Effects of chronic noise stress on spatial memory of rats in relation to neuronal dendritic alteration and free radical-imbalance in hippocampus and medial prefrontal cortex

• Published in: Neuroscience letters Vol. 399; no. 1; pp. 17 - 22
• Main Authors: Manikandan, Sundaramahalingam, Padma, Moorthy K, Srikumar, Ramasundaram, Jeya Parthasarathy, Narayanaperumal, Muthuvel, Arumugam, Devi, Rathinasamy Sheela
• Format: Journal Article
• Language: English
• Published: Shannon Elsevier Ireland Ltd 15-05-2006; Elsevier
• Subjects: Animals; Antioxidants - metabolism; Biological and medical sciences; Chronic Disease; Corticosterone - blood; Dendrites - pathology; Eight-arm radial maze; Free Radicals - metabolism; Frontal Lobe - enzymology; Frontal Lobe - metabolism; Frontal Lobe - pathology; Fundamental and applied biological sciences. Psychology; Hippocampus; Hippocampus - enzymology; Hippocampus - metabolism; Hippocampus - pathology; Male; Maze Learning; Medial prefrontal cortex; Memory; Noise - adverse effects; Noise stress; Oxidative stress; Rats; Rats, Wistar; Stress, Psychological - metabolism; Stress, Psychological - physiopathology; Vertebrates: nervous system and sense organs; Noise stress; Eight-arm radial maze; Medial prefrontal cortex; Oxidative stress; Hippocampus; Rat; Noise; Rodentia; Central nervous system; Prefrontal cortex; Free radical; Encephalon; Vertebrata; Chronic; Mammalia; Animal; Spatial memory
• ISSN: 0304-3940; 1872-7972
• DOI: 10.1016/j.neulet.2006.01.037

Spatial memory is coordinated with different brain regions especially hippocampus (HIP) and medial prefrontal cortex (mPFC). Influence of noise stress on working and reference memory error in rats was evaluated by radial eight-arm maze experiment. Changes in the dendritic count were observed in the brain regions such as CA1, CA3 regions of HIP and layers II, III of mPFC. In order to understand the possible mechanism behind noise stress-induced changes, free radical status and acetylcholinesterase (AChE) activity in HIP and mPFC were evaluated. Plasma corticosterone level was also evaluated. Results obtained in this study showed that after noise-stress exposure, 100
dBA/4
h per day for 30 days, working and reference memory error increased significantly (
P
<
0.05) when compared to control animals. Neuronal dendritic count in the HIP was reduced in the 2nd and 3rd order dendrites but not in the mPFC. Superoxide dismutase, lipid peroxidation, plasma corticosterone level and AChE activity were significantly increased in the 1 day, 15 days and 30 days stress groups animal significantly. Catalase and glutathione peroxidase activity were increased in the 1 day and 15 days noise-stress groups but decreased in the 30 days noise-stress group and GSH level was decreased in all the stress exposed animals. In conclusion, oxidative stress, increased AChE activity, reduced dendritic count in HIP, mPFC regions and elevated plasma corticosterone level which develops in long-term noise-stress exposed rats, might have caused the impairment of spatial memory.