ABSTRACT
@#Objectives: Calcitonin gene-related peptide (CGRP) is currently considered to be a major contributing factor in migraine headache. Botulinum toxin type A (BTXA) was found to be effective in migraine prevention. However, the mechanism of action in patients was unknown. Using injection as in clinical setting, the study aimed to determine whether BTXA could decrease the sensitization of the trigeminovascular nociceptive system through the reduction of CGRP action. Methods: Adult male Wistar rats were pretreated with normal saline solution or BTXA before KCl application to induce cortical spreading depression (CSD) or NaCl application as a control. Regional cerebral blood flow at parietal cortex was measured for 90 min after KCl or NaCl application. Tissues from trigeminal ganglion (TG) and trigeminal nucleus caudalis (TNC) were then collected for CGRP and c-Fos measurement respectively. Results: BTXA pretreatment significantly decreased the cumulative blood flow and number of hyperemic peaks induced by KCl. Numbers of CGRP positive cells at TG and c-Fos positive cells at TNC were also reduced by BTXA.Conclusion: BTXA pretreatment reduced CGRP production and release from the TG leading to lessen CSD production and persistent activation of TNC which played a major role in migraine headache.
ABSTRACT
Background and objective: Although the electromagnetic radiation (EMR) emitted by mobile phones does not possess high energy like those of much higher frequencies such as X-rays and gamma-rays, several studies were reported with results showing that mobile phone use could produce hazardous health effects. These include headaches, changes in sleep patterns, electroencephalogram (EEG) and blood pressure. The present study was aimed to examine the effect of mobile phone exposure on brain oxidative stress. Methods: A group of about 300 g body weight male Wistar rats (EMR-exposed group) was put into re-straining cages and, after an equilibration period of at least 30 minutes, was exposed to a 900 MHz electromagnetic signal from two mobile phones (GSM system) at less than 10 cm distance for one hour in a day. This exposure was repeated for one week. Another group of animals (control group) served as a control and were subject to the same procedure but at more than 10 cm distance from the mobile phones. After the last exposure, the brains were removed, weighed and homogenized for determination of malondialdehyde (MDA) and glutathione (GSH). Results: The MDA concentrations in brain homogenates of the animals in the EMR-exposed group were not different from the control group of animals. Also, the GSH concentrations in the EMR-exposed group were at about the same levels as those in the control group. Conclusion: The present study provided no additional data indicating the probable role of oxidative stress in producing health effects of EMR exposure from mobile phone use.