PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
15644873-3	2005	In fura-2-loaded neurons, nAChR activation evoked a transient increase in [Ca(2+)](I), which was inhibited reversibly and selectively by clinically relevant concentrations of thiopental.	Thiopental	175-185	cholinergic receptor nicotinic beta 1 subunit	Rattus norvegicus	26-31	
15644873-4	2005	The half-maximal concentration for thiopental inhibition of nAChR-induced [Ca(2+)](i) transients was 28 microM, close to the estimated clinical EC(50) (clinically relevant (half-maximal) effective concentration) of thiopental.	Thiopental	35-45	cholinergic receptor nicotinic beta 1 subunit	Rattus norvegicus	60-65	
15644873-4	2005	The half-maximal concentration for thiopental inhibition of nAChR-induced [Ca(2+)](i) transients was 28 microM, close to the estimated clinical EC(50) (clinically relevant (half-maximal) effective concentration) of thiopental.	Thiopental	215-225	cholinergic receptor nicotinic beta 1 subunit	Rattus norvegicus	60-65	
15644873-5	2005	In fura-2-loaded neurons, voltage clamped at -60 mV to eliminate any contribution of voltage-gated Ca(2+) channels, thiopental (25 microM) simultaneously inhibited nAChR-induced increases in [Ca(2+)](i) and peak current amplitudes.	Thiopental	116-126	cholinergic receptor nicotinic beta 1 subunit	Rattus norvegicus	164-169	
15644873-6	2005	Thiopental inhibited nAChR-induced peak current amplitudes in dialysed whole-cell recordings by approximately 40% at -120, -80 and -40 mV holding potential, indicating that the inhibition is voltage independent.	Thiopental	0-10	cholinergic receptor nicotinic beta 1 subunit	Rattus norvegicus	21-26	
9366473-12	1997	CONCLUSIONS: Thiopental, whose reported EC50 for general anesthesia is 25 microM, inhibited the neuronal nAchR-mediated current but not the P2X receptor-mediated response in PC12 cells at clinically relevant concentrations.	Thiopental	13-23	cholinergic receptor nicotinic beta 1 subunit	Rattus norvegicus	105-110