Overexpression of the immediate-early genes Egr1, Egr2, and Egr3 in two strains of rodents susceptible to audiogenic seizures.

Genetic animal models of epilepsy are an important tool for further understanding the basic cellular mechanisms underlying epileptogenesis and for developing novel antiepileptic drugs. We conducted a comparative study of gene expression in the inferior colliculus, a nucleus that triggers audiogenic seizures, using two animal models, the Wistar audiogenic rat (WAR) and the genetic audiogenic seizure hamster (GASH:Sal). For this purpose, both models were exposed to high intensity auditory stimulation, and 60min later, the inferior colliculi were collected. As controls, intact Wistar rats and Syrian hamsters were subjected to stimulation and tissue preparation protocols identical to those performed on the experimental animals. Ribonucleic acid was isolated, and microarray analysis comparing the stimulated Wistar and WAR rats showed that the genomic profile of these animals displayed significant (fold change, |FC|≥2.0 and p<0.05) upregulation of 38 genes and downregulation of 47 genes. Comparison of gene expression profiles between stimulated control hamsters and stimulated GASH:Sal revealed the upregulation of 10 genes and the downregulation of 5 genes. Among the common genes that were altered in both models, we identified the zinc finger immediate-early growth response gene Egr3. The Egr3 protein is a transcription factor that is induced by distinct stress-elicited factors. Based on immunohistochemistry, this protein was expressed in the cochlear nucleus complex, the inferior colliculus, and the hippocampus of both animal models as well as in lymphoma tumors of the GASH:Sal. Our results support that the overexpression of the Egr3 gene in both models might contribute to neuronal viability and development of lymphoma in response to stress associated with audiogenic seizures. This article is part of a Special Issue entitled "Genetic and Reflex Epilepsies, Audiogenic Seizures and Strains: From Experimental Models to the Clinic".

ACTUALIZACIÓN EN MEDICINA DE FAMILIA: Síndrome de Sudeck (distrofia simpático refleja) / UP-DATE IN FAMILY MEDICINE: Sudeck's syndrome (reflex sympathetic dystrophy syndrome)

Desde que Mitchel en 1864 la denominara causalgia y en1909 Paul Sudeck la bautizara, a día de hoy continúa siendoun reto para la clínica médica. Su inespecificidad diagnóstica,añadida al gran número de factores precipitantes y a suetiopatogenia no claramente esclarecida y de terapéuticacontrovertida hacen de esta enfermedad un cuadro clínicocomplejo tanto para el paciente como para quien lo asiste.Llegar a un diagnóstico precoz es el eje principal del tratamientodel síndrome de Sudeck.Puede afectar a cualquier edad y tanto a hombres como amujeres, aunque estadísticamente es más frecuente en mujeresjóvenes.La incidencia de la enfermedad es variable, oscilando entreel 2 y el 25% de la población, aunque en nuestro país noconocemos cifras. Indudablemente es una entidad que pasahabitualmente desapercibida para nuestra comunidad médicaen general (AU)

Since Mitchell coined the term causalgia in 1864 and PaulSudeck baptized it in 1909, this disease continues to be achallenge for the medical clinician. Its non-specific diagnosisas well as its large number of precipitating factors, this alladded to its etiopathogenesis that cannot be clearly clarifiedand its controversial treatment, makes this disease a complexclinical picture for both the patient and treating clinician.Reaching an early diagnostic is fundamental in the treatmentof Sudeck’s syndrome. It can affect any age group andboth men as well as women, although it is more frequent inyoung women statistically.The incidence of the illness is variable, ranging from 2%to 25% of the population. Although there are no known valuesin our country, it is undoubtedly a condition that generallygoes unnoticed in our medical community (AU)