Name: BRUNA ZANETTI ROHOR
Type: MSc dissertation
Publication date: 11/12/2015
Advisor:

Namesort descending Role
RITA GOMES WANDERLEY PIRES Advisor *

Examining board:

Namesort descending Role
CRISTINA MARTINS E SILVA Co advisor *
LÍVIA CARLA DE MELO RODRIGUES External Examiner *
RITA GOMES WANDERLEY PIRES Advisor *

Summary: The environment is formed by a set of situations around the individual and has influence on all organisms. A stressor environment has negative influences in a subject, but an enriched environment (EE) has positive influences. In animals, the AE is defined as a combination of inanimate and social complex stimuli that can improve motor, cognitive and sensory functions. The EE is composed of different objects of different shapes, sizes, colors, textures, among others. Environmental novelty, voluntary physical activity and social interaction are also part of EE. The EE is capable of promoting increased visual, sensory, cognitive and motor functions. Cognitive improvement, increased synaptic plasticity, adult hippocampal neurogenesis, modulation of gene expression and changes in levels of neurotransmitters and neurotrophic factors are EE-induced alterations already described. However, several EE paradigms are found in the literature, and this variety of protocols produces a range of controversial results on the effects induced by EE. Time is an important factor that influences the effects induced by the EE. In this context, the aim of this study was to evaluate the cognitive and molecular changes observed in mice exposed to EE or SE (stardard environment) for 30 or 60 days, to check if the exposure time affects those parameters. We performed object recognition and social memory tests, social interaction test, and evaluated components belonging to cholinergic and glutamatergic neurotransmitter systems, endocannabinoid system and neurotrophic factors, such as BDNF and GDNF, which are all associated to cognitive processes in the cortex. The EE exposure for 30 or 60 days did not induce effects on object recognition and social memories, but both exposure times increased social interaction in mice. The EE for 30 days causes a decreased gene expression of α7, M1, mGluR5 receptors, and an increase in the gene expression of MAGL. The EE for 60 days decreased the gene expression of M1 and DAGL, but increased the gene expression of ChAT and FAAH. Both exposure times increased the protein expression of BDNF. In this context, this study demonstrates that different exposure times to EE can induce different responses to cognitive and molecular parameters evaluated. It also suggests that more studies regarding the different effects of time exposure to EE must be conducted in order to define the different protocols that could be used in the prevention and/ou treatment of neurodegenerative diseases´s such as Parkinson´s disease, Huntington´s disease, Alzheimer disease, drug addiction, among others.

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