Changes in stimuli and feeding in pregnant mothers alter the behavior of offspring. Since behavior is mediated by brain activity, it is expected that postnatal changes occur at the level of currents, receptors or soma and dendrites structure and modulation. In this work, we explore at the mechanism level the effects on Sprague–Dawley rat offspring following the administration of serotonin (5-HT) agonist 5-methoxytryptamine (5-MT). We analyzed whether 5-HT affects the glutamate-activated (IGlut) and N-methyl-D-aspartate (NMDA)-activated currents (IGlut, INMDA) in dissociated pyramidal neurons from the prefrontal cortex (PFC). For this purpose, we performed voltage-clamp experiments on pyramidal neurons from layers V-VI of the PFC of 40-day-old offspring born from 5-MT-treated mothers at the gestational days (GD) 11 to 21. We found that the pyramidal-neurons from the PFC of offspring of mothers treated with 5-MT exhibit a significant increased reduction in both the IGlut and INMDA when 5-HT was administered. Our results suggest that the concentration increase of a neuromodulator during the gestation induces changes in its modulatory action over the offspring ionic currents during the adulthood thus contributing to possible psychiatric disorders.
La depresión es un problema de salud mundial. La sertralina, un antidepresivo de uso común, puede ocasionar efectos secundarios en la fertilidad. El tratamiento con alucinógenos, por ejemplo, la psilocibina, se considera un procedimiento alternativo para tratar la depresión. El objetivo de este trabajo fue comparar los efectos de la administración sub-crónica del extracto metanólico de P. cubensis o de sertralina sobre la calidad espermática de ratas macho. Treinta ratas machos Sprague-Dawley se distribuyeron en cinco grupos (n=6). Un grupo testigo absoluto (TA) de animales no separados de la madre; animales separados de la madre (Vetulani, 2013; DEP); medicados diariamente con sertralina (5 mg/kg; DEP+SERT); administrados con extracto metanólico de P. cubensis (0.1 mg/kg; DEP+EXTR); y con solución salina + 1% de Tween 80 como vehículo (DEP+VH). La administración se realizó desde el día 45 de edad y hasta el día 60. Los animales fueron sacrificados a los seis meses de edad. Se disecaron los epidídimos y se obtuvieron espermatozoides de la cola. Se cuantificó el número total y la viabilidad de los espermatozoides, así como el porcentaje de espermatozoides con motilidad progresiva rápida, lenta, in situ e inmóviles. La concentración (F=1.25624; p=0.3133), el porcentaje de viabilidad (F=0.96249; p=0.44528), de inmovilidad (F=2.31662; p=0.08509), y de motilidad progresiva lenta (F= 0.09148; p= 0.98428) de los espermatozoides no mostraron diferencias significativas entre grupos. La prueba de comparación de medias de Tukey arrojo que el porcentaje de motilidad progresiva rápida en SERT es menor con respecto a TA (α=0.05; p=0.04166), y EXTR (α=0.05; p=0.01971). Además, el porcentaje de espermatozoides in situ en EXTR es más bajo con respecto VH (α=0.05; p=0.00348), y TA (α=0.05; p=0.00619). Nuestros resultados sugieren que el uso del extracto metanólico de P. cubensis no afecta los parámetros de fertilidad a diferencia de la sertralina que afecta principalmente la motilidad.
Huntington’s Disease (HD) is a degenerative disease which produces cognitive and motor disturbances. Treatment with GABAergic agonists improves the behavior and activity of mitochondrial complexes in rodents treated with 3-nitropropionic acid to mimic HD symptomatology. Apparently, GABA receptors activity may protect striatal medium spiny neurons (MSNs) from excitotoxic damage. This study evaluates whether mitochondrial inhibition with 3-NP that mimics the early stages of HD, modifies the kinetics and pharmacology of GABA receptors in patch clamp recorded dissociated MSNs cells. The results show that MSNs from mice treated with 3-NP exhibited differences in GABA-induced dose-response currents and pharmacological responses that suggests the presence of GABAC receptors in MSNs. Furthermore, there was a reduction in the effect of the GABAC antagonist that demonstrates a lessening of this GABA receptor subtype activity as a result of mitochondria inhibition.
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