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By integrating magnetic resonance-visible components with scaffold materials, hydrogel microspheres (HMs) become visible under magnetic resonance imaging(MRI), allowing for non-invasive, continuous, and dynamic monitoring of the distribution, degradation, and relationship of the HMs with local tissues. However, when these visualization components are physically blended into the HMs, it reduces their relaxation rate and specificity under MRI, weakening the efficacy of real-time dynamic monitoring. To achieve MRI-guided in vivo monitoring of HMs with tissue repair functionality, we utilized airflow control and photo-crosslinking methods to prepare alginate-gelatin-based dual-network hydrogel microspheres (G-AlgMA HMs) using gadolinium ions (Gd (III)), a paramagnetic MRI contrast agent, as the crosslinker. When the network of G-AlgMA HMs degrades, the cleavage of covalent bonds causes the release of Gd (III), continuously altering the arrangement and movement characteristics of surrounding water molecules. This change in local transverse and longitudinal relaxation times results in variations in MRI signal values, thus enabling MRI-guided in vivo monitoring of the HMs. Additionally, in vivo data show that the degradation and release of polypeptide (K2 (SL)6 K2 (KK)) from G-AlgMA HMs promote local vascular regeneration and soft tissue repair. Overall, G-AlgMA HMs enable non-invasive, dynamic in vivo monitoring of biomaterial degradation and tissue regeneration through MRI, which is significant for understanding material degradation mechanisms, evaluating biocompatibility, and optimizing material design.
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Alginatos , Meios de Contraste , Gadolínio , Hidrogéis , Imageamento por Ressonância Magnética , Microesferas , Imageamento por Ressonância Magnética/métodos , Gadolínio/química , Animais , Alginatos/química , Hidrogéis/química , Meios de Contraste/química , Cicatrização/efeitos dos fármacos , Reagentes de Ligações Cruzadas/química , Gelatina/química , Camundongos , Alicerces Teciduais/químicaRESUMO
Seawater electrolysis is an attractive way of making H2 in coastal areas, and NiFe-based materials are among the top options for alkaline seawater oxidation (ASO). However, ample Cl- in seawater can severely corrode catalytic sites and lead to limited lifespans. Herein, we report that in situ carbon oxyanion self-transformation (COST) from oxalate to carbonate on a monolithic NiFe oxalate micropillar electrode allows safeguard of high-valence metal reaction sites in ASO. In situ/ex situ studies show that spontaneous, timely, and appropriate COST safeguards active sites against Cl- attack during ASO even at an ampere-level current density (j). Our NiFe catalyst shows efficient and stable ASO performance, which requires an overpotential as low as 349â mV to attain a j of 1â A cm-2 . Moreover, the NiFe catalyst with protective surface CO3 2- exhibits a slight activity degradation after 600â h of electrolysis under 1â A cm-2 in alkaline seawater. This work reports effective catalyst surface design concepts at the level of oxyanion self-transformation, acting as a momentous step toward defending active sites in seawater-to-H2 conversion systems.
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The cellular functions, such as tissue-rebuilding ability, can be directly affected by the metabolism of cells. Moreover, the glucose metabolism is one of the most important processes of the metabolism. However, glucose cannot be efficiently converted into energy in cells under ischemia hypoxia conditions. In this study, a high-energy intermediate fructose hydrogel (HIFH) is developed by the dynamic coordination between sulfhydryl-functionalized bovine serum albumin (BSA-SH), the high-energy intermediate in glucose metabolism (fructose-1,6-bisphosphate, FBP), and copper ion (Cu2+ ). This hydrogel system is injectable, self-healing, and biocompatible, which can intracellularly convert energy with high efficacy by regulating the glucose metabolism in situ. Additionally, the HIFH can greatly boost cell antioxidant capacity and increase adenosine triphosphate (ATP) in the ischemia anoxic milieu by roughly 1.3 times, improving cell survival, proliferation and physiological functions in vitro. Furthermore, the ischemic skin tissue model is established in rats. The HIFH can speed up the healing of damaged tissue by promoting angiogenesis, lowering reactive oxygen species (ROS), and eventually expanding the healing area of the damaged tissue by roughly 1.4 times in vivo. Therefore, the HIFH can provide an impressive perspective on efficient in situ cell energy supply of damaged tissue.
