• Korean Journal of Veterinary Research
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• v.37 no.1
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• pp.9-13
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• 1997

The gastrointestinal endocrine cells of the African clawed toad, Xenopus laevis have been investigated immunohistochemically using the avidin-biotin method. Seven antisera were tested and three endocrine cell types immunoreacted with antisera to neurotensin, GRP and substance P. A moderate number of neurotensin-immunoreactive cells were weakly reacted in the small intestine. GRP-immunoreactive cells were mainly situated among the upper portion in the fundic glands, and the basal portion in the pyloric glands. These cells were oval and round in shape. On the other hand, in the intestine they were thin spindly cells with the epithelium. Substance P-immunoreactive cells were observed in among intestinal epithelium. However, no secretin-, motilin-, M-Enk- and PYY-immunoreactive cells were found in the GIT of the African clawed toads.

• The Korean Journal of Physiology and Pharmacology
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• v.9 no.4
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• pp.223-230
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• 2005

The purpose of the present study was to examine the effect of naltrexone, an opioid antagonist, on secretion of catecholamines (CA) evoked by cholinergic nicotinic stimulation and membrane-depolarization from the isolated perfused rat adrenal gland and to establish the mechanism of its action. Naltrexone $(3{\times}10^{-6}M)$ perfused into an adrenal vein for 60 min produced time-dependent inhibition in CA secretory responses evoked by ACh $(5.32{\times}10^{-3}M)$ , high $K^+$ $(5.6{\times}10^{-2}M)$ , DMPP ($10^{-4}$ M) and McN-A-343 $(10^{-4}M)$ . Naltrexone itself did also fail to affect basal CA output. In adrenal glands loaded with naltrexone $(3{\times}10^{-6}M)$ , the CA secretory responses evoked by Bay-K-8644, an activator of L-type $Ca^{2+}$ channels and cyclopiazonic acid, an inhibitor of cytoplasmic $Ca^{2+}-ATPase$, were also inhibited. However, in the presence of met-enkephalin $(5{\times}10^{-6}M)$ , a well-known opioid agonist, the CA secretory responses evoked by ACh, high $K^+$, DMPP, McN-A-343, Bay-K-8644 and cyclopiazonic acid were also significantly inhibited. Collectively, these experimental results demonstrate that naltrexone inhibits greatly CA secretion evoked by stimulation of cholinergic (both nicotinic and muscarinic) receptors as well as that by membrane depolarization. It seems that this inhibitory effect of naltrexone does not involve opioid receptors, but might be mediated by blocking both the calcium influx into the rat adrenal medullary chromaffin cells and the uptake of $Ca^{2+}$ into the cytoplasmic calcium store, which are at least partly relevant to the direct interaction with the nicotinic receptor itself.

• Archives of Pharmacal Research
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• v.28 no.6
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• pp.699-708
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• 2005

The present study was designed to investigate the effect of naloxone, a well known opioid antagonist, on the secretion of catecholamines (CA) evoked by cholinergic stimulation and membrane-depolarization in the isolated perfused rat adrenal glands, and to establish its mechanism of action. Naloxone ($10^{-6}\~10^{-5}$ M), perfused into an adrenal vein for 60 min, produced dose- and time-dependent inhibition of CA secretory responses evoked by ACh ($5.32\times10^{-3}$ M), high K+ ($5.6\times10^{-2}$ M), DMPP ($10^{-4}$ M) and McN-A-343 ($10^{-4}$ M). Naloxone itself also failed to affect the basal CA output. In adrenal glands loaded with naloxone ($3\times10^{-6}$ M), the CA secretory responses evoked by Bay-K-8644, an activator of L-type $Ca^{2+}$ channels, and cyclopiazonic acid, an inhibitor of cytoplasmic $Ca^{2+}$-ATPase, were also inhibited. In the presence of met-enkephalin ($5\times10^{-6}$ M), a well known opioid agonist, the CA secretory responses evoked by ACh, high $K^+$, DMPP, McN-A-343, Bay-K-8644 and cyclopiazonic acid were also significantly inhibited. Taken together, these results suggest that naloxone greatly inhibits the CA secretion evoked by stimulation of cholinergic (both nicotinic and muscarinic) receptors as well as that by membrane depolarization. It seems that these inhibitory effects of naloxone does not involve opioid receptors, but might be mediated by blocking both the calcium influx into the rat adrenal medullary chromaffin cells and the uptake of $Ca^{2+}$ into the cytoplasmic calcium store, which are at least partly relevant to the direct interaction with the nicotinic receptor itself.

• Molecules and Cells
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• v.45 no.8
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• pp.537-549
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• 2022

Preproenkephalin (PPE) is a precursor molecule for multiple endogenous opioid peptides Leu-enkephalin (ENK) and Met-ENK, which are involved in a wide variety of modulatory functions in the nervous system. Despite the functional importance of ENK in the brain, the effect of brain-derived factor(s) on PPE expression is unknown. We report the dual effect of neural epidermal growth factor (EGF)-like-like 2 (NELL2) on PPE gene expression. In cultured NIH3T3 cells, transfection of NELL2 expression vectors induced an inhibition of PPE transcription intracellularly, in parallel with downregulation of protein kinase C signaling pathways and extracellular signal-regulated kinase. Interestingly, these phenomena were reversed when synthetic NELL2 was administered extracellularly. The in vivo disruption of NELL2 synthesis resulted in an increase in PPE mRNA level in the rat brain, suggesting that the inhibitory action of intracellular NELL2 predominates the activation effect of extracellular NELL2 on PPE gene expression in the brain. Biochemical and molecular studies with mutant NELL2 structures further demonstrated the critical role of EGF-like repeat domains in NELL2 for regulation of PPE transcription. These are the first results to reveal the spatio-specific role of NELL2 in the homeostatic regulation of PPE gene expression.

• The Korean Journal of Pharmacology
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• v.30 no.3
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• pp.299-311
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• 1994

The present study was attempted to investigate whether pentazocine, which is known to possess both opioid agonistic and antagonistic properties, produces catecholamines (CA) secretion from the isolated perfused rat adrenal gland, and to establish the mechanism of its action, and also to compare its action with that of some opioids. Pentazocine (30 to 300 ug) injected into an adrenal vein caused a dose-dependent secretory response of CA from the rat adrenal medulla. The pentazocine-evoked secretion of CA was remarkably diminished by the preloading with chlorisondamine $(10^{-6}\;M)$, naloxone $(1.22{\times}10^{-7}\;M)$, morphine $(1.7{\times}10^{-5}\;M)$, met-enkephalin $(9.68{\times}10^{-6}\;M)$, nicardipine $(10^{-6}\;M)$ and TMB-8 $(10^{-5}\;M)$ while was not influenced by the pretreatment of pirenzepine $(2{\times}10^{-6}\;M)$. The perfusion of $Ca^{++}$-free Krebs solution for 30 min into the gland also led to the marked reduction in CA secretion evoked by pentazocine. Furthermore, the CA release evoked by ACh and/or DMPP was greatly inhibited by the pretreatment with pentazocine $(1.75{\times}10^{-4}\;M)$ for 20 min. From these experimental results, it is thought that pentazocine causes markedly the increased secretion of CA from the isolated perfused rat adrenal medulla by a calcium-dependent exocytotic mechanism. The secretory effect of pentazocine appears to be mediated through activation of opioid receptors located on adrenal chromaffin cells, which may be also associated with stimulation of cholinergic nicotinic receptors.