RESUMEN
The use of mobile phones is increasing, and the main health concern is the possible deleterious effects of radiation on brain functioning. The present study aimed to examine the effects of exposure to a global system for mobile communication (GSM) with mobile phones on inhibitory avoidance (IA) memory performance as well as the involvement of endogenous opioids and nitric oxide (NO) in this task. Male Wistar rats, 10-12â¯weeks old, were used. The results showed that four weeks of mobile phone exposure impaired IA memory performance in rats. The results also revealed that post-training, but not pre-training, as well as pre-test intracerebroventricular (i.c.v.) injections of naloxone (0.4, 4 and 40â¯ng/rat), dose-dependently recovered the impairment of IA memory performance induced by GSM radiation. Additionally, the impairment of IA memory performance was completely recovered in the exposed animals with post-training treatment of naloxone (40â¯ng/rat) plus pre-test i.c.v. injections of L-arginine (100 and 200â¯nmol/rat). However, pre-test i.c.v. injections of L-NAME (10 and 20â¯nmol/rat), impaired IA memory performance in the animals receiving post-training naloxone (40â¯ng/rat). In the animals receiving post-training naloxone treatment, the impairment of IA memory performance due to pre-test i.c.v. injections of L-NAME was recovered by the pre-test co-administration of L-arginine. It was concluded that the recovery from impairment of IA memory in GSM-exposed animals with post-training naloxone treatment was the result of blockade of the opioidergic system in early memory consolidation as well as activation of the nitrergic system in the retrieval phase of memory.
Asunto(s)
Reacción de Prevención/efectos de la radiación , Uso del Teléfono Celular/efectos adversos , Consolidación de la Memoria/efectos de la radiación , Animales , Arginina/farmacología , Masculino , Memoria/fisiología , Consolidación de la Memoria/efectos de los fármacos , Morfina/farmacología , NG-Nitroarginina Metil Éster/farmacología , Naloxona/farmacología , Neuronas Nitrérgicas/efectos de la radiación , Óxido Nítrico/fisiología , Radiación , Ratas , Ratas Wistar , Receptores Opioides/efectos de la radiaciónRESUMEN
A single intraperitoneal injection of a gram-positive pathogen Clostridium perfringens (Cp) causes a remarkable down-regulation the constitutive nitric oxide synthase (cNOS) with a simultaneous increase in the activity of inducible NOS (iNOS) and the level of reactive nitrogen species in the rat brain major regions (cortex, striatum, hippocampus and hypothalamus) at 48 h post-administration of Cp. Treatment by both a semiconductor laser (SCL) and/or a light-emitting diode (LED) with same wavelength, energy density and time exposure (continuous wave, λ=654 nm, fluence=1.27 J/cm(2), time exposure=600 s) could modulate brain nitrergic response following Cp-infection. Besides, unlike the LED, the SCL-irradiation prevents the cNOS inhibition in all the studied brain regions and might be useful in restoring its function in neurotransmission and cerebral blood flow, along with providing a protective effect against nitrosative stress-induced iNOS-mediated injury in the brain regions.
Asunto(s)
Infecciones por Clostridium/radioterapia , Clostridium perfringens/efectos de la radiación , Hipotálamo/efectos de la radiación , Láseres de Semiconductores/uso terapéutico , Neuronas Nitrérgicas/efectos de la radiación , Animales , Infecciones por Clostridium/enzimología , Hipotálamo/enzimología , Hipotálamo/microbiología , Masculino , Neuronas Nitrérgicas/metabolismo , Óxido Nítrico Sintasa de Tipo I/efectos adversos , Óxido Nítrico Sintasa de Tipo I/antagonistas & inhibidores , Óxido Nítrico Sintasa de Tipo I/metabolismo , Óxido Nítrico Sintasa de Tipo II/metabolismo , Distribución Aleatoria , Ratas , Especies de Nitrógeno Reactivo/biosíntesis , Especies de Nitrógeno Reactivo/efectos de la radiación , Resultado del TratamientoRESUMEN
Using a nitric oxide (NO)-specific fluorescent probe, we have examined the location of NO generation in the urethra from sheep and rat when induced by either electrical field- or light-stimulation (EFS and LS, respectively). In addition, we studied the effect of specific glutathione (GSH) modifiers, acting upon different cellular GSH pools, on NO release and on urethral relaxation. Both EFS and LS led to fluorescence emission from a fiber network associated with neuronal NO synthase (nNOS) immunoreactive nerves. Both the relaxation and the fluorescence elicited by EFS were blocked by specific nNOS inhibitors, but these parameters were not significantly modified by endogenous GSH depletion. In contrast, the opposite was found for LS-induced responses. Moreover, when the mitochondrial pool was effectively reduced by incubation with ethacrynic acid, the responses to LS were further reduced until they disappeared after intensive LS. Our results confirm that while NO is released by nNOS activation, the photolytic breakdown of an endogenous nitro-compound, probably S-nitroso-glutathione, in nitrergic nerves (and in the vascular endothelium) is the only factor responsible for photo-relaxation. The possible role of this mechanism in NO inactivation and as a protective mechanism in NO-generating structures is further discussed.