PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
11356984-1	2001	The goal of this article is to summarize available data examining the physiological significance of brain corticotropin-releasing factor (CRF) systems in mediating the behavioral and physiological effects of several classes of abused drugs, including opioid and psychostimulant drugs, alcohol and sedative hypnotics, nicotine, and cannabinoids.	Nicotine	317-325	corticotropin releasing hormone	Homo sapiens	106-136	
18337407-0	2008	Nicotine self-administration differentially regulates hypothalamic corticotropin-releasing factor and arginine vasopressin mRNAs and facilitates stress-induced neuronal activation.	Nicotine	0-8	corticotropin releasing hormone	Homo sapiens	67-97	
16269317-0	2005	The role of corticotropin-releasing factor-like peptides in cannabis, nicotine, and alcohol dependence.	Nicotine	70-78	corticotropin releasing hormone	Homo sapiens	12-42	
24755994-2	2014	Animal studies indicate that the dysphoric state associated with nicotine withdrawal is at least partly mediated by an increase in corticotropin-releasing factor (CRF) release in the central nucleus of the amygdala (CeA).	Nicotine	65-73	corticotropin releasing hormone	Homo sapiens	131-161	
9449645-7	1998	Nicotine and KCl depolarization stimulated the secretion of CRH, whereas interleukin-1beta, glucocorticoids, and nerve growth factor stimulated its synthesis.	Nicotine	0-8	corticotropin releasing hormone	Homo sapiens	60-63	
32190681-10	2020	In the nicotine exposed group, maternal hypothalamic corticotropin releasing hormone (CRH) level decreased, but pituitary adrenocorticotropic hormone (ACTH) and serum Cort levels increased.	Nicotine	7-15	corticotropin releasing hormone	Homo sapiens	86-89	
32190681-13	2020	In the nicotine exposed group, maternal hypothalamic corticotropin releasing hormone (CRH) level decreased, but pituitary adrenocorticotropic hormone (ACTH) and serum Cort levels increased.	Nicotine	7-15	corticotropin releasing hormone	Homo sapiens	86-89	
28222901-6	2017	In the present review, we analyze reports studying the role of Corticotropin Releasing Factor (CRF), the principle neuroendocrine mediator of the stress response and its two receptors (CRF1 and CRF2) in the withdrawal phase as well as in the abstinence from nicotine use.	Nicotine	258-266	corticotropin releasing hormone	Homo sapiens	63-93	
25402857-3	2014	We provide further evidence in rodents that chronic nicotine exposure upregulates Crh mRNA (encoding CRF) in dopaminergic neurons of the posterior VTA, activates local CRF1 receptors and blocks nicotine-induced activation of transient GABAergic input to dopaminergic neurons.	Nicotine	52-60	corticotropin releasing hormone	Homo sapiens	82-85	
25402857-3	2014	We provide further evidence in rodents that chronic nicotine exposure upregulates Crh mRNA (encoding CRF) in dopaminergic neurons of the posterior VTA, activates local CRF1 receptors and blocks nicotine-induced activation of transient GABAergic input to dopaminergic neurons.	Nicotine	194-202	corticotropin releasing hormone	Homo sapiens	82-85	
25402857-4	2014	Local downregulation of Crh mRNA and specific pharmacological blockade of CRF1 receptors in the VTA reversed the effect of nicotine on GABAergic input to dopaminergic neurons, prevented the aversive effects of nicotine withdrawal and limited the escalation of nicotine intake.	Nicotine	123-131	corticotropin releasing hormone	Homo sapiens	24-27