INT8362
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
These results are consistent with differences in NT receptors localization in these three dopaminergic structures. | |||||||||||||||
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The 5HT-releasing effect of NT was completely inhibited by tetrodotoxin suggesting that NT receptors involved in the control of 5-HT release are not located on 5-HT terminals. | |||||||||||||||
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NT(1-13) and NT(8-13) increased (3H)5HT release with EC50 values in the nanomolar range and Emax values in the range of 100% of control, whereas D-tyr11-NT was inactive. | |||||||||||||||
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SR 48527 also antagonized NT induced (3H)5HT release with an IC50 value of 0.95+/-0.06 nM whereas the inactive R(-) enantiomer SR 49711 only inhibited this effect with IC50 value close to 10(-6)M. | |||||||||||||||
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NT(1-13) and NT(8-13) increased (3H)5HT release with EC50 values in the nanomolar range and Emax values in the range of 100% of control, whereas D-tyr11-NT was inactive. | |||||||||||||||
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The previous study described in detail the localization of immunohistochemical NT in the rat brain. | |||||||||||||||
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The fact that all these responsive brain areas contain NT indicates that the microinjection of NT may be mimicking the effects of endogenously released NT, thus supporting the possible physiological significance of NT as an endogenous modulator of body temperature or nociceptive sensory information. | |||||||||||||||
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Pretreatment of the 1% bile extract with the bile salt-sequestering resin cholestyramine (2%, wt/vol) abolished NT-LI release. | |||||||||||||||
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These results show that the tauro-conjugated forms of cholic and deoxycholic acid are strong stimulants of NT-LI release. | |||||||||||||||
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Bolus injections of neurotensin (NT) in the rat perfused heart elicited a transient, dose-dependent histamine release. | |||||||||||||||
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The nicotinic receptor agonist DMPP (10(-4) M) had no significant effect on NT-LI release. | |||||||||||||||
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Our results indicate that additionally to the secretion of NT induced by cholinergic agents and bombesin, substance P and to a lesser extent Leu-enkephalin are capable of stimulating NT release in the rat. | |||||||||||||||
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G-amino-n-butyric acid (GABA), histamine, serotonin and dopamine administered at final concentrations up to 10(-5) M had no effect on NT-LI release. | |||||||||||||||
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Finally, bile salt-induced NT-LI release is not mediated by intramural nerves and is not dependent on the activation of calcium channels. | |||||||||||||||
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Luminal administration of crude ox bile extract (0.25-1.5%, wt/vol) produced a dose-dependent release of NT-like immunoreactivity (NT-LI), with a maximal effect after infusion of 1% bile extract (500% of basal). | |||||||||||||||
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Bile salts in the distal small intestine are strong stimulants of neurotensin (NT) release, but the underlying mechanisms are not known. | |||||||||||||||
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The maximal secretion of NT-LI was observed after infusion of 20 mM TC (400% of basal). | |||||||||||||||
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Taurodeoxycholate (20 mM) was as potent as TC in stimulating NT-LI release, but the threshold concentration of taurodeoxycholate for NT-LI secretion was lower than that of TC. | |||||||||||||||
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To investigate the functional relationship between the enteric nervous system and the intestinal neurotensin (N) cells, the release of neurotensin (NT) was measured upon vascular 8-min infusion periods of various neurotransmitters and neuropeptides in an isolated vascularly perfused rat jejunoileum. | |||||||||||||||
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In contrast, the micellar form of oleic acid (20 and 100 mM) in bile extract (1%) or TC (20 mM) dose dependently reduced the release of NT-LI induced by bile extract or TC alone. | |||||||||||||||
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General Comments
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