ABSTRACT
Electromagnetic field [EMF] radiation affects cellular and brain chemistry and function, resulting in deleterious effects such as free radicals formation, impaired DNA repair, reduced melatonin and blood brain barrier protection, and defects on learning and memory and other higher brain functions. In this paper the effects of low frequency EMF of 50- and 217 Hz, ranges often associated with common electronic devices such as televisions and cell phones were examined on learning and memory in adult male mice. Five groups [n=10 mice/group] of mice [1 control and 4 experimental] were initially trained for the passive avoidance [PA] test. They were then placed in devices creating EMF radiation with varying intensities [0.5 to 2 milli-Tesla, mT] and frequencies [50- and 217-Hz] for 2-weeks [16 hrs/day]. Control mice received no radiation. Learning and memory was tested by the PA test and evaluated based on the following parameters: mean step through latency [STL], number of crossing [Cr#] and time in dark compartment [TDC]. Results showed significant deficiencies in learning and memory in the EM-exposed mice compared to controls: mean STL decreased significantly [p<0.001] in the 50 Hz group [1 and 1.5 mT intensities]. In the 217 Hz group, STL also decreased in the 0.5 and 2 mT groups [p< 0.05]. There was a notable increase in mean Cr# for both groups and TDC for 50 Hz group. Results confirm that long-term exposure to EMF radiation of 50 and 217 Hz, imparts significant harmful changes on memory and learning, reiterating the need for preventive measures against such exposures
ABSTRACT
One of the side effects of diabetes epidemic today in the world is painful neuropathy, the reasons and treatments of which are un- known. Due to the importance of the problem of pain treatment as one of the harmful phenomena in life, this research studies the effect of continued diabetes on the formalin induced pain and Baclofen analgesia in rats. Moreover, the effect of Baclofen as a non-opiate, analgesic drug on the increased pains in the quiescent phase as the model of diabetic pain is investigated. The method is experimental, evaluating the pain level through conducting the formalin test in 3 groups of rats. The first group was divided to control [injection normal saline] and diabetic [injection aloxan 100 mg/kg] which were tested, after one to four weeks from the beginning of diabetes, the second one was divided to a new control and diabetic group, and before performing formalin test, the Baclofen [10 mg/kg] was injected to them. And the third one was divided to two diabetic groups that received Baclofen and normal saline and then the pain of the quiescent phase was compared in them. The results indicate that diabetes increases formalin induced pain [P<0.05] and remained with continued diabetes. It also indicates that diabetes establishes increased pain in the quiescent phase [P<0.05], yet, it has had no influence on the Baclofen analgesic effect on the first phase of formalin test but increased it on the second phase. Moreover, Baclofen can quiet the increased pain in quiescent phase [P<0.05] very well. Due to the results of this study it seems that diabetes, with the changes in the central and peripheral pathways of the pain and also pain control, increases the pain. More studies are required for determining its mechanisms. These changes are accompanied with weakening the internal anti pain systems such as Gaba ergic, which can be treated with Baclofen. Diabetes has no interaction with the Baclofen's analgesic effect, so, Baclofen may be recommended as an effective drug to comfort painful diabetic Neuropathy