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Synthesis of green ammonia (NH3 ) via electrolysis of nitric oxide (NO) is extraordinarily sustainable, but multielectron/proton-involved hydrogenation steps as well as low concentrations of NO can lead to poor activities and selectivities of electrocatalysts. Herein, it is reported that oxygen-defective TiO2 nanoarray supported on Ti plate (TiO2- x /TP) behaves as an efficient catalyst for NO reduction to NH3 . In 0.2 m phosphate-buffered electrolyte, such TiO2- x /TP shows competitive electrocatalytic NH3 synthesis activity with a maximum NH3 yield of 1233.2 µg h-1 cm-2 and Faradaic efficiency of 92.5%. Density functional theory calculations further thermodynamically faster NO deoxygenation and protonation processes on TiO2- x (101) compared to perfect TiO2 (101). And the low energy barrier of 0.7 eV on TiO2- x (101) for the potential-determining step further highlights the greatly improved intrinsic activity. In addition, a Zn-NO battery is fabricated with TiO2- x /TP and Zn plate to obtain an NH3 yield of 241.7 µg h-1 cm-2 while providing a peak power density of 0.84 mW cm-2 .
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Electroreduction of nitrite (NO2 - ) to valuable ammonia (NH3 ) offers a sustainable and green approach for NH3 synthesis. Here, a Cu3 P@TiO2 heterostructure is rationally constructed as an active catalyst for selective NO2 - -to-NH3 electroreduction, with rich nanosized Cu3 P anchored on a TiO2 nanoribbon array on Ti plate (Cu3 P@TiO2 /TP). When performed in the 0.1 m NaOH with 0.1 m NaNO2 , the Cu3 P@TiO2 /TP electrode obtains a large NH3 yield of 1583.4 µmol h-1 cm-2 and a high Faradaic efficiency of 97.1%. More importantly, Cu3 P@TiO2 /TP also delivers remarkable long-term stability for 50 h electrolysis. Theoretical calculations indicate that intermediate adsorption/conversion processes on Cu3 P@TiO2 interfaces are synergistically optimized, substantially facilitating the conversion of NO2 - -to-NH3 .
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Ammonia (NH3 ) is an indispensable feedstock for fertilizer production and one of the most ideal green hydrogen rich fuel. Electrochemical nitrate (NO3 - ) reduction reaction (NO3 - RR) is being explored as a promising strategy for green to synthesize industrial-scale NH3 , which has nonetheless involved complex multi-reaction process. This work presents a Pd-doped Co3 O4 nanoarray on titanium mesh (Pd-Co3 O4 /TM) electrode for highly efficient and selective electrocatalytic NO3 - RR to NH3 at low onset potential. The well-designed Pd-Co3 O4 /TM delivers a large NH3 yield of 745.6 µmol h-1 cm-2 and an extremely high Faradaic efficiency (FE) of 98.7% at -0.3 V with strong stability. These calculations further indicate that the doping Co3 O4 with Pd improves the adsorption characteristic of Pd-Co3 O4 and optimizes the free energies for intermediates, thereby facilitating the kinetics of the reaction. Furthermore, assembling this catalyst in a Zn-NO3 - battery realizes a power density of 3.9 mW cm-2 and an excellent FE of 98.8% for NH3 .
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Electrochemical nitrate (NO3-) reduction is a potential approach to produce high-value ammonia (NH3) while removing NO3- pollution, but it requires electrocatalysts with high efficiency and selectivity. Herein, we report the development of Fe3O4 nanoparticles decorated TiO2 nanoribbon array on titanium plate (Fe3O4@TiO2/TP) as an efficient electrocatalyst for NO3--to-NH3 conversion. When operated in 0.1 M phosphate-buffered saline and 0.1 M NO3-, such Fe3O4@TiO2/TP achieves a prominent NH3 yield of 12394.3 µg h-1 cm-2 and a high Faradaic efficiency of 88.4%. In addition, it exhibits excellent stability during long-time electrolysis.
