Hippocampal damage after traumatic brain injury (TBI) is associated with late posttraumatic conditions, such as depression, cognitive decline and epilepsy. Mechanisms of selective hippocampal damage after TBI are not well understood. In this study, using rat TBI model (lateral fluid percussion cortical injury), we assessed potential association of immediate posttraumatic seizures and changes in corticosterone (CS) levels with neuroinflammation and neuronal cell loss in the hippocampus. Indices of distant hippocampal damage (neurodegeneration and neuroinflammation) were assessed using histological analysis (Nissl staining, Iba-1 immunohistochemical staining) and ELISA (IL-1β and CS) 1, 3, 7 and 14 days after TBI or sham operation in male Wistar rats (n = 146). IL-1β was elevated only in the ipsilateral hippocampus on day 1 after trauma. CS peak was detected on day 3 in blood, the ipsilateral and contralateral hippocampus. Neuronal cell loss in the hippocampus was demonstrated bilaterally; in the ipsilateral hippocampus it started earlier than in the contralateral. Microglial activation was evident in the hippocampus bilaterally on day 7 after TBI. The duration of immediate seizures correlated with CS elevation, levels of IL-1β and neuronal loss in the hippocampus. The data suggest potential association of immediate post-traumatic seizures with CS-dependent neuroinflammation-mediated distant hippocampal damage.
This study aimed to examine the behavioral and neural correlates of facial emotion recognition in young women with subsyndromal panic disorder (SPD). In the experiment 15 non-medicated women with SPD and 17 matched healthy controls were tasked with recognizing angry, fearful, happy, and neutral facial expressions, and accuracy, reaction time (RT), and event-related potentials (ERPs) were recorded. Significant between-group differences in behavioral characteristics (accuracy of emotion recognition and RT) were not found, however, the SPD subjects demonstrated a slower response to fearful expressions compared to neutral and happy expressions. More distinct between-group differences were observed for the EPRs. The SPD subjects demonstrated increased amplitudes of the P100 ERP component in the occipital area and the P200 component over the occipital and temporal regions. In the frontal regions the SPD group showed a greater amplitude of the N200 component and also an increased negativity 350−450 ms after stimulus presentation. According to the dipole source modeling data, the SPD subjects showed enhanced activation in the extra-striate cortex which increased in intensity when angry and fearful faces were presented. Thus, young women with SPD which manifested in infrequent panic attacks showed significant alterations in ERP characteristics of emotional processing, which may be considered as a more sensitive indicator of early-stage panic disorder than the observed behavioral measures.
K+ channels are of great interest to epilepsy research as mutations in their genes are found in humans with inherited epilepsy. At the level of cellular physiology, K+ channels control neuronal intrinsic excitability and are the main contributors to membrane repolarization of active neurons. Recently, a genetically modified voltage-dependent K+ channel has been patented as a remedy for epileptic seizures.
Neuroscience and Behavioral Physiology publishes original contributions of international importance in the fields of brain physiology, psychopharmacology, neuroendocrinology, neurogenetics, psychophysiology and neurochemistry, as well as in the anatomy and pathology of the nervous system. The focus of the journal is basic research related to brain function and behavior, cellular and molecular mechanisms underlying higher brain functions.