or desensitize nicotinic acetylcholine receptors20, 21 and may enhance nicotine self-administration in rats possibly by increasing the dose needed to produce a particular level of reinforcement.22 Stress hormones also influence the severity of nicotine withdrawal in rats23 and potentially, relapse to smoking in humans.24, 25 Thus, FKBP5, a stress-response gene, may function in pathways that modulate sensitivity to nicotine and the severity of nicotine withdrawal. To our knowledge, no previous studies have examined the modulation of nicotine responses and withdrawal severity by FKBP5.
