PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
26549202-10	2017	These data suggest that CIE specifically disrupts mGlu1/5 -LTD, representing a possible connection between NMDAR and mGlu receptor signaling.	chlorimuron ethyl	24-27	glutamate receptor, ionotropic, NMDA1 (zeta 1)	Mus musculus	107-112	
28656742-3	2018	Following a CIE-induced escalation of ethanol consumption, NMDAR (N-methyl-D-aspartate receptor)-dependent long-term depression in D1 dopamine receptor expressing medium spiny neurons of the NAc shell was markedly altered with no changes in plasticity in D1 dopamine receptor medium spiny neurons from the NAc core.	chlorimuron ethyl	12-15	glutamate receptor, ionotropic, NMDA1 (zeta 1)	Mus musculus	59-64	
28656742-3	2018	Following a CIE-induced escalation of ethanol consumption, NMDAR (N-methyl-D-aspartate receptor)-dependent long-term depression in D1 dopamine receptor expressing medium spiny neurons of the NAc shell was markedly altered with no changes in plasticity in D1 dopamine receptor medium spiny neurons from the NAc core.	chlorimuron ethyl	12-15	glutamate receptor, ionotropic, NMDA1 (zeta 1)	Mus musculus	66-95	
28656742-10	2018	This CIE-induced alteration in AMPAR subunit composition may contribute to the loss of NMDAR-dependent long-term depression in the NAc shell and therefore may constitute a critical neuroadaptive response underlying the escalation of ethanol intake in the CIE model.	chlorimuron ethyl	5-8	glutamate receptor, ionotropic, NMDA1 (zeta 1)	Mus musculus	87-92	
28656742-10	2018	This CIE-induced alteration in AMPAR subunit composition may contribute to the loss of NMDAR-dependent long-term depression in the NAc shell and therefore may constitute a critical neuroadaptive response underlying the escalation of ethanol intake in the CIE model.	chlorimuron ethyl	255-258	glutamate receptor, ionotropic, NMDA1 (zeta 1)	Mus musculus	87-92	
26687341-7	2017	Ex vivo reverse transcription polymerase chain reaction analysis of brain tissue found reduced sensitivity to punished EtOH seeking after CIE exposure was accompanied by a significant increase in gene expression of the GluN1 and GluN2A subunits of the N-methyl-d-aspartate receptor, specifically in the medial orbitofrontal cortex.	chlorimuron ethyl	138-141	glutamate receptor, ionotropic, NMDA1 (zeta 1)	Mus musculus	219-224	
22941108-3	2012	CIE impaired extinction encoding by infralimbic mPFC neurons in vivo and functionally downregulated burst-mediating NMDA GluN1 receptors.	chlorimuron ethyl	0-3	glutamate receptor, ionotropic, NMDA1 (zeta 1)	Mus musculus	121-126	
22666364-4	2012	Consistent with this, Western blot analysis of the postsynaptic density fraction showed that while there was no change in expression of the AMPA GluR1 subunit, NMDA NR1 and NRB subunits were significantly increased in CIE exposed mice when examined immediately after the last episode of alcohol exposure.	chlorimuron ethyl	218-221	glutamate receptor, ionotropic, NMDA1 (zeta 1)	Mus musculus	165-168	
16839855-1	2006	We examined the mRNA and protein levels of GABA(A) and NMDA receptor (NMDAR) subunits in cultured mouse cortical neurons following exposure to chronic ethanol (CE) or chronic intermittent ethanol (CIE), and after 5 days of withdrawal.	chlorimuron ethyl	197-200	glutamate receptor, ionotropic, NMDA1 (zeta 1)	Mus musculus	70-75