Neuroscience
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Prenatal stress and overexposure to glucocorticoids (GC) during development may be associated with an increased susceptibility to a number of diseases in adulthood including neuropsychiatric disorders, such as depression and anxiety. In animal models, prenatal overexposure to GC results in hyper-responsiveness to stress in adulthood, and females appear to be more susceptible than males. Here, we tested the hypothesis that overexposure to GC during fetal development has sex-specific programming effects on the brain, resulting in altered behaviors in adulthood. ⋯ Prenatal DEX increased TpH2 mRNA selectively in the female caudal DRN at P7, whereas it decreased TpH2 mRNA selectively in the female caudal DRN in adulthood. In animals challenged with restraint stress in adulthood, TpH2 mRNA was significantly lower in rostral DRN of prenatal DEX-treated females compared to vehicle-treated females. These data demonstrated that prenatal overexposure to GC alters the development of TpH2 gene expression and these alterations correlated with lasting behavioral changes found in adult female offspring.
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Cognitive flexibility is the ability to switch between different rules or concepts and behavioral flexibility is the overt physical manifestation of these shifts. Behavioral flexibility is essential for adaptive responses and commonly measured by reversal learning and set-shifting performance in rodents. Both tasks have demonstrated vulnerability to stress with effects dependent upon stressor type and number of repetitions. ⋯ Enhancing post-synaptic norepinephrine function, serotonin availability, and dopamine receptor activation rescues and/or prevents behavioral flexibility performance following stress. While this review highlights a lack of a standardization of stress paradigms, some consistent effects are apparent. Future studies are necessary to specify the mechanisms underlying the stress-induced impairments of behavioral flexibility, which will aid in alleviating these symptoms in patients with some psychiatric disorders.
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To thrive in a changing environment, organisms evolved strategies for rapidly modifying their behavioral responses to sensory stimuli. In this review, we investigate the role of sensory cortical circuits in these flexible behaviors. ⋯ Last, we discuss inactivation studies which indicate that sensory cortex facilitates behavioral flexibility, but is not always required for adapting to changes in environmental conditions. This analysis provides insights into the contributions of cortical and subcortical sensory circuits to flexibility in behavior.
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Monoamine neurotransmitter, serotonin (5-HT) has its own specific receptors in both pre- and post-synapse. In the present study the role of carnosine on aging-induced changes of [(3)H]-5-HT receptor binding in different brain regions in a rat model was studied. The results showed that during aging (18 and 24 months) the [(3)H]-5-HT receptor binding was reduced in hippocampus, hypothalamus and pons-medulla with a decrease in their both Bmax and KD but in cerebral cortex the [(3)H]-5-HT binding was increased with the increase of its only Bmax. ⋯ The decrease in pons-medullary [(3)H]-5-HT binding including its Bmax of 18-month-aged rats was promoted with carnosine without any significant change in its cerebral cortex. The [(3)H]-5-HT receptor binding with the same dosages of carnosine in 4-month-young rats (a) increased in the cerebral cortex and hippocampus with the increase in their only Bmax whereas (b) decreased in hypothalamus and pons-medulla with a decrease in their both Bmax and KD. These results suggest that carnosine treatment may (a) play a preventive role in aging-induced brain region-specific changes in serotonergic activity (b) not be worthy in 4-month-young rats in relation to the brain regional serotonergic activity.
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The objective of the study was to examine whether axotomy and 17β-estradiol affects P2X7 receptor expression and distribution in the hypoglossal nucleus. The left hypoglossal nerve of ovariectomized mice was cut and animals received a single injection of 17β-estradiol (25 μg/100g b.w. in 20% (2-hydroxypropyl)-β-cyclodextrin) or vehicle one hour after axotomy. Mice were sacrificed on day 4 following surgery. ⋯ The CD11b immunoreactive microglia area fraction increased significantly following axotomy, but was not affected by 17β-estradiol. Neither ER alpha, nor beta colocalized with CD11b. Our results suggest that axotomy induces cell-type specific changes in P2X7 receptor expression, which may be directly regulated by 17β-estradiol through ER alpha or beta in neurons, but not in activated microglia.