scholarly journals Vasopressin gene products are colocalised with corticotrophin‐releasing factor within neurosecretory vesicles in the external zone of the median eminence of the Japanese macaque monkey ( Macaca fuscata )

2020 ◽  
Vol 32 (8) ◽  
Author(s):  
Akito Otubo ◽  
Natsuko Kawakami ◽  
Sho Maejima ◽  
Yasumasa Ueda ◽  
John F. Morris ◽  
...  
Keyword(s):  
Median Eminence ◽  
Macaca Fuscata ◽  
Japanese Macaque ◽  
Macaque Monkey ◽  
Gene Products ◽  
External Zone ◽  
Corticotrophin Releasing Factor ◽  
Vasopressin Gene

Molecular histology of spermatogenesis in the Japanese macaque monkey (Macaca fuscata)

Primates ◽  
2020 ◽  
Author(s):  
Sawako Okada ◽  
Kota Kuroki ◽  
Cody A. Ruiz ◽  
Anthony J. Tosi ◽  
Masanori Imamura
Keyword(s):  
Macaca Fuscata ◽  
Japanese Macaque ◽  
Macaque Monkey

scholarly journals Spontaneous Peritoneal Malignant Mesothelioma in a Geriatric Japanese Macaque (Macaca fuscata)

2007 ◽  
Vol 56 (2) ◽  
pp. 155-159 ◽  
Author(s):  
Jyoji YAMATE ◽  
Akitada TOMITA ◽  
Mitsuru KUWAMURA ◽  
Fusako MITSUNAGA ◽  
Shin NAKAMURA
Keyword(s):  
Malignant Mesothelioma ◽  
Macaca Fuscata ◽  
Japanese Macaque

Mother to Fetus Transfer of Hydroxylated Polychlorinated Biphenyl Congeners (OH-PCBs) in the Japanese Macaque (Macaca fuscata): Extrapolation of Exposure Scenarios to Humans

2020 ◽  
Vol 54 (18) ◽  
pp. 11386-11395
Author(s):  
Kei Nomiyama ◽  
Yusuke Tsujisawa ◽  
Emiko Ashida ◽  
Syuji Yachimori ◽  
Akifumi Eguchi ◽  
...  
Keyword(s):  
Macaca Fuscata ◽  
Polychlorinated Biphenyl ◽  
Japanese Macaque

scholarly journals Asbestosis in a Japanese Macaque (Macaca fuscata)

2015 ◽  
Vol 43 (7) ◽  
pp. 1035-1039
Author(s):  
Kosuke Tsugo ◽  
Akane Kashimura ◽  
Yumi Une
Keyword(s):  
Macaca Fuscata ◽  
Japanese Macaque

scholarly journals Acute hypoxia activates neuroendocrine, but not presympathetic, neurons in the paraventricular nucleus of the hypothalamus: differential role of nitric oxide

2017 ◽  
Vol 312 (6) ◽  
pp. R982-R995 ◽  
Author(s):  
K. Max Coldren ◽  
De-Pei Li ◽  
David D. Kline ◽  
Eileen M. Hasser ◽  
Cheryl M. Heesch
Keyword(s):  
Nitric Oxide ◽  
Paraventricular Nucleus ◽  
Median Eminence ◽  
Nucleus Tractus Solitarius ◽  
Acute Hypoxia ◽  
Ventrolateral Medulla ◽  
Specific Cell ◽  
External Zone ◽  
Cell Phenotypes

