Neuroscience
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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.
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Surgery endangers the integrity of the body through a continuous stream of noxious stimuli. General anesthesia helps patients cope with the surgery situation. In the first part of our literature review, we present our new knowledge about nociception as described by Sherrington. ⋯ Maintaining the unconscious state created by anesthetics during surgery is only possible by continuously counteracting nociception. Finally, we present the role of the opioid receptor system in antinociception. Understanding all these processes can help expand our knowledge about nociception, pain and formation of consciousness.
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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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Due to the increasing prevalence of depressive and anxiety disorders in youth, a growing interest in the endocannabinoid system (ECS) as a potential alternative target point for treatment arised. This study aimed to investigate whether chronic administration of escitalopram reverses behavioral changes induced by maternal separation in male adolescent Wistar rats and explore the corresponding neurochemical changes in the ECS. The pups were separated from their dams for 360 min daily from postnatal day (PND) 2 until PND 15. ⋯ Escitalopram reversed anxiety-like behavior and attenuated signs of despair behavior. The escitalopram administration has been followed by a decrease in the studied genes expression in the amygdala, the hypothalamus, and the hippocampus, what might suggest that the endocannabinoid system is involved in the mechanism of its action in adolescents. However Western blot analysis did not indicate significant alterations in the protein levels, so more detailed studies are needed to verify this hypothesis.
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Neurodegenerative disorders (NDDs) have been prevalent for more than a decade, and the number of individuals affected per year has increased exponentially. Among these NDDs, Alzheimer's disease, which causes extreme cognitive impairment, and Parkinson's disease, characterized by impairments in motor activity, are the most prevalent. While few treatments are available for clinical practice, they have minimal effects on reversing the neurodegeneration associated with these debilitating diseases. ⋯ The potential CRMs discussed in this review are quercetin, chrysin, astragalin, apigenin, curcumin, epigallocatechin-3-gallate, and NAD+ precursors. This review aims to provide an overview of these CRMs' effectiveness in preventing neurodegenerative disorders associated with aging. Moreover, we highlight the clinical relevance of these compounds by discussing in detail the results of clinical trials on them.