Background: Nightmares (NM) are one of the core symptoms of PTSD (DSM-5). NM have been associated with rapid eye movement (REM) sleep. It is recognized that REM sleep plays a central role in emotional regulation. We examined the frequency of suicidal behavior (SB) and depression in PTSD patients who sought medical attention for nightmares (PTSD1NM) versus all other PTSD visits (PTSD-NM), in a nationally representative US sample. Methods: We examined an estimated6SE 27,588,1096 2,900,885 (unweighted count53341) PTSD-related patient visits (mean 6 SE age: 39.2860.65 years; 67.0% 62.1%, female) from 1995-2011 in the National Ambulatory Medical Care Survey and National Hospital Ambulatory Medical Care Survey. Each patient visit is assigned up to 3 ICD9CM diagnoses and up to 3 Reasons for Visit(RFV). Variables were dened as follows: PTSD ICD9CM code 309.81; Nightmares (NM)- ICD9CM code 307.49 or RFV Nightmares; Suicidal Behavior (SB)- ICD9CM codes E950-E959 or RFV Suicide attemptor Intentional overdose; Depression- ICD9CM codes 296.2, 296.3, 296.82, 311, 296.20-296.36, 300.4. Results: There were an estimated6SE 498,169 6 143,660 (unweighted count557; 1.8% 6 0.4% of all PTSD visits) NM visits and an estimated6SE 93,813 6 40,633 (unweighted count531; 0.3% 6 0.1% of all PTSD visits) SB visits. Interestingly, there was no SB in the PTSD1NM group. Depression was not signi cantly different between the PTSD1NM versus PTSD-NM groups (OR51.43, 95% CI 0.77- 2.65) Conclusions: PTSD patients with NM had signicantly less SB but not lower depression scores. This previously unreported nding suggests that NM (possibly through mechanisms associated with REM sleep) have a protective effect against SB. Keywords: PTSD, Nightmares, Emotional Regulation, REM sleep, Suicide 219. HAB/LAB Rats A Model of Opioid Tone Elizabeth Perkins University of Miami Jackson Memorial Hospital Background: Rats bred for anxiety based on their performance on an elevated plus maze have been considered the gold standard genetic animal model for anxiety. However, many of the behaviors observed in these rats including alcohol self- administration, pain tolerance, and aggression - are the opposite of what we have observed in humans with chronic anxiety. Interestingly, monogamous voles (MV) and polygamous voles (PV) mirror the behavioral proles of HAB and LAB rats. Methods: Literature on both animal models was reviewed by search on PUBMED. The terms HAB rats, polygamous voles, AVP and opioidarticles were reviewed on PUBMED as both animal models have AVP mutations and display behaviors that are known to be controlled by the endogenous opioid system. Results: These two animal models have different AVP mutations which lead to the same physiological outcome. HAB/PVs have higher levels of AVP activity, while comparatively LAB/MVs have lower levels of AVP activity. This leads to different baseline levels of endorphins affecting a range of behaviors such as bonding, addiction, pain sensitivity and aggression. Conclusions: While HAB rats exhibit traits of chronic anxiety, it is not the result of an anxiety geneit is simply an example of stress-diathesis. The genetic make-up of the HAB group gives them higher opioid tone (via greater AVP activity) making the lab environment, one of forced social interaction, an adverse environment with no way for the rats to naturally modulate their endogenous opioid levels to lower, less dysphoric levels and inducing chronic anxiety. Keywords: anxiety, attachment, opioid, addiction, AVP 220. Molecular Indicators of Stress-Induced Neuroin- ammation in a Mouse Model Simulating Features of Post-Traumatic Stress Disorder Seid Muhie 2 , Aarti Gautam 3 , Nabarun Chakraborty 2 , Allison Hoke 2 , James Meyerhoff 2 , Rasha Hammamieh 3 , Marti Jett 3 , and James Meyerhoff 1 1 Georgetown University School of Medicine, 2 Geneva Foundation, 3 Integrative Systems Biology Program, US Army Center for Environmental Health Research Background: PTSD is a growing problem. Identication of targets for early intervention requires understanding of pathogenesis. Accordingly, we examined alterations in signaling pathways following exposure to stress. Methods: A social-stress model involving exposure of an intruder (male C57BL/6) mouse to a resident aggressor (male SJL) mouse was used to simulate features of PTSD. Transcriptome changes in the blood, brain regions and spleen, as well as DNA methylome changes in hemi-brain of stressed vs control C57BL/6 mice were assayed at one, 10 and 42 days post-trauma. Transcripts and methylation states meeting criteria p , 0.01 and fold changes . 2 were used to identify enriched pathways and processes. Results: Differentially expressed genes (DEGs) and methylated promoter regions were associated with activated inammatory pathways (IP), inhibited neurogenesis (NG) and synaptic plasticity (SP). In amygdala (AY), hippocampus (HC), and medial pre- frontal cortex (MPFC), all 3 pathways were activated during the early response. While NG/SP were inhibited at later times in AY, they persisted at 42 days post-trauma in HC and mPFC. NG/SP changes were corroborated by impaired Y-maze responses of aggressor-exposed mice. Conclusions: Activated inammation might inhibit neurogenesis (relatable to cognitive decits), and physical complaints in PTSD patients. Processes associated with NG/SP might be mediating the effects of neuroinammation in behavioral manifestations of PTSD. Also, inammation could be involved in tissue damage underlying somatic comorbidity. Identi cation of correlated DEGs and pathways between blood and brain suggests that blood might serve as an accessible brain surrogate for clinical investigation. Supported By: MOMRP/TAWT/869 Keywords: PTSD MICE GENES BRAIN BLOOD 221. Interaction of Early Life Stress (ELS) 1 Short Allele of Serotonin Transporter Gene (STG) and Reduced Macaque Neurogenesis Nishant Gupta 1 , Anna Rosenboym 2 , Sasha Fulton 3 , Lakshmi Thiramangalakdi 3 , Tarique Perera 3 , and Jeremy Coplan 4 Biological Psychiatry S90 Biological Psychiatry May 15, 2017; 81:S1S139 www.sobp.org/journal Thursday Abstracts