PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 12714357-2 2003 The GLP-1/2-containing neural pathways have been suggested to play a role in taste aversion and nausea because LiCl activates these neurons, and LiCl-induced suppression of food intake can be blocked by the GLP-1 receptor antagonist exendin-9. Lithium Chloride 111-115 glucagon Rattus norvegicus 4-9 26211731-0 2016 The Aversive Agent Lithium Chloride Suppresses Phasic Dopamine Release Through Central GLP-1 Receptors. Lithium Chloride 19-35 glucagon Rattus norvegicus 87-92 15459118-1 2005 In rats, central administration of glucagon-like peptide-1 (GLP-1) elicits symptoms of visceral illness like those caused by the toxin lithium chloride (LiCl), including anorexia, conditioned taste aversion (CTA) formation, and neural activation in the hypothalamus and hindbrain including activation of brainstem preproglucagon cells. Lithium Chloride 135-151 glucagon Rattus norvegicus 35-58 15459118-1 2005 In rats, central administration of glucagon-like peptide-1 (GLP-1) elicits symptoms of visceral illness like those caused by the toxin lithium chloride (LiCl), including anorexia, conditioned taste aversion (CTA) formation, and neural activation in the hypothalamus and hindbrain including activation of brainstem preproglucagon cells. Lithium Chloride 135-151 glucagon Rattus norvegicus 60-65 15459118-1 2005 In rats, central administration of glucagon-like peptide-1 (GLP-1) elicits symptoms of visceral illness like those caused by the toxin lithium chloride (LiCl), including anorexia, conditioned taste aversion (CTA) formation, and neural activation in the hypothalamus and hindbrain including activation of brainstem preproglucagon cells. Lithium Chloride 153-157 glucagon Rattus norvegicus 35-58 15459118-1 2005 In rats, central administration of glucagon-like peptide-1 (GLP-1) elicits symptoms of visceral illness like those caused by the toxin lithium chloride (LiCl), including anorexia, conditioned taste aversion (CTA) formation, and neural activation in the hypothalamus and hindbrain including activation of brainstem preproglucagon cells. Lithium Chloride 153-157 glucagon Rattus norvegicus 60-65 24183963-6 2014 Furthermore, our data in the present study suggested that GLP-1 regulated tau phosphorylation induced by AGEs through a signaling pathway involving glycogen synthase kinase 3beta (GSK-3beta), similarly to the GSK-3beta inhibitor, lithium chloride. Lithium Chloride 230-246 glucagon Rattus norvegicus 58-63 12714357-2 2003 The GLP-1/2-containing neural pathways have been suggested to play a role in taste aversion and nausea because LiCl activates these neurons, and LiCl-induced suppression of food intake can be blocked by the GLP-1 receptor antagonist exendin-9. Lithium Chloride 145-149 glucagon Rattus norvegicus 4-9 10662851-0 2000 The role of CNS glucagon-like peptide-1 (7-36) amide receptors in mediating the visceral illness effects of lithium chloride. Lithium Chloride 108-124 glucagon Rattus norvegicus 16-39 10444567-7 1999 The majority of GLP-1 neurons were activated to express c-Fos after LiCl, LPS, or CCK treatment, including (in LiCl-treated rats) those projecting to the PVN. Lithium Chloride 68-72 glucagon Rattus norvegicus 16-21 10444567-7 1999 The majority of GLP-1 neurons were activated to express c-Fos after LiCl, LPS, or CCK treatment, including (in LiCl-treated rats) those projecting to the PVN. Lithium Chloride 111-115 glucagon Rattus norvegicus 16-21 10564228-0 1999 A functional role for central glucagon-like peptide-1 receptors in lithium chloride-induced anorexia. Lithium Chloride 67-83 glucagon Rattus norvegicus 30-53 10564228-1 1999 The present study sought to determine whether central glucagon-like peptide-1 (GLP-1)-receptor signalling contributes to the anorexigenic effects of systemically administered lithium chloride (LiCl). Lithium Chloride 175-191 glucagon Rattus norvegicus 54-77 10564228-1 1999 The present study sought to determine whether central glucagon-like peptide-1 (GLP-1)-receptor signalling contributes to the anorexigenic effects of systemically administered lithium chloride (LiCl). Lithium Chloride 193-197 glucagon Rattus norvegicus 54-77 10564228-6 1999 These results support the view that central mechanisms underlying LiCl-induced anorexia include a prominent role for endogenous GLP-1 neural pathways. Lithium Chloride 66-70 glucagon Rattus norvegicus 128-133 9729361-0 1998 Central infusion of glucagon-like peptide-1-(7-36) amide (GLP-1) receptor antagonist attenuates lithium chloride-induced c-Fos induction in rat brainstem. Lithium Chloride 96-112 glucagon Rattus norvegicus 20-43