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Nanopartículas , Nanotubos de Carbono , Nitratos , AmôniaRESUMO
Electrocatalytic nitrite (NO2-) reduction offers the potential to synthesize high-value ammonia (NH3) while simultaneously removing NO2- pollution from aqueous solutions, but it requires high-efficiency catalysts to drive the complex six-electron reaction. Herein, cobalt-nanoparticle-decorated 3D porous nitrogen-doped carbon network (Co@NC) is proven as a high-efficiency catalyst for the selective electroreduction of NO2- to NH3. Such Co@NC attains a large NH3 yield of 922.7 µmol h-1 cm-2 and a high Faradaic efficiency of 95.4% under alkaline conditions. Furthermore, it shows remarkable electrochemical stability during cyclic electrolysis.
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Electrochemical nitrite (NO2-) reduction is recognized as a promising strategy for synthesizing valuable ammonia (NH3) and degrading NO2- pollutants in wastewater. The six-electron process for the NO2- reduction reaction is complex and necessitates a highly selective and stable electrocatalyst for efficient conversion of NO2- to NH3. Herein, a FeP nanoparticle-decorated TiO2 nanoribbon array on a titanium plate (FeP@TiO2/TP) is proposed as an efficient catalyst for NH3 production under ambient conditions. In 0.1 M NaOH with 0.1 M NO2-, such a FeP@TiO2/TP affords a large NH3 yield of 346.6 µmol h-1 cm-2 and a high Faradaic efficiency of 97.1%. Additionally, it demonstrates excellent stability and durability during long-term cycling tests and electrolysis experiments.
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Constructing efficient and low-cost oxygen evolution reaction (OER) catalysts operating in seawater is essential for green hydrogen production but remains a great challenge. In this study, we report an iron doped cobalt carbonate hydroxide nanowire array on nickel foam (Fe-CoCH/NF) as a high-efficiency OER electrocatalyst. In alkaline seawater, such Fe-CoCH/NF demands an overpotential of 387 mV to drive 500 mA cm-2, superior to that of CoCH/NF (597 mV). Moreover, it achieves excellent electrochemical and structural stability in alkaline seawater.
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Seawater electrolysis has great potential to generate clean hydrogen energy, but it is a formidable challenge. In this study, we report CoFe-LDH nanosheet uniformly decorated on a CuO nanowire array on Cu foam (CuO@CoFe-LDH/CF) for seawater oxidation. Such CuO@CoFe-LDH/CF exhibits high oxygen evolution reaction electrocatalytic activity, demanding only an overpotential of 336 mV to generate a current density of 100 mA cm-2 in alkaline seawater. Moreover, it can operate continuously for at least 50 h without obvious activity attenuation.
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Overexpression of inflammatory cytokines and chemokines occurs at deep soft tissue injury sites impeding the inflammation self-limiting and impairing the tissue remodeling process. Inspired by the electrostatically extracellular matrix (ECM) binding property of the inflammatory signals, an inflammation self-limiting fibrous tape is designed by covalently modifying the thermosensitive methacrylated gelatin (GelMA) and negatively charged methacrylated heparin (HepMA) hydrogel mixture with proper ratio onto the electrospun fibrous membrane by mild alkali hydrolysis and carboxyl-amino condensation reaction to restore inflammation self-limiting and promote tissue repair via regional immunity regulation. While the GelMA guarantees cell compatibility, the negatively charged HepMA successfully adsorbs the inflammatory cytokines and chemokines by electrostatic interactions and inhibits immune cell migration in vitro. Furthermore, in vivo inflammation self-limiting and regional immunity regulation efficacy is evaluated in a rat abdominal hernia model. Reduced local inflammatory cytokines and chemokines in the early stage and increased angiogenesis and ECM remodeling in the later phase confirm that the tape is an approach to maintain an optimal regional immune activation level after soft tissue injury. Overall, the reported electrospun fibrous tape will find its way into clinical transformation and solve the challenges of deep soft tissue injury.
