Investigation of the effects of IL-1B on neuroplasticity and the Endocannabinoid System of hippocampal neurons

Abstract

Neuroinflammation is a term used to describe the immune responses of the Central Nervous System (CNS). Although the response is initiated to protect the CNS, the effect generated can be toxic, which can lead to neural death. In this sense, the Endocannabinoid System (ECB) appears as neuroprotective, capable of preventing or delaying neuronal loss caused by neuroinflammation, thus contributing to the management of synaptic plasticity. In view of the importance of SECB for neural homeostasis, it is necessary to understand whether this system can be affected by IL-1², since it is one of the main cytokines released in the context of neuroinflammation, in addition to playing an important role in homeostasis synaptic. From this, the effects of IL-1² on neuroplasticity and SECB signaling in primary culture of hippocampal neurons will be evaluated. Therefore, it will be investigated whether IL-1² can alter the expression of SECB molecules and proteins involved in synaptogenesis. In addition, the effect of this cytokine on the release of GABA, glutamate and BDNF will be analyzed, as well as whether IL-1² can alter the morphology and extent of neuritic processes. The knowledge generated by the present study will contribute to a better understanding of the mechanisms involved in neuroinflammation.