EXPRESSION OF SINAPTO-VESICULAR PROTEINS IN BRAIN AREAS OF AN ANIMAL MODEL OF METABOLIC SYNDROME

Introduction: Metabolic syndrome (MetS) is characterized by obesity, dyslipidemia, hypertension and insulin resistance (IR). MetS and its components induce neuroinflammation and cerebrovascular disease (CVD). CVD refers to a group of conditions that affects the blood circulation. This process in the cerebral arteries may cause stroke and/or mild cognitive impairment. Vascular dementia (VaD) is the most important disorder that can be associated with inflammation, type-2 diabetes mellitus(T2DM), obesity and hypertension. Leptin level is associated with a lower cognitive decline incidence. Thus, the obese Zucker rats (OZRs), with mutation (fa/fa) in the gene encoding the leptin receptor and as control Zucker lean (LZR) were used. To demonstrate a connection between dementia and obesity, the synaptic transmission was investigated. Methods: Male OZRs and the littermate LZRs of different ages were used. The rats were monitored for body weight, food intake, blood pressure and blood levels of triglycerides, cholesterol and glucose. Behavioral tests were performed. In OZRs, some behavioral tasks were changed. Brains were processed for the immunochemical and immunohistochemical analysis of pre- and postsynaptic proteins as synaptophysin (Syp), vesicular protein SV2A, SV2B, SV2C and PSD-95, respectively. Results: The results show a reduction of synaptic proteins in brain. A decrease of SV2B, Syp and PSD-95 in the frontal cortex of 20-weeks-old OZRs was observed. Conclusions: SV2B probably controls synaptic vesicle release. Its decrease was also found in hippocampus and cortex in Alzheimer’s disease and VaD patients. Therefore, a decrease of synaptic proteins can be related to the cerebrovascular alterations both in the frontal cortex and in the hippocampus.