The effect of pulsed electromagnetic radiation from mobile phone on the levels of monoamine neurotransmitters in four different areas of rat brain.

BACKGROUND: The use of mobile phones is rapidly increasing all over the world. Few studies deal with the effect of electromagnetic radiation (EMR) on monoamine neurotransmitters in the different brain areas of adult rat. AIM: The aim of the present study was to investigate the effect of EMR on the concentrations of dopamine (DA), norepinephrine (NE) and serotonin (5-HT) in the hippocampus, hypothalamus, midbrain and medulla oblongata of adult rats. MATERIALS AND METHODS: Adult rats were exposed daily to EMR (frequency 1800 MHz, specific absorption rate 0.843 W/kg, power density 0.02 mW/cm2, modulated at 217 Hz) and sacrificed after 1, 2 and 4 months of daily EMR exposure as well as after stopping EMR for 1 month (after 4 months of daily EMR exposure). Monoamines were determined by high performance liquid chromatography coupled with fluorescence detection (HPLC-FD) using their native properties. RESULTS: The exposure to EMR resulted in significant changes in DA, NE and 5-HT in the four selected areas of adult rat brain. CONCLUSIONS: The exposure of adult rats to EMR may cause disturbances in monoamine neurotransmitters and this may underlie many of the adverse effects reported after EMR including memory, learning, and stress.

Cerebrolysin attenuates cerebral and hepatic injury due to lipopolysaccharide in rats.

This study aimed to investigate the effect of cerebrolysin on oxidative stress in the brain and liver during systemic inflammation. Rats were intraperitoneally challenged with a single subseptic dose of lipopolysaccharide (LPS; 300 µg/kg) without or with cerebrolysin at doses of 21.5, 43 or 86 mg/kg. After 4 h, rats were euthanized and the brain and liver tissues were subjected to biochemical and histopathological analyses. Cerebrolysin revealed inhibitory effects on the elevation of lipid peroxidation and nitric oxide induced by LPS. In contrast, the decrease in reduced glutathione level and paraoxonase activity induced by LPS was attenuated by an injection of cerebrolysin in a dose-dependent manner. Moreover, cerebrolysin reduced LPS-induced activation of brain NF-κB and reversed LPS-induced decline of brain butyrylcholinesterase and acetylcholinesterase activities in a dose-dependent manner. Histopathological analyses revealed that neuronal damage and liver necrosis induced by LPS were ameliorated by cerebrolysin dose-dependently. Cerebrolysin treatment dose-dependently attenuated LPS-induced expressions in cyclooxygenase 2, inducible nitric oxide synthase, and caspase-3 in the cortex or striatum as well as the liver. These results suggest that cerebrolysin treatment might have beneficial therapeutic effects in cerebral inflammation. Cerebrolysin might also prove of value in liver disease and this possibility requires further exploration.

Nicotine restores monoamine neurotransmitter changes in the cortex and hippocampus of reserpinized rats as a model of depression.

BACKGROUND AND OBJECTIVES: A number of studies have shown that nicotine has an antidepressant-like effect. The prevalence of smoking is much higher in people suffering from depression. In addition, the administration of nicotine from transdermal nicotine patch can exert antidepressant activity in nonsmokers and the continuous infusion of nicotine to rats attenuates learned helplessness, a putative behavioral model of depression. The aim of the present study is to elucidate the neurochemical effect of nicotine on monoamine levels in the cerebral cortex and hippocampus of reserpinized rats as a model of depression. MATERIALS AND METHODS: In the present study, rats were divided into control animals treated with saline and reserpinized group which received a daily i.p injection of reserpine for 15 days to establish the animal model of depression. Starting from the 16th day, the reserpinized rats were divided into reserpinized rats, and reserpinized rats treated daily with nicotine (0.4 mg/kg) for 15 and 30 days. After decapitation, the cerebral cortex and hippocampus of each rat were dissected out. The levels of monoamine neurotransmitters (serotonin, norepinephrine and dopamine) were measured in each area using a spectrofluorimeter. RESULTS: The daily i.p injection of reserpine induced a significant decrease in monoamine levels in the cortex and hippocampus. Nicotine administration restored the changes in monoamine neurotransmitters induced by reserpine in both areas after 30 days. DISCUSSION: The data of the present study suggest that the antidepressant-like effect of nicotine could be mediated by the effect of nicotine on monoamine neurotransmitters in the cortex and hippocampus of rat brain.