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GRUPO DE NEURONAS ESENCIAL EN EL MECANISMO POR EL QUE DEJAMOS DE SENTIR MIEDO: El Instituto
Nacional de Salud Mental en Estados Unidos estima que en el país, en un año dado, cerca de 40 millones de adultos (con 18 o más años
de edad) sufrirán de alguna forma de ansiedad, incluyendo fobias, trastornos de ansiedad y estrés postraumático.
Allanando el camino hacia formas más efectivas de tratamiento para los problemas de ansiedad, en un estudio reciente, Denis Paré (de la
Universidad Rutgers en Newark) ha identificado un componente crítico de la red neuronal de la amígdala, que suele intervenir en la extinción
de los miedos asociados a recuerdos.
Nature. 2008 Jul 31;454(7204):642-5. Epub 2008 Jul 9. Comment in: Nature. 2008 Jul 31;454(7204):589-90. Amygdala intercalated neurons are required for expression of fear extinction. Likhtik E, Popa D, Apergis-Schoute J, Fidacaro GA, Paré D. Center for Molecular and Behavioral Neuroscience, Rutgers, The State University of New Jersey, Newark, New Jersey 07102, USA. Congruent findings from studies of fear learning in animals and humans indicate that research on the circuits mediating fear constitutes our best hope of understanding human anxiety disorders. In mammals, repeated presentations of a conditioned stimulus that was previously paired to a noxious stimulus leads to the gradual disappearance of conditioned fear responses. Although much evidence suggests that this extinction process depends on plastic events in the amygdala, the underlying mechanisms remain unclear. Intercalated (ITC) amygdala neurons constitute probable mediators of extinction because they receive information about the conditioned stimulus from the basolateral amygdala (BLA), and contribute inhibitory projections to the central nucleus (CEA), the main output station of the amygdala for conditioned fear responses. Thus, after extinction training, ITC cells could reduce the impact of conditioned-stimulus-related BLA inputs to the CEA by means of feed-forward inhibition. Here we test the hypothesis that ITC neurons mediate extinction by lesioning them with a toxin that selectively targets cells expressing micro-opioid receptors (microORs). Electron microscopic observations revealed that the incidence of microOR-immunoreactive synapses is much higher in ITC cell clusters than in the BLA or CEA and that microORs typically have a post-synaptic location in ITC cells. In keeping with this, bilateral infusions of the microOR agonist dermorphin conjugated to the toxin saporin in the vicinity of ITC neurons caused a 34% reduction in the number of ITC cells but no significant cell loss in surrounding nuclei. Moreover, ITC lesions caused a marked deficit in the expression of extinction that correlated negatively with the number of surviving ITC neurons but not CEA cells. Because ITC cells exhibit an unusual pattern of receptor expression, these findings open new avenues for the treatment of anxiety disorders.
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