Abstract: |
Antisense (AS) oligodeoxynucleotides targeting G-protein α-subunits distinguish feeding responses of morphine and its metabolite, as well as nocturnal and deprivation-induced feeding. The present study examined whether feeding elicited by β-endorphin (βEND) or dynorphin A1-17 was altered by ventricularly-applied Giα1, Giα2, Giα3, Gsα, Goα, Gqα or Gx/zα AS probes, or a nonsense (NS) control. The βEND-induced feeding was reduced by the Giα1 and Gx/zα AS probes, and increased by Giα2 or Giα3 AS treatment. Dynorphin-induced feeding was attenuated by Giα1 and Goα AS treatment. Yet, Gsα or Gqα AS and NS treatments failed to alter opioid agonist-induced feeding. These data provide initial characterization of potential effector signaling pathways mediating βEND and dynorphin-induced feeding. © 2002 Elsevier Science Inc. All rights reserved. |
Keywords: |
signal transduction; controlled study; unclassified drug; drug potentiation; nonhuman; protein function; animal; metabolism; animals; animal experiment; gtp-binding proteins; feeding behavior; drug effect; feeding; chemistry; drug mechanism; rat; protein structure, tertiary; rats; protein subunit; rats, sprague-dawley; guanine nucleotide binding protein; protein tertiary structure; sprague dawley rat; complementary dna; narcotic agent; oligonucleotides, antisense; dynorphin; beta-endorphin; antisense oligonucleotide; narcotics; male; priority journal; article; beta endorphin; support, non-u.s. gov't; support, u.s. gov't, p.h.s.; support, u.s. gov't, non-p.h.s.; dynorphins; β-endorphin; dynorphin a1-17; g-protein α-subunit antisense; beta endorphin derivative; beta endorphin[1-17]; dna probe
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