title: Cortisol responses to ipsapirone challenge correlate with aggression, while basal cortisol levels correlate with impulsivity, in personality disorder and healthy volunteer subjects.
abstract: BACKGROUND
  This study was performed to test the hypothesis that 5-HT-1a receptors, as assessed by the cortisol (post-synaptic) and temperature (pre-synaptic) responses to the 5-HT-1a agonist, Ipsapirone (IPSAP), play a role in the regulation of impulsive aggressive behavior in human subjects.
  
  
  METHODS
  Fifty-two healthy subjects (28 with Personality Disorder: PD; 24 Healthy Volunteers: HV) underwent acute challenge with the selective 5-HT-1a agonist, ipsaprione (IPSAP: .3 mg/kg po). Residual Peak Delta Cortisol (ΔCORT[IPSAP]-R; after removal of Basal CORT and IPSAP plasma levels) was used as the primary 5-HT-1a post-synaptic receptor variable. Residual Nadir Delta Temperature (ΔTEMP[IPSAP]-R; after removal of Basal TEMP) was used as the primary 5-HT-1a somatodendritic (pre-synaptic) receptor variable. Measures of trait aggression included the Aggression scales of the Buss-Durkee Hostility Inventory (BDHI) and the Life History of Aggression (LHA); trait impulsivity was assessed with the Impulsivity scale of the Eysenck Personality Questionnaire (EPQ-II).
  
  
  RESULTS
  Correlations between ΔCORT[IPSAP]-R responses and BDHI Aggression scores varied by group. Specifically, BDHI Aggression correlated inversely with ΔCORT[IPSAP]-R values in PD subjects but directly in HV subjects. While EPQ-II Impulsivity did not correlate with ΔCORT[IPSAP]-R responses, this measure of impulsivity correlated directly with Basal CORT levels in all subjects. ΔTEMP[IPSAP]-R responses did not correlate with measures of trait aggression or trait impulsivity.
  
  
  CONCLUSIONS
  Physiologic responses of 5-HT-1a post-synaptic receptors may be reduced as a function of trait aggression, but not impulsivity, in PD subjects. In contrast, pre-synaptic 5-HT-1a receptors may not play a role in the regulation of aggression or impulsivity in human subjects.
authors.affiliation: Clinical Neuroscience & Psychopharmacology Research Unit, Department of Psychiatry and Behavioral Neuroscience, Division of Biological Sciences and Pritzker School of Medicine, The University of Chicago, Chicago, IL 60637, USA.
authors.forename: Marcela
authors.initials: M
authors.lastname: Almeida
authors.forename: Royce
authors.initials: R
authors.lastname: Lee
authors.forename: Emil F
authors.initials: EF
authors.lastname: Coccaro
mesh_terms: D000328:Adult; D000374:Aggression / Q000187:drug effects; D015415:Biomarkers / Q000097:blood; D001831:Body Temperature; D003712:Dendrites / Q000187:drug effects / Q000378:metabolism; D039721:Diagnostic and Statistical Manual of Mental Disorders; D005260:Female; D006801:Humans; D006854:Hydrocortisone / Q000097:blood*; D007175:Impulsive Behavior / Q000097:blood*; D008297:Male; D008875:Middle Aged; D010554:Personality Disorders / Q000097:blood*; D010555:Personality Inventory; D011569:Psychiatric Status Rating Scales; D011743:Pyrimidines / Q000494:pharmacology*; D058825:Serotonin 5-HT1 Receptor Agonists / Q000494:pharmacology*; D011795:Surveys and Questionnaires; D013570:Synaptic Membranes / Q000187:drug effects / Q000378:metabolism; D013997:Time Factors
chemical_list: D015415:Biomarkers; D011743:Pyrimidines; D058825:Serotonin 5-HT1 Receptor Agonists; C043077:ipsapirone; D006854:Hydrocortisone