Topic: post-traumatic stress disorder

Scott J. Russo presents cross-species research on how immune cells outside the brain influence neural circuits implicated in anxiety and depression. The session examines stress-related disruption of neuroimmune communication, including inflammation and increased monocyte abundance. It connects these mechanisms with translational efforts to develop targeted interventions for major depression and post-traumatic stress disorder.

Matthew J. Girgenti discusses how research on individual brain cells and the three-dimensional organization of DNA is changing the biological understanding of post-traumatic stress disorder. The seminar examines how these approaches reveal trauma-associated brain changes and identify possible targets for more effective, personalized treatments. Girgenti is a neuroscientist in Yale School of Medicine’s Department of Psychiatry. Jeffrey Borenstein moderates this Meet the Scientist session. Online via the BBRF Zoom webinar. Tuesday 13 October 2026, 14:00 EDT (America/New_York; UTC−4). Follow Reg

Maladaptive emotional memories contribute to the persistence of numerous mental health disorders, including post-traumatic stress disorder (PTSD), drug addiction and obsessive-compulsive disorder (OCD). Using rodent behavioural models of the psychological processes relevant to these disorders, it is possible to identify potential treatment targets for the development of new therapies, including those based upon disrupting the reconsolidation of maladaptive emotional memories. Using examples from rodent models relevant to multiple mental health disorders, this talk will consider some of the opp

50 years ago it was found that sleep somehow made memories better and more permanent, but neither sleep nor memory researchers knew enough about sleep and memory to devise robust, effective tests. Today the fields of sleep and memory have grown and what is now understood is astounding. Still, great mysteries remain. What is the functional difference between the subtly different slow oscillation vs the slow wave of sleep and do they really have opposite memory consolidation effects? How do short spindles (e.g. <0.5 s as in schizophrenia) differ in function from longer ones and are longer spindl

While many individuals experience traumatic events during their lifetimes, only some go on to develop post-traumatic stress disorder (PTSD). This susceptibility and resilience can be modelled in rodents using the stress-enhanced fear learning (SEFL) procedure, in which rats are exposed to a session of massed, unpredictable footshocks and subsequently assessed on tasks of adaptive fear learning. It has previously been observed that subpopulations of rats are susceptible or resilient to showing the PTSD-like phenotype following SEFL, and that these rats show differences in glutamate receptor sub

Understanding the neural circuitry involved in fear memory is expected to provide implications for mental disorders such as post-traumatic stress disorder. The basolateral amygdala (BLA) and the medial prefrontal cortex (mPFC) are essential for the consolidation of fear memories. This consolidation occurs in particular when BLA neurons responding to aversive stimuli are reactivated during non-REM sleep. However, the neural circuit mechanism during non-REM sleep remains unclear. We focus on the role of neocortical slow waves, a hallmark of non-REM sleep, in fear memory formation. By recording l

Post-traumatic stress disorder (PTSD) emerges in the aftermath of a traumatic event, underscoring the pressing need for research into preventive treatments. Adrenal glucocorticoids induce short-term physiological adaptations necessary to cope with the threat. Evidence indicates that when administrated after trauma, glucocorticoids prevent the development of PTSD. The basolateral amygdala (BLA) is a key structure for processing positive and negative valence which communicates bidirectionally with other regions to regulate the stress responses. The present study evaluates the efficacy of cortico

Life experiences wield particular influence over brain development during restricted time windows (i.e., critical periods), when the brain is more responsive to environmental stimuli. Positive experiences during critical periods lead to healthy brain wiring and development of proper behavioral skills. Conversely, diverse traumatic life experiences (e.g., physical/sexual abuse, prolonged hospitalization, warfare) can damage the brain structure and connectivity, increasing the risk for neuropsychiatric disorders (e.g. depression, anxiety, post-traumatic stress disorder, attention-deficit/hyperac

