Detail of "133156-06-6"

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Role of NK-2 receptors in the antidipsogenic activity of neurokinins in the mouse

Role of NK-2 receptors in the antidipsogenic activity of neurokinins in the mouse. Walsh, Delia M.; Elliott, Peter J.; Hagan, Russell M. (Neuropharmacol. Dep., Glaxo Group Res. Ltd.Some commonly used reagents like 7732-18-5 and 133156-06-6 are used in this experiment., Ware SG12 0DP, UK). Gen. Pharmacol., 23(2), 231-3 (English) 1992. CODEN: GEPHDP. ISSN: 0306-3623. DOCUMENT TYPE: Journal CA Section: 2 (Mammalian Hormones) The receptors involved in the antidipsogenic activity of neurokinin (NK) agonists were investigated in water-deprived mice. Intracerebral administration of agonists selective at all 3 NK receptors (NK-1, NK-2, NK-3) caused inhibition of drinking in this model. However, only the NK-2 receptor agonist GR 64349 inhibited drinking without producing other behavioral effects. Both NK-1 (GR 73632) and NK-3 (senktide) agonists induced a variety of behavioral effects which appeared to compete with the drinking response. The inhibitory effect on drinking obsd. after central injection of the NK-2 agonist was attenuated by co-administration of the NK-2 antagonist L 659,877, but not by the NK-1 antagonist GR 82334. These results illustrate that the antidipsogenic activity of the NKs in mice is mediated via NK-2 receptors. .

Differential effects of NK1 receptors in the midbrain periaqueductal gray upon defensive rage and predatory attack in the cat

Differential effects of NK1 receptors in the midbrain periaqueductal gray upon defensive rage and predatory attack in the cat. Gregg, Thomas R.; Siegel, Allan (Graduate School of the Biomedical Sciences, Department of Neurosciences, University of Medicine and Dentistry of New Jersey, Newark, NJ 07103, USA). Brain Research, 994(1), 55-66 (English) 2003 Elsevier Science B.V. CODEN: BRREAP. ISSN: 0006-8993.Some commonly used reagents like 33507-63-0 and 133156-06-6 are used in this experiment. DOCUMENT TYPE: Journal CA Section: 2 (Mammalian Hormones) This study utilized anatomical and behavioral-pharmacol. to det. the role of NK1-Substance P receptors in the midbrain periaqueductal gray (PAG) in defensive rage behavior in cats. For behavioral pharmacol. expts., monopolar stimulating electrodes were implanted in the medial hypothalamus for elicitation of defensive rage behavior and cannula-electrodes were implanted in the PAG for microinjections of receptor compds. Microinjections of the NMDA antagonist, AP-7 (2 nmol), into the dorsal PAG blocked defensive rage elicited by medial hypothalamic stimulation, thus establishing the PAG as a synaptic region that receives hypothalamic inputs linked to defensive rage behavior. Microinjections of the NK1 agonist, GR73632, into the same injection sites facilitated defensive rage in a dose-dependent manner, and also induced spontaneous hissing in five cats. The effects of GR73632 were reduced by pretreatment of the PAG with the NK1 antagonist, GR82334 (16 nmol), microinjected into the same sites. Microinjections of GR73632 (8 nmol) into the PAG also suppressed predatory attack elicited by stimulation of the lateral hypothalamus. Immunohistochem. utilized to detect Substance P and Fos immunoreactivity revealed that neurons in the PAG activated after defensive rage-inducing medial hypothalamic stimulation lie in the same region as Substance-P-immunoreactive processes. Fos immunoreactivity was highest in the dorsomedial aspect of the rostral PAG after medial hypothalamic stimulation. Cats that were unstimulated or that exhibited predatory attack after lateral hypothalamic stimulation had low c-fos expression levels in the PAG. Substance P immunoreactivity was high throughout the dorsal PAG. The results indicate that NK1 receptors in the PAG potentiate defensive rage and suppress predatory aggression in the cat. .