Résumé
Depression causes mental and physical changes which affect quality of life. It is estimated to become the second most prevalent disease, but despite its commonness, the pathophysiology of depression remains unclear and medicine is not sufficiently protective. p-Coumaric acid (p-CA) is a dietary phenolic acid which has been proven to have antifungal, anti-HIV, anti-melanogenic, antioxidant and anti-inflammatory effects. Considering these effects, we investigated whether p-CA can prevent depressive symptoms by reducing inflammatory cytokines in animals injected with lipopolysaccharide (LPS). Changes in despair-related behaviors, inflammatory cytokines, neurotrophic factors and synaptic activity were measured. In these animals, p-CA improved despair-related behavioral symptoms induced by LPS in the forced swim test (FST), tail suspension test (TST) and sucrose splash test (SST). p-CA also prevented the increase of inflammatory cytokines in the hippocampus such as cycloxigenase-2 and tumor necrosis factor-α due to LPS. Similarly, it prevented the reduction of brain-derived neurotrophic factor (BDNF) by LPS. Electrophysiologically, p-CA blocked the reduction of long-term depression in LPS-treated organotypic tissue slices. In conclusion, p-CA prevented LPS-induced depressive symptoms in animals, as determined by behavioral, biochemical and electrophysiological measures. These findings suggest the potential use of p-CA as a preventive and therapeutic medicine for depression.
Sujets)
Animaux , Rats , Symptômes comportementaux , Facteur neurotrophique dérivé du cerveau , Cytokines , Dépression , Suspension des membres postérieurs , Hippocampe , Nécrose , Facteurs de croissance nerveuse , Phénol , Qualité de vie , SaccharoseRésumé
La neuroplasticidad es la potencialidad del sistema nervioso de modificarse para formar conexiones nerviosas en respuesta a la información nueva, la estimulación sensorial, el desarrollo, la disfunción o el daño. En general, la neuroplasticidad suele asociarse al aprendizaje que tiene lugar en la infancia, pero sus definiciones van más allá y tienen un recorrido histórico. Hay diversos componentes bioquímicos y fisiológicos detrás de un proceso de neuroplasticidad y esto lleva a diferentes reacciones biomoleculares químicas, genómicas y proteómicas que requieren de acciones intra y extra neuronales para generar una respuesta neuronal.
Neuroplasticity is the potentiality of the nervous system to change itself and to form neural connections in response to a new information, sensorial stimulation, development, dysfunction or damage. In general, neuroplasticity is often associated with learning during the childhood, but their definitions its going further, and it has an historical follow-up. There are many biochemical and physiological components behind neuroplasticity process, and this leads to biomolecular, chemical, genomics and proteomics processes, that requiring intra and extra-neuronal actions to generate a neural response.
Résumé
Long-term potentiation (LTP) and long-term depression (LTD) of synaptic transmission are forms of synaptic plasticity that have been studied extensively and are thought to contribute to learning and memory. The reversal of LTP, known as depotentiation (DP) has received far less attention however, and its role in behavior is also far from clear. Recently, deficits in depotentiation have been observed in models of schizophrenia, suggesting that a greater understanding of this form of synaptic plasticity may help reveal the physiological alterations that underlie symptoms experienced by patients. This review therefore seeks to summarize the current state of knowledge on DP, and then put the deficits in DP in models of disease into this context.
Sujets)
Humains , Dépression , Apprentissage , Potentialisation à long terme , Dépression synaptique à long terme , Mémoire , Plasticité neuronale , Matières plastiques , Schizophrénie , Transmission synaptiqueRésumé
Long-term potentiation (LTP) and long-term depression (LTD) of synaptic transmission are forms of synaptic plasticity that have been studied extensively and are thought to contribute to learning and memory. The reversal of LTP, known as depotentiation (DP) has received far less attention however, and its role in behavior is also far from clear. Recently, deficits in depotentiation have been observed in models of schizophrenia, suggesting that a greater understanding of this form of synaptic plasticity may help reveal the physiological alterations that underlie symptoms experienced by patients. This review therefore seeks to summarize the current state of knowledge on DP, and then put the deficits in DP in models of disease into this context.