PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
14642446-7	2003	Conversely, after TBI in rats treated with fentanyl, CMRglu increased markedly and bilaterally in CA1 and CA3 (p<0.05 vs. fentanyl uninjured), but not ipsilateral parietal cortex.	Fentanyl	43-51	carbonic anhydrase 1	Rattus norvegicus	98-101	
16473332-12	2006	Rats receiving fentanyl pre- and post-TBI had the worst CA1 neuronal survival of all groups.	Fentanyl	15-23	carbonic anhydrase 1	Rattus norvegicus	56-59	
15114213-9	2004	The percent alive CA1 neurons in the fentanyl-nitrous oxide group increased with duration of recovery (P = 0.004).	Fentanyl	37-45	carbonic anhydrase 1	Rattus norvegicus	18-21	
14642446-1	2003	Despite common use of narcotics in the clinical management of severe traumatic brain injury (TBI), in experimental models rats treated with fentanyl have exhibited worse functional outcome and more CA1 hippocampal death than rats treated with standard isoflurane anesthesia.	Fentanyl	140-148	carbonic anhydrase 1	Rattus norvegicus	198-201	
14642446-8	2003	In contralateral CA1, CMRglu was nearly two times greater after TBI in fentanyl vs. isoflurane treated rats (p<0.05).	Fentanyl	71-79	carbonic anhydrase 1	Rattus norvegicus	17-20	
14642446-9	2003	Hyperglycolysis was exacerbated in CA1 and CA3 hippocampus after TBI in rats treated with fentanyl vs. isoflurane anesthesia.	Fentanyl	90-98	carbonic anhydrase 1	Rattus norvegicus	35-38	
14642446-10	2003	This post-traumatic hyperglycolysis suggests greater excitotoxicity and concurs with reports of worse functional outcome and more CA1 hippocampal death after TBI with fentanyl vs. isoflurane anesthesia.	Fentanyl	167-175	carbonic anhydrase 1	Rattus norvegicus	130-133	
9661548-0	1998	The effect of fentanyl on electrophysiologic recovery of CA 1 pyramidal cells from anoxia in the rat hippocampal slice.	Fentanyl	14-22	carbonic anhydrase 1	Rattus norvegicus	57-61	
9661548-2	1998	We evaluated the effect of fentanyl on anoxic injury to CA 1 pyramidal cells in the rat hippocampus.	Fentanyl	27-35	carbonic anhydrase 1	Rattus norvegicus	56-60	
26578961-0	2015	Effect of acute fentanyl treatment on synaptic plasticity in the hippocampal CA1 region in rats.	Fentanyl	16-24	carbonic anhydrase 1	Rattus norvegicus	77-80	
9339403-8	1997	Fentanyl caused preischemic evidence of epileptoid activity but decreased the percentage of neurons that died in the CA1 sector of the hippocampus relative to control (p = 0.0005).	Fentanyl	0-8	carbonic anhydrase 1	Rattus norvegicus	117-120	
26578961-4	2015	Therefore, we investigated the effect of fentanyl, a strong agonist of MOR and often used for anesthesia and analgesia in clinical settings, on hippocampal synaptic plasticity in the Schaffer-collateral CA1 pathway during acute exposure and washout in vitro.	Fentanyl	41-49	carbonic anhydrase 1	Rattus norvegicus	203-206	
26578961-7	2015	These results demonstrated that fentanyl acute exposure and washout increases hippocampal excitability in the Schaffer-collateral CA1 pathway, depending on disinhibiting interneurons after MOR activation.	Fentanyl	32-40	carbonic anhydrase 1	Rattus norvegicus	130-133	
25972075-9	2015	On day 5, significantly more apoptosis in the CA1 segment of the hippocampus was found in the sevoflurane/fentanyl group.	Fentanyl	106-114	carbonic anhydrase 1	Rattus norvegicus	46-49	
18706433-0	2008	Fentanyl treatment reduces GABAergic inhibition in the CA1 area of the hippocampus 24 h after acute exposure to the drug.	Fentanyl	0-8	carbonic anhydrase 1	Rattus norvegicus	55-58	
18706433-1	2008	The effect of in vivo fentanyl treatment on synaptic transmission was studied in the CA1 area of the rat hippocampus.	Fentanyl	22-30	carbonic anhydrase 1	Rattus norvegicus	85-88