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Lesões dos Tecidos Moles , Alicerces Teciduais , Álcalis , Animais , Citocinas/metabolismo , Matriz Extracelular/química , Gelatina/química , Heparina , Hidrogéis/química , Inflamação/metabolismo , Ratos , Lesões dos Tecidos Moles/metabolismo , Engenharia Tecidual , Alicerces Teciduais/químicaRESUMO
The least damaging and most economical method to deliver drugs or carriers into the inner ear for treatment of disease is through the middle ear. However, the retention of drug in the middle ear is an obstacle. Here, inspired by the adhesion of mussels, a methacrylate gelatin microspheres (GM) coupling polydopamine (PDA) layer (GM@PDA) with excellent adhesive ability is constructed, and Ebselen liposomes are further loaded into the GM@PDA (GM@PDA@Lipo-Ebselen). The loading capacity of GM@PDA for Ebselen liposomes is 25 ± 1 µg mg-1 microspheres. GM@PDA@Lipo-Ebselen could be injected on round windows membrane (RWM) and tightly adheres to the surface of RWM by PDA, and the microspheres are even still attached to the RWM after 360° rotation and inverted shaking. The in vivo imaging system shows that the adhesive microspheres can prolong the retention of the middle ear cavity for more than 7 days. The hearing of mice in the GM@PDA@Lipo-Ebselen group is significantly recovered, especially on day 14 after noise exposure, and the hearing of each frequency is restored to baseline level. At 32 kHz frequency, the survival of outer hair cells recovers from 48 0± 6% to 93 ± 2%. Therefore, the adhesive and injectable hydrogel microspheres provide a promising strategy for the treatment of hearing loss.
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Orelha Interna , Hidrogéis , Adesivos , Animais , Gelatina , Lipossomos , Camundongos , MicroesferasRESUMO
The ideal bone repair material should firstly recognize and recruit osteoblast precursor cells to initiate the repair process, then promote the differentiation of osteoblasts and accelerate the mineralization of the extracellular matrix (ECM). Here, a bioinspired staged bone regeneration strategy which loads bone morphogenetic protein2 (BMP2 )-modified black phosphorus (BP@BMP2 ) nanosheets to a polylactic acid (PLLA) electrospun fibrous scaffold, with a combination of recruiting osteoblast precursor cells and biomineralization properties for bone regeneration, is constructed successfully by micro-sol electrospinning technique. BP, acting as carriers, can not only provide a negative surface and a strong BMP2 loading ability but can also promote biomineralization in a 3D manner on the electrospun fibrous scaffold, while the BMP2 is to target osteoblast precursor cells for recruitment and osteogenesis differentiation, which endows BP@BMP2 nanosheets with staged bone regeneration ability. Furthermore, the in vitro and in vivo data showed that the BP@BMP2 loaded electrospun fibrous scaffold have good biocompatibility and a strong osteogenesis ability resulting in rapid new bone tissue regeneration. Altogether, this newly developed bioinspired BMP2 -modified BP electrospun fiber with staged bone regeneration properties via recruiting osteoblast precursor cells to the bone injured site and accelerating biomineralization can be a promising approach in physiologic bone repair.
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Biomineralização , Alicerces Teciduais , Proteína Morfogenética Óssea 2 , Regeneração Óssea , Diferenciação Celular , Osteoblastos , Osteogênese , FósforoRESUMO
We report on comprehensive results identifying the ground state of a triangular-lattice structured YbZnGaO_{4} as a spin glass, including no long-range magnetic order, prominent broad excitation continua, and the absence of magnetic thermal conductivity. More crucially, from the ultralow-temperature ac susceptibility measurements, we unambiguously observe frequency-dependent peaks around 0.1 K, indicating the spin-glass ground state. We suggest this conclusion holds also for its sister compound YbMgGaO_{4}, which is confirmed by the observation of spin freezing at low temperatures. We consider disorder and frustration to be the main driving force for the spin-glass phase.