Post-traumatic stress disorder (PTSD) can develop after exposure to severe traumatic event. PTSD is associated with changes in behavior and reduced neurogenesis. Available data suggests that antipsychotics or enriched environment may positively affect behavioral outcomes and increase neurogenesis in PTSD patients. Our aim was to determine whether aripiprazole, enriched environment or their combination in the PTSD animal model will positively affect behavioral outcomes and hippocampal neurogenesis. We used the single prolonged stress paradigm to induce PTSD related symptoms in animals. Animals

Post-traumatic stress disorder (PTSD) is a multifaceted psychological disorder characterized by deregulated fear and stress responses. Etiology and progression of PTSD involve multiple neurochemical factors that interact in complex ways and consequently alter range of neurotransmitters systems. One of the most important is CRH system, which involvement in fear and stress response is well established. CRH acts through two receptors, CRHR1 that plays role in stress responding and anxious arousal and CRHR2 that is responsible for dampening the stress response initiated by activation of CRHR1. In

Overgeneralization and sleep quality disruption are major components of anxiety and post-traumatic stress disorder (PTSD). This study attempts to elucidate potential links between these elements. We designed a paradigm wherein participants learned associations between three faces and positive, negative, or neutral outcomes. Subsequently, we evaluated their generalization of these faces by examining responses to morphed faces resembling the initially associated faces before and after consolidation during daytime wakefulness or full-night sleep. Our findings reveal that post-sleep, participants

Exposure-based therapies can be highly effective for patients with post-traumatic stress disorder (PTSD) but up to one third of patients do not respond adequately. Repeated exposure to fear-evoking cues is hypothesized to suppress fear responses through the acquisition and recall of new safety learning in a process termed fear extinction. Transcranial direct current stimulation (tDCS) has gained interest as a non-invasive neuromodulation technique that may suppress fear expression or augment fear extinction. We previously established that in mice, repeated anodal tDCS applied over the prefront

The experience of aversive events is a component of everyone’s lives. People perceive aversive events and traumas in distinct ways, but the explanation of this different perception is poorly understood. In some cases, maladaptive responses to traumatic events may leads to chronic fear disorders, including post-traumatic stress disorder (PTSD). Despite the high prevalence of such disorders, effective treatments for trauma remain scarce. Recently, psilocybin has emerged as a promising drug for major depressive disorder (MDD) and potentially PTSD. However, its mechanism of action and how it could

Fear is essential to an individual's survival. Abnormal fear will make people or animals more vulnerable to danger, and even lead to a series of neuropsychiatric diseases. Previous studies have suggested that functional abnormalities of the ventral tegmental area (VTA) may lead to fear-related neuropsychiatric diseases, such as post-traumatic stress disorder and schizophrenia, but the underlying mechanisms remain unclear. Our preliminary data has first shown that the projection from the central amygdala (CeA) to the ventral tegmental area could regulate fear. However, the specific cell types a

Post-traumatic stress disorder affects millions worldwide, with low therapeutic success. Research confirms the involvement of memory processes in pathological and persistent traumatic memories that are difficult to overwrite. Previously, in an animal model, we demonstrated that the extinction can be expedited by closed-loop (CL) stimulation of the medial forebrain bundle (MFB) triggered by sharp-wave ripple (SWR) patterns. Similarly, stimulation of the infralimbic cortex (IL) timed to SWR also maintained a low level of fear response over the long term.We aimed to investigate if the manipulatio

Although fear is known to serve essential purposes in protecting individuals from dangerous situations and threats, dysfunction of fear response can lead to neuropsychiatric disorders – such as pathological anxiety and post-traumatic stress disorder. The understanding of the neuropathophysiology of those disorders is still limited, and therapeutic options (psychotherapy or medication) remain in some cases ineffective. Works investigating the function of neuronal networks helped highlight the implication of the dorsomedial prefrontal cortex (dmPFC) in fear response. Moreover studies on mice hav