Physiological characteristics of gastric contractions and circadian gastric motility in the free-moving conscious house musk shrew (Suncus murinus). Am J Physiol Regul Integr Comp Physiol 299: R1106 -R1113, 2010. First published August 4, 2010 doi:10.1152/ajpregu.00278.2010.-Although many studies have demonstrated the physiological action of motilin on the migrating motor complex, the precise mechanisms remain obscure. To obtain new insights into the mechanisms, we focused on the house musk shrew (Suncus murinus, suncus used as a laboratory name) as a small model animal for in vivo motilin study, and we studied the physiological characteristics of suncus gastrointestinal motility. Strain gauge transducers were implanted on the serosa of the gastric body and duodenum, and we recorded gastrointestinal contractions in the free-moving conscious suncus and also examined the effects of intravenous infusion of various agents on gastrointestinal motility. During the fasted state, the suncus stomach and duodenum showed clear migrating phase III contractions (intervals of 80 -150 min) as found in humans and dogs. Motilin (bolus injection, 100-300 ng/kg; continuous infusion, 10-100 ng · kg Ϫ1 · min Ϫ1 ) and erythromycin (80 g·kg Ϫ1 · min Ϫ1 ) induced gastric phase III contractions, and motilin injection also increased the gastric motility index in a dose-dependent manner (P Ͻ 0.05, vs. saline). Pretreatment with atropine completely abolished the motilin-induced gastric phase III contractions. On the other hand, in the free-feeding condition, the suncus showed a relatively long fasting period in the light phase followed by spontaneous gastric phase III contractions. The results suggest that the suncus has almost the same gastrointestinal motility and motilin response as those found in humans and dogs, and we propose the suncus as a new small model animal for studying gastrointestinal motility and motilin in vivo.suncus; migrating motor complex; motilin; ghrelin; gastric motility DURING A FASTED STATE, THE stomach and small intestine undergo a temporally coordinated cyclic motor pattern known as migrating motor complex (MMC) in dogs (38) and humans (44). It has been established that these coordinated contractions consist of three phases, phase I (period of motor quiescence), phase II (period of preceding irregular contractions), and phase III (period of clustered potent contractions), and the MMC is stimulated by endogenous motilin that is released in the fasted state.Motilin was originally purified from porcine intestinal mucosa in the 1970s, and its molecular structure was determined to be a 22-amino-acid polypeptide. It has been demonstrated that plasma motilin is released at ϳ100-min intervals at the interdigestive state (20,21). Physiological study of motilin in vivo has been mainly performed by using dogs and humans, and endogenous motilin and exogenous motilin have been shown to induce phase III contractions through the cholinergic pathway because atropine pretreatment completely abolished the motilin-induced contra...
Thyroid-stimulating hormone (TSH)-producing cells (TSH cells), which account for a large fraction of the cells in the rat pars tuberalis (PT), have been found to express MT1 melatonin receptor and mammalian clock genes at high densities. Although these findings suggest that TSH production in the rat PT is regulated by melatonin and/or the biological clock, there have been no studies focusing on the diurnal change and regulation mechanism of TSH production in the rat PT. Therefore, in the present study, we examined diurnal changes of in TSH beta and alpha-glycoprotein subunit (alpha GSU) mRNA expression and TSH immunoreactivity (-ir) in the rat PT, and also examined the relationship between melatonin and TSH production in vivo. Both TSH beta mRNA expression and alpha GSU mRNA expression in the PT showed diurnal variations: the expression levels were lowest at the light phase [Zeitgeber time (ZT)4] and high at the dark phase (ZT12 and ZT20). TSH-ir in the PT showed the lowest level at ZT4, as was found for mRNA expression. Interestingly, TSH-ir, which was confined to the Golgi apparatus at ZT4, spread to the cytoplasm, and most of the TSH cells in the PT were uniformly immunostained in the cytoplasm at ZT20. Despite the fact that chronic administration of melatonin suppressed TSH beta and alpha GSU mRNA expression, TSH-ir in the PT was significantly enhanced. These findings results clearly show that there are diurnal changes in TSH expression and accumulation in rat PT-TSH cells and suggest that these fluctuations are regulated by melatonin.
We investigated the role of macrophage colony-stimulating factor (M-CSF) in the pituitary gland to understand the effect of M-CSF on pituitary hormones and the relationship between the endocrine and immune systems. When we attempted to establish pituitary cell lines from a thyrotropic pituitary tumor (TtT), a macrophage cell line, TtT/M-87, was established. We evaluated M-CSF-like activity in conditioned media (CM) from seven pituitary cell lines using TtT/M-87 cells. TtT/M-87 proliferation significantly increased in the presence of CM from TtT/GF cells, a pituitary folliculostellate (FS) cell line. M-CSF mRNA was detected in TtT/GF and MtT/E cells by reverse transcriptase-polymerase chain reaction (RT-PCR), and its expression in TtT/GF cells was increased in a lipopolysaccharide (LPS) dose-dependent manner. M-CSF mRNA expression was also increased in rat anterior pituitary glands by LPS. M-CSF receptor (M-CSFR) mRNA was only detected in TtT/ M-87 cells and increased in the LPS-stimulated rat pituitary glands. In rat pituitary glands, M-CSF and M-CSFR were found to be localized in FS cells and prolactin (PRL)-secreting cells, respectively, by immunohistochemistry. The PRL concentration in rat sera was significantly increased at 24 h after M-CSF administration, and mRNA levels significantly increased in primary culture cells of rat anterior pituitary glands. In addition, TNF-α mRNA was increased in the primary culture cells by M-CSF. These results revealed that M-CSF was secreted from FS cells and M-CSF regulated PRL expression in rat pituitary glands.
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