Prepulse inhibition deficits in schizophrenia are modified by smoking status

• Published in: Schizophrenia research 2009-07, Vol.112 (1), p.86-90
• Main Authors: Woznica, Andrea A, Sacco, Kristi A, George, Tony P
• Format: Article
• Language: English
• Subjects: Acoustic Stimulation - methods; Addiction vulnerability; Addictive behaviors; Adult; Adult and adolescent clinical studies; Analysis of Variance; Biological and medical sciences; Cigarette smoking; Gait Disorders, Neurologic - etiology; Humans; Inhibition (Psychology); Medical sciences; Middle Aged; Prepulse inhibition; Psychiatric Status Rating Scales; Psychiatry; Psychology. Psychoanalysis. Psychiatry; Psychopathology. Psychiatry; Psychoses; Reaction Time - physiology; Reflex, Startle - physiology; Schizophrenia; Schizophrenia - complications; Schizophrenic Psychology; Smoking - psychology; Smoking status; Startle response; Time Factors; Tobacco smoking; Tobacco, tobacco smoking; Toxicology
• ISSN: 0920-9964; 1573-2509
• DOI: 10.1016/j.schres.2009.04.016

Abstract Background Schizophrenia is associated with high rates of cigarette smoking and deficits in sensorimotor gating, as measured by prepulse inhibition (PPI) of the startle response. However, the relationship between PPI deficits and smoking status is unclear. We examined whether smoking status modifies PPI deficits in schizophrenia. Methods We studied PPI as a function of smoking status and schizophrenia diagnosis in four groups using a cross-sectional design: Smokers with schizophrenia (SS; n = 14), non-smokers with schizophrenia (SNS; n = 15), control smokers (CS; n = 11), and control non-smokers (CNS; n = 10). PPI in smokers was recorded under conditions of smoking satiation, and smoking status was verified biochemically. Results The Diagnosis × Smoking Status × Prepulse Interval interaction was significant ( F11,140 = 5.01, p < 0.001). At all prepulse to pulse intervals (PPTPIs; 30, 60 and 120 ms), we found that SNS had reductions (~ 50%; p < 0.01) in PPI compared to CNS. However, when SS were compared to CS under conditions of smoking satiation, SS had comparable levels of PPI to CS, and significantly higher levels of PPI than SNS. Conclusions Our findings suggest that PPI deficits are present in nonsmokers with schizophrenia, and may be modified by smoking status. Acute smoking in schizophrenia is associated with an elevation of PPI to the levels in non-psychiatric control smokers. These findings have significant implications for understanding vulnerability to tobacco dependence in schizophrenia, which may lead to the development of more effective treatments for PPI deficits and tobacco dependence in this population.