Hypoxia results in decreased arterial Po2, arterial chemoreflex activation, and compensatory increases in breathing, sympathetic outflow, and neuroendocrine secretions, including increased secretion of AVP, corticotropin-releasing hormone (CRH), adrenocorticotropin hormone (ACTH), and corticosterone. In addition to a brain stem pathway, including the nucleus tractus solitarius (nTS) and the rostral ventrolateral medulla (RVLM), medullary pathways to the paraventricular nucleus of the hypothalamus (PVN) contribute to chemoreflex responses. Experiments evaluated activation of specific cell phenotypes within the PVN following an acute hypoxic stimulus (AH; 2 h, 10% O2) in conscious rats. Retrograde tracers (from spinal cord and RVLM) labeled presympathetic (PreS) neurons, and immunohistochemistry identified AVP- and CRH-immunoreactive (IR) cells. c-Fos-IR was an index of neuronal activation. Hypoxia activated AVP-IR (~6%) and CRH-IR (~15%) cells, but not PreS cells in the PVN, suggesting that sympathoexcitation during moderate AH is mediated mainly by a pathway that does not include PreS neurons in the PVN. Approximately 14 to 17% of all PVN cell phenotypes examined expressed neuronal nitric oxide synthase (nNOS-IR). AH activated only nNOS-negative AVP-IR neurons. In contrast ~23% of activated CRH-IR neurons in the PVN contained nNOS. In the median eminence, CRH-IR terminals were closely opposed to tanycyte processes and end-feet (vimentin-IR) in the external zone, where vascular NO participates in tanycyte retraction to facilitate neuropeptide secretion into the pituitary portal circulation. Results are consistent with an inhibitory role of NO on AVP and PreS neurons in the PVN and an excitatory role of NO on CRH secretion in the PVN and median eminence.

Mechanism of restoration of ACTH release in rats with long-term lesions of the paraventricular nuclei

1986 ◽  
Vol 111 (1) ◽  
pp. 75-82 ◽  
Author(s):  
J. Dohanics ◽  
G. Kapócs ◽  
T. Janáky ◽  
J. Z. Kiss ◽  
G. Rappay ◽  
...  
Keyword(s):  
Median Eminence ◽  
Plasma Concentrations ◽  
Plasma Acth ◽  
Corticotrophin Releasing Factor ◽  
Paraventricular Nuclei ◽  
Basal Plasma ◽  
Corticosterone Response ◽  
Intact Rats ◽  
Acth Release

ABSTRACT The effects of lesions in the paraventricular nucleus (PVN) on the adrenocortical response to ether stress were investigated in neurohypophysectomized and intact rats. During the first 4 days after placement of lesions in the PVN, the corticosterone response to ether stress was almost completely inhibited. It then gradually increased and, within 4–6 weeks of surgery, was restored to about 60% of that in sham-operated rats. Basal plasma concentrations of corticosterone were low in rats after placement of lesions in the PVN and/or after neurointermediate lobectomy (NILX). Corticosterone responses to ether stress were similar in groups submitted to PVN lesions and/or NILX, and lower than those in the appropriate sham-operated groups. In all lesioned groups, plasma ACTH concentrations after a combination of stressors (ether plus laparotomy) were also lower than those in the sham-operated groups. Six weeks after lesioning of the PVN, immunoreactive rat corticotrophin-releasing factor-41 (rCRF-41) concentrations in stalk-median eminence (SME) extract fell to about 5% of that in sham-operated rats, while immunoreactive arginine vasopressin (AVP) concentrations did not change. Immunohistochemistry revealed a substantial decrease in rCRF-41 immunostaining of the median eminence 6 weeks after lesioning of the PVN, though randomly located clusters of stained terminals were still seen in the whole rostro-caudal extent of the median eminence. A mixture containing synthetic rCRF-41 and AVP, in proportions similar to those in SME extracts from sham-operated rats, caused significantly less release of ACTH from anterior pituitary cell cultures than did SME extracts from sham-operated rats. Extracts of SME from PVN-lesioned rats released as much ACTH as a mixture containing synthetic rCRF-41 and AVP in proportions similar to those in the SME extracts from PVN-lesioned rats. Extracts of SME from either PVN-lesioned or sham-operated rats did not cause a significant increase in the amount of ACTH released when preincubated with antisera to both rCRF-41 and AVP. It is suggested that (1) the restoration of the adrenocortical reponse to ether stress, evident within a few days of placement of lesions in the PVN, occurs independently of neurohypophysial function; (2) the full corticosterone and ACTH response to ether or ether plus laparotomy stress requires not only an intact PVN but also an intact neurointermediate lobe; (3) SME extracts from sham-operated rats contain a factor(s) with the ability to potentiate the ACTHreleasing effect of rCRF-41 and AVP; and (4) the ACTH-releasing activity of SME extract obtained from rats with long-term PVN lesions is probably due to its remaininJ content of rCRF-41 and AVP. J. Endocr. (1986) 111, 75–82

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