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The hematopoietic growth factor erythropoietin (EPO) has been shown to be neuroprotective against hypoxia-ischemia (HI) in Postnatal Day 7 (P7)-P10 or adult animal models. The current study was aimed to determine whether EPO also provides long-lasting neuroprotection against HI in P5 rats, which is relevant to immature human infants. Sprague-Dawley rats at P5 were subjected to right common carotid artery ligation followed by an exposure to 6% oxygen with balanced nitrogen for 1.5 h. Human recombinant EPO (rEPO, at a dose of 5 units/g) was administered intraperitoneally one hour before or immediately after insult, followed by additional injections at 24 and 48 h post-insult. The control rats were injected with normal saline following HI. Neurobehavioral tests were performed on P8 and P20, and brain injury was examined on P21. HI insult significantly impaired neurobehavioral performance including sensorimotor, locomotor activity and cognitive ability on the P8 and P20 rats. HI insult also resulted in brain inflammation (as indicated by microglia activation) and neuronal death (as indicated by Jade B positive staining) in the white matter, striatum, cortex, and hippocampal areas of the P21 rat. Both pre- and post-treatment with rEPO significantly improved neurobehavioral performance and protected against the HI-induced neuronal death, microglia activation (OX42+) as well as loss of mature oligodendrocytes (APC-CC1+) and hippocampal neurons (Nissl+). The long-lasting protective effects of rEPO in the neonatal rat HI model suggest that to exert neurotrophic activity in the brain might be an effective approach for therapeutic treatment of neonatal brain injury induced by hypoxia-ischemia.
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Eritropoetina/uso terapêutico , Hipocampo/fisiopatologia , Hipóxia-Isquemia Encefálica/tratamento farmacológico , Transtornos Motores/tratamento farmacológico , Fármacos Neuroprotetores/uso terapêutico , Animais , Astrócitos/metabolismo , Astrócitos/patologia , Eritropoetina/farmacologia , Hipocampo/citologia , Hipocampo/efeitos dos fármacos , Hipocampo/crescimento & desenvolvimento , Humanos , Hipóxia-Isquemia Encefálica/complicações , Locomoção , Transtornos Motores/etiologia , Neurônios/metabolismo , Neurônios/patologia , Fármacos Neuroprotetores/farmacologia , Ratos , Ratos Sprague-DawleyRESUMO
Serotonin (5-hydroxytryptamine, 5-HT) has been implicated to play critical roles in early neural development. Recent reports have suggested that perinatal exposure to selective serotonin reuptake inhibitors (SSRIs) resulted in cortical network miswiring, abnormal social behavior, callosal myelin malformation, as well as oligodendrocyte (OL) pathology in rats. To gain further insight into the cellular and molecular mechanisms underlying SSRIs-induced OL and myelin abnormalities, we investigated the effect of 5-HT exposure on OL development, cell death, and myelination in cell culture models. First, we showed that 5-HT receptor 1A and 2A subtypes were expressed in OL lineages, using immunocytochemistry, Western blot, as well as intracellular Ca(2+) measurement. We then assessed the effect of serotonin exposure on the lineage development, expression of myelin proteins, cell death, and myelination, in purified OL and neuron-OL myelination cultures. For pure OL cultures, our results showed that 5-HT exposure led to disturbance of OL development, as indicated by aberrant process outgrowth and reduced myelin proteins expression. At higher doses, such exposure triggered a development-dependent cell death, as immature OLs exhibited increasing susceptibility to 5-HT treatment compared to OL progenitor cells (OPC). We showed further that 5-HT-induced immature OL death was mediated at least partially via 5-HT2A receptor, since cell death could be mimicked by 5-HT2A receptor agonist 1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane hydrochloride, (±)-2,5-dimethoxy-4-iodoamphetamine hydrochloride, but atten-uated by pre-treatment with 5-HT2A receptor antagonist ritanserin. Utilizing a neuron-OL myelination co-culture model, our data showed that 5-HT exposure significantly reduced the number of myelinated internodes. In contrast to cell injury observed in pure OL cultures, 5-HT exposure did not lead to OL death or reduced OL density in neuron-OL co-cultures. However, abnormal patterns of contactin-associated protein (Caspr) clustering were observed at the sites of Node of Ranvier, suggesting that 5-HT exposure may affect other axon-derived factors for myelination. In summary, this is the first study to demonstrate that manipulation of serotonin levels affects OL development and myelination, which may contribute to altered neural connectivity noted in SSRIs-treated animals. The current in vitro study demonstrated that exposure to high level of serotonin (5-HT) led to aberrant oligodendrocyte (OL) development, cell injury, and myelination deficit. We propose that elevated extracellular serotonin levels in the fetal brain, such as upon the use of selective serotonin reuptake inhibitors (SSRIs) during pregnancy, may adversely affect OL development and/or myelination, thus contributing to altered neural connectivity seen in Autism Spectrum Disorders. OPC = oligodendrocyte progenitor cell.
