PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
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	
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	
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	
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	
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	
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	
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	
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	
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	
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