates that contribution of Cl− channels to agonist-induced arterial contraction and depolarization decreases during postnatal development. This postnatal decline is associated with sympathetic nerves development.


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