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<title>Pharmacology, Department of</title>
<link>http://hdl.handle.net/2027.42/78407</link>
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<pubDate>Fri, 24 May 2013 13:22:07 GMT</pubDate>
<dc:date>2013-05-24T13:22:07Z</dc:date>
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<title>Pharmacology, Department of</title>
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<title>Hypocretin-1 causes G protein activation and increases ACh release in rat pons</title>
<link>http://hdl.handle.net/2027.42/75751</link>
<description>Hypocretin-1 causes G protein activation and increases ACh release in rat pons
Bernard, René; Lydic, Ralph; Baghdoyan, Helen A.
The effects of the arousal-promoting peptide hypocretin on brain stem G protein activation and ACh release were examined using 16 adult Sprague-Dawley rats. In vitro [ 35 S]GTPγS autoradiography was used to test the hypothesis that hypocretin-1-stimulated G protein activation is concentration-dependent and blocked by the hypocretin receptor antagonist SB-334867. Activated G proteins were quantified in dorsal raphe nucleus (DR), locus coeruleus (LC) and pontine reticular nucleus oral part (PnO) and caudal part (PnC). Concentration–response data revealed a significant ( P  &lt; 0.001) effect of hypocretin-1 (2–2000 nm) in all brain regions examined. Maximal increases over control levels of [ 35 S]GTPγS binding were 37% (DR), 58% (LC), 52% (PnO) and 44% (PnC). SB-334867 (2 µm) significantly ( P  &lt; 0.002) blocked hypocretin-1 (200 nm)-stimulated [ 35 S]GTPγS binding in all four nuclei. This is the first autoradiographic demonstration that hypocretin-1 activates G proteins in arousal-related brain stem nuclei as a result of specific receptor interactions. This finding suggests that some hypocretin receptors in brain stem couple to inhibitory G proteins. In vivo microdialysis was used to test the hypothesis that PnO administration of hypocretin-1 increases ACh release in PnO. Dialysis delivery of hypocretin-1 (100 µm) significantly ( P  &lt; 0.002) increased (87%) ACh release. This finding is consistent with the interpretation that one mechanism by which hypocretin promotes arousal is by enhancing cholinergic neurotransmission in the pontine reticular formation.
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<pubDate>Wed, 01 Oct 2003 00:00:00 GMT</pubDate>
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<dc:date>2003-10-01T00:00:00Z</dc:date>
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<title>Roles of residues 3 and 4 in cyclic tetrapeptide ligand recognition by the Κ -opioid receptor</title>
<link>http://hdl.handle.net/2027.42/75723</link>
<description>Roles of residues 3 and 4 in cyclic tetrapeptide ligand recognition by the Κ -opioid receptor
Przydzial, M. J.; Pogozheva, I. D.; Bosse, K. E.; Andrews, S. M.; Tharp, T. A.; Traynor, John R.; Mosberg, Henry I.
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<pubDate>Tue, 01 Mar 2005 00:00:00 GMT</pubDate>
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<dc:date>2005-03-01T00:00:00Z</dc:date>
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<title>VISUALLY EVOKED RESPONSE IN ANESTHETIZED MAN WITH AND WITHOUT INDUCED MUSCLE PARALYSIS *</title>
<link>http://hdl.handle.net/2027.42/75634</link>
<description>VISUALLY EVOKED RESPONSE IN ANESTHETIZED MAN WITH AND WITHOUT INDUCED MUSCLE PARALYSIS *
Domino, Edward F.; Corssen, Guenter
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<pubDate>Fri, 01 May 1964 00:00:00 GMT</pubDate>
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<dc:date>1964-05-01T00:00:00Z</dc:date>
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<title>EFFECT OF INFARCT SIZE LIMITATION BY PROPRANOLOL ON VENTRICULAR ARRHYTHMIAS AFTER MYOCARDIAL INFARCTION</title>
<link>http://hdl.handle.net/2027.42/75625</link>
<description>EFFECT OF INFARCT SIZE LIMITATION BY PROPRANOLOL ON VENTRICULAR ARRHYTHMIAS AFTER MYOCARDIAL INFARCTION
Stewart, James R.; Gibson, John K.; Lucchesi, Benedict R.
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<pubDate>Mon, 01 Mar 1982 00:00:00 GMT</pubDate>
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<dc:date>1982-03-01T00:00:00Z</dc:date>
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