Palmitoylethanolamide Reduces Neuropsychiatric Behaviors by Restoring Cortical Electrophysiological Activity in a Mouse Model of Mild Traumatic Brain Injury

摘要: Traumatic brain injury (TBI) represents a major public health problem, which is associated with neurological dysfunction. In severe or moderate cases of TBI, in addition to its high mortality rate, subjects may encounter diverse behavioural dysfunctions. Previous reports suggest that an association between TBI and chronic pain syndromes tends be more common patients mild forms injury. Despite causing minimal damage, (mTBI) often leads persistent psychologically debilitating symptoms, can include anxiety, various memory learning deficits, depression. At present, no effective treatment options are available for these little known about the complex cellular activity affecting neuronal occurs response during late phase. Here, we used mouse model investigate effect Palmitoylethanolamide (PEA) on both sensorial neuropsychiatric dysfunctions mTBI through behavioural, electrophysiological, biomolecular approaches. Fourteen-day mice developed anxious, aggressive, reckless behaviour, whilst depressive-like behaviour impaired social interactions were observed from 60th day onwards. Altered was changes interleukin 1 beta (IL-1β) expression levels firing medial prefrontal cortex (m-PFC). Compared vehicle, PEA restored phenotype partially normalised biochemical functional occurring at supraspinal level. conclusion, our findings reveal some modifications responsible alterations as pharmacological tool ameliorate dysfunction induced by trauma.