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Neurokinin 3 receptor-selective agonist, senktide, decreases core temperature in Japanese Black cattle.
Domestic Animal Endocrinology ( IF 1.9 ) Pub Date : 2020-07-28 , DOI: 10.1016/j.domaniend.2020.106522
S Nakamura 1 , M Miwa 2 , Y Morita 3 , S Ohkura 3 , T Yamamura 4 , Y Wakabayashi 5 , S Matsuyama 6
Affiliation  

Heat stress disrupts reproductive function in cattle. In summer, high ambient temperature and humidity elevate core body temperature, which is considered to be detrimental to reproductive abilities in cattle. Neurokinin B (NKB) is a factor that generates pulsatile GnRH and subsequent LH secretion in mammals. Recent studies have reported that NKB-neurokinin 3 receptor (NK3R) signaling is associated with heat-defense responses in rodents. The present study aimed to clarify the role of NKB-NK3R signaling in thermoregulation in cattle. We examined the effects of an NK3R-selective agonist, senktide, on vaginal temperature as an indicator of core body temperature in winter and summer. In both seasons, continuous infusion of senktide for 4 h immediately decreased vaginal temperature, and the mean temperature change in the senktide-treated group was significantly lower than that of both vehicle- and GnRH-treated groups. Administration of GnRH induced LH elevation, but there was no significant difference in vaginal temperature change between GnRH- and vehicle-treated groups. Moreover, we investigated the effects of senktide on ovarian temperature. Senktide treatment seemed to suppress the increase in ovarian temperature from 2 h after the beginning of administration, although the difference between groups was not statistically significant. Taken together, these results suggest that senktide infusion caused a decline in the vaginal temperature of cattle, in both winter and summer seasons, and this effect was not due to the gonadotropin-releasing action of senktide. These findings provide new therapeutic options for senktide to support both heat-defense responses and GnRH/LH pulse generation.



中文翻译:

神经激肽 3 受体选择性激动剂 senktide 可降低日本黑牛的核心温度。

热应激会破坏牛的生殖功能。夏季,高环境温度和湿度会升高核心体温,这被认为不利于牛的繁殖能力。神经激肽 B (NKB) 是一种在哺乳动物中产生脉动 GnRH 和随后 LH 分泌的因子。最近的研究报告称,NKB-神经激肽 3 受体 (NK3R) 信号传导与啮齿动物的热防御反应有关。本研究旨在阐明 NKB-NK3R 信号在牛体温调节中的作用。我们研究了 NK3R 选择性激动剂 senktide 对作为冬季和夏季核心体温指标的阴道温度的影响。在两个季节,连续输注森克肽 4 小时都会立即降低阴道温度,senktide 治疗组的平均温度变化显着低于载体和 GnRH 治疗组。GnRH 的给药诱导 LH 升高,但 GnRH 治疗组和载体治疗组之间的阴道温度变化没有显着差异。此外,我们研究了senktide对卵巢温度的影响。Senktide 治疗似乎从给药开始后 2 小时起抑制了卵巢温度的升高,尽管组间差异无统计学意义。综上所述,这些结果表明,在冬季和夏季,森克肽输注导致牛的阴道温度下降,这种影响不是由于森克肽的促性腺激素释放作用。

更新日期:2020-07-28
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