PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
16384857-6	2006	Of the CCK-responsive neurons 60% (18 of 30) were capsaicin-sensitive.	Capsaicin	50-59	cholecystokinin	Homo sapiens	7-10	
16384857-10	2006	Of these CCK-responsive neurons 80% (12 of 15) were capsaicin sensitive.	Capsaicin	52-61	cholecystokinin	Homo sapiens	9-12	
21543639-8	2011	Perivagal capsaicin, which is supposed to induce a selective degeneration of C-fibers, decreased the number of cNTS neurons responding to capsaicin or CCK-8s but not those responding to alpha,beta-Met-ATP.	Capsaicin	10-19	cholecystokinin	Homo sapiens	151-154	
10408253-15	1999	The present results suggest that: (1) both CCK1 and CCK2 receptors mediate the peptic secretory responses induced by CCK-like peptides; (2) the excitatory inputs of CCK-8S and gastrin-I to chief cells are not driven through acid-dependent mechanisms or capsaicin-sensitive afferent sensory nerves; and (3) under in vivo conditions, the stimulant actions of CCK-like peptides on pepsinogen secretion are mediated, at least in part, by an increase in NO generation.	Capsaicin	253-262	cholecystokinin	Homo sapiens	43-46	
10408253-15	1999	The present results suggest that: (1) both CCK1 and CCK2 receptors mediate the peptic secretory responses induced by CCK-like peptides; (2) the excitatory inputs of CCK-8S and gastrin-I to chief cells are not driven through acid-dependent mechanisms or capsaicin-sensitive afferent sensory nerves; and (3) under in vivo conditions, the stimulant actions of CCK-like peptides on pepsinogen secretion are mediated, at least in part, by an increase in NO generation.	Capsaicin	253-262	cholecystokinin	Homo sapiens	52-55	
10408253-15	1999	The present results suggest that: (1) both CCK1 and CCK2 receptors mediate the peptic secretory responses induced by CCK-like peptides; (2) the excitatory inputs of CCK-8S and gastrin-I to chief cells are not driven through acid-dependent mechanisms or capsaicin-sensitive afferent sensory nerves; and (3) under in vivo conditions, the stimulant actions of CCK-like peptides on pepsinogen secretion are mediated, at least in part, by an increase in NO generation.	Capsaicin	253-262	cholecystokinin	Homo sapiens	52-55	
2428085-6	1986	Moreover, capsaicin, a primary afferent neurotoxin, depleted sP IR and CCK IR only from the intact side.	Capsaicin	10-19	cholecystokinin	Homo sapiens	71-74	
15905220-3	2005	Because CCK enhances behavioral and electrophysiological responses to gastric distension in rats and people, we hypothesized that CCK might enhance the vagal afferent response to gastric distension via an action on capsaicin-insensitive vagal afferents.	Capsaicin	215-224	cholecystokinin	Homo sapiens	130-133	
3420015-0	1988	Capsaicin application to central or peripheral vagal fibers attenuates CCK satiety.	Capsaicin	0-9	cholecystokinin	Homo sapiens	71-74	
3420015-2	1988	Intraperitoneal, fourth ventricular or perivagal application of capsaicin attenuated or abolished cholecystokinin (CCK)-induced suppression of food intake.	Capsaicin	64-73	cholecystokinin	Homo sapiens	98-113	
3420015-2	1988	Intraperitoneal, fourth ventricular or perivagal application of capsaicin attenuated or abolished cholecystokinin (CCK)-induced suppression of food intake.	Capsaicin	64-73	cholecystokinin	Homo sapiens	115-118	
3420015-8	1988	These data indicate that localized capsaicin application attenuates CCK-induced suppression of food intake by impairing the function of either central or peripheral portions of vagal afferent neurons.	Capsaicin	35-44	cholecystokinin	Homo sapiens	68-71	
3420015-9	1988	The data also support the conclusion that intraperitoneal capsaicin attenuates CCK-induced suppression of feeding by impairing vagal sensory function.	Capsaicin	58-67	cholecystokinin	Homo sapiens	79-82	
21543639-3	2011	Since it has been suggested that cholecystokinin (CCK), exerts its gastrointestinal (GI)-related effects via paracrine activation of vagal afferent C-fibers, we tested whether CCK-sensitive fibers impinging upon cNTS neurons are responsive to vanilloid but not purinergic agonists.	Capsaicin	243-252	cholecystokinin	Homo sapiens	33-48	
21543639-7	2011	All neurons responding to either alpha,beta-Met-ATP or CCK-8s were also responsive to capsaicin.	Capsaicin	86-95	cholecystokinin	Homo sapiens	55-58	
21543639-10	2011	Our data also indicate that CCK-8s increases glutamate release from purinergic and vanilloid responsive fibers impinging on cNTS neurons.	Capsaicin	83-92	cholecystokinin	Homo sapiens	28-31	
21316356-5	2011	Many capsaicin-sensitive vagal afferents participate in peripheral satiety signaling that includes cholecystokinin (CCK) sensitive neurons.	Capsaicin	5-14	cholecystokinin	Homo sapiens	99-114	
21316356-5	2011	Many capsaicin-sensitive vagal afferents participate in peripheral satiety signaling that includes cholecystokinin (CCK) sensitive neurons.	Capsaicin	5-14	cholecystokinin	Homo sapiens	116-119	
21316356-10	2011	However CCK evoked inward currents only on capsaicin-sensitive neurons and 28% of the CCK-sensitive neurons expressed TRPA1.	Capsaicin	43-52	cholecystokinin	Homo sapiens	8-11