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Linhagem da Célula/efeitos dos fármacos , Regulação da Expressão Gênica/efeitos dos fármacos , Oligodendroglia/efeitos dos fármacos , Serotonina/efeitos adversos , Animais , Morte Celular/efeitos dos fármacos , Células Cultivadas , Técnicas de Cocultura , Relação Dose-Resposta a Droga , Embrião de Mamíferos , Células-Tronco Embrionárias/efeitos dos fármacos , Feminino , Proteínas da Mielina/genética , Proteínas da Mielina/metabolismo , Bainha de Mielina/metabolismo , Neurônios/efeitos dos fármacos , Neurônios/fisiologia , Oligodendroglia/metabolismo , Gravidez , Ratos , Ratos Sprague-Dawley , Receptor 5-HT1A de Serotonina/metabolismo , Receptor 5-HT2A de Serotonina/metabolismoRESUMO
Our previous study showed that a single lipopolysaccharide (LPS) treatment to neonatal rats could induce a long-lasting neuroinflammatory response and dopaminergic system injury late in life. This is evidenced by a sustained activation of microglia and elevated interleukin-1ß (IL-1ß) levels, as well as reduced tyrosine hydroxylase (TH) expression in the substantia nigra (SN) of P70 rat brain. The object of the current study was to test whether co-administration of IL-1 receptor antagonist (IL-1ra) protects against LPS-induced neurological dysfunction later in life. LPS (1 mg/kg) with or without IL-1ra (0.1 mg/kg), or sterile saline was injected intracerebrally into postnatal day 5 (P5) Sprague-Dawley male rat pups. Motor behavioral tests were carried out from P7 to P70 with subsequent examination of brain injury. Our results showed that neonatal administration of IL-1ra significantly attenuated LPS-induced motor behavioral deficits, loss of TH immunoreactive neurons, as well as microglia activation in the SN of P70 rats. These data suggest that IL-1ß may play a pivotal role in mediating a chronic neuroinflammation status by a single LPS exposure in early postnatal life, and blockading IL-1ß might be a novel approach to protect the dopaminergic system against perinatal infection/inflammation exposure.
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Neurônios Dopaminérgicos/efeitos dos fármacos , Proteína Antagonista do Receptor de Interleucina 1/farmacologia , Lipopolissacarídeos/farmacologia , Fármacos Neuroprotetores/farmacologia , Transtornos Psicomotores/prevenção & controle , Animais , Animais Recém-Nascidos , Neurônios Dopaminérgicos/imunologia , Complexo I de Transporte de Elétrons/metabolismo , Locomoção , Masculino , Microglia/imunologia , Microglia/metabolismo , Transtornos Psicomotores/imunologia , Ratos Sprague-Dawley , Substância Negra/efeitos dos fármacos , Substância Negra/imunologia , Substância Negra/patologiaRESUMO
Serotonin (5-HT) plays a key role in early brain development, and manipulation of 5-HT levels during this period can have lasting neurobiological and behavioral consequences. It is unclear how perinatal exposure to drugs, such as selective serotonin reuptake inhibitors (SSRIs), impacts cortical neural network function and what mechanism(s) may elicit the disruption of normal neuronal connections/interactