Neuroscience
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Beauty judgments are common in daily life, but rarely studied in cognitive neuroscience. Here, in three studies, we searched for the neural mechanisms of musical beauty using a naturalistic free-listening paradigm applied to behavioral and neuroimaging recordings and validated by experts' judgments. In Study 1, 30 adults continuously rated the perceived beauty of three musical pieces using a motion sensor. ⋯ Effective connectivity analysis discovered inhibition of auditory activation and neural communication with the right orbitofrontal cortex for listening to beautiful passages vs. intrinsic activation of auditory cortices and decreased coupling to orbitofrontal cortex for not-beautiful passages. Experts' questionnaires indicated that the beautiful passages were more melodic, calm, sad, slow, tonal, traditional, and simple than the ones rated negatively. In sum, we identified neural and psychological underpinnings of musical beauty, irrespectively of individual taste and listening biography.
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Major depressive disorder (MDD) is a complex neuropsychiatric disorder potentially influenced by factors such as stress and inflammation. Chronic stress can lead to maladaptive brain changes that may trigger immune hyperactivation, contributing to MDD's pathogenesis. While the involvement of inflammation in MDD is well established, the effects of inflammatory preconditioning in animals subsequently exposed to chronic stress remain unclear. ⋯ A trend toward elevated IL-17 levels was also observed at the peripheral level. These findings indicate that inflammatory preconditioning contributes significantly to behaviors phenotypically associated with MDD. Furthermore, the study suggests that these behavioral changes are linked to a dysfunctional immune response and impaired neuroplasticity.
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Peripuberty is a significant period of neurodevelopment with long-lasting effects on the brain and behavior. Blocking type 1 corticotropin-releasing factor receptors (CRFR1) in neonatal and peripubertal rats attenuates detrimental effects of early-life stress on neural plasticity, behavior, and stress hormone action, long after exposure to the drug has ended. CRFR1 antagonism can also impact neural and behavioral development in the absence of stressful stimuli, suggesting sustained alterations under baseline conditions. ⋯ In the adult amygdala, peripubertal CRFR1a induced alterations in pathways related to neural plasticity and stress in males. In females, pathways related to central nervous system myelination, cell junction organization, and glutamatergic regulation of synaptic transmission were affected. Understanding how acute exposure to neuropharmacological agents can have sustained impacts on brain and behavior, in the absence of further exposures, has important clinical implications for developing adolescents.
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Attention deficit hyperactivity disorder (ADHD) is one of the most frequent and disabling neurodevelopmental disorders. Recent research on cerebral blood flow (CBF) has enhanced understanding of the underlying pathophysiology in neuropsychiatric disorders. This systematic review aims to synthesize the existing literature on CBF anomalies among individuals with ADHD in comparison to controls. ⋯ This review highlights diverse CBF anomalies in ADHD. The most consistently reported findings suggest hypoperfusion during resting state in prefrontal and temporal areas, along with the basal ganglia, while there is a hyperperfusion in frontal, parietal and occipital regions. Further research, including longitudinal studies, is essential to develop a comprehensive understanding of CBF implications in ADHD.
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In this special issue to celebrate the 30th anniversary of the Uruguayan Society for Neuroscience (SNU), we find it pertinent to highlight that research on glial cells in Uruguay began almost alongside the history of SNU and contributed to the understanding of neuron-glia interactions within the international scientific community. Glial cells, particularly astrocytes, traditionally regarded as supportive components in the central nervous system (CNS), undergo notable morphological and functional alterations in response to neuronal damage, a phenomenon referred to as glial reactivity. Among the myriad functions of astrocytes, metabolic support holds significant relevance for neuronal function, given the high energy demand of the nervous system. ⋯ Thus, exploring mitochondrial activity and metabolic reprogramming within glial cells may provide valuable insights for developing innovative therapeutic approaches to mitigate neuronal damage. In this review, we focus on studies supporting the emerging paradigm that metabolic reprogramming occurs in astrocytes following damage, which is associated with their phenotypic shift to a new functional state that significantly influences the progression of pathology. Thus, exploring mitochondrial activity and metabolic reprogramming within glial cells may provide valuable insights for developing innovative therapeutic approaches to mitigate neuronal damage.