« Previous AbstractDetection of conspecific pheromones elicits fos expression in GABA and calcium-binding cells of the rat vomeronasal system-medial extended amygdala    Next AbstractContrasting Volatilomes of Livestock Dung Drive Preference of the Dung Beetle Bubas bison (Coleoptera: Scarabaeidae) »

Exp Toxicol Pathol

Title:		Kainic acid-induced early genes activation and neuronal death in the medial extended amygdala of rats
Author(s):		Pereno GL; Balaszczuk V; Beltramino CA;
Address:		"Catedra de Neurofisiologia y Psicofisiologia, Facultad de Psicologia, Universidad Nacional de Cordoba 5000, Cordoba, Argentina. gpereno@psyche.unc.edu.ar"
Journal Title:		Exp Toxicol Pathol
Year:		2011
Volume:		20100224
Issue:		3
Page Number:		291 - 299
DOI:		10.1016/j.etp.2010.02.001
ISSN/ISBN:		1618-1433 (Electronic) 0940-2993 (Linking)
Abstract:		"The medial extended amygdala modulates pheromonal perception, influencing emotional and social behavior. As the amygdala is part of neuronal circuits that are very sensitive to excitability, its neurons are targets of seizures in temporal lobe epilepsy. It has been suggested that the hippocampus is strongly involved this pathology. There is less consistent information, however, on the effects of this disease in the amygdala. The effects of status epilepticus on the medial extended amygdala were analyzed by immunohistochemistry for neural stress and by the amino-cupric-silver technique for neuronal death in rats after kainic acid (KA) administration. Sixty adult Wistar male rats were used. Thirty animals received an injection of KA, and 30 were injected with saline. After 2, 4, 12, 24 and 48 h survival the brains were stained for Fos and FosB and for neuronal death. In the present study we show that KA induces Fos and FosB expression in neurons of the medial extended amygdala after 2, 4-48 h, with time courses that are different between them and from control animals. While Fos-IR peaks at 2-4 h post KA and then decreases, FosB-IR increases in the same period reaching its highest expression at 24-48 h. Moreover, KA injection produced massive neuronal death with a peak at 24 h. This neurodegeneration paralleled FosB-IR protein expression. These findings show that KA produces neuronal stress and activation of early genes and neuronal death in the medial extended amygdala, demonstrating the vulnerability of its neurons to the epileptogenic effects of KA"
Keywords:		"Amygdala/drug effects/metabolism/*pathology Animals Cell Death/drug effects Gene Expression/*drug effects Genes, Immediate-Early/*drug effects Kainic Acid/*toxicity Male Nerve Degeneration/chemically induced/genetics/pathology Neurons/drug effects/metabol;"
Notes:		"MedlinePereno, German L Balaszczuk, Veronica Beltramino, Carlos A eng Research Support, Non-U.S. Gov't Germany 2010/02/27 Exp Toxicol Pathol. 2011 Mar; 63(3):291-9. doi: 10.1016/j.etp.2010.02.001. Epub 2010 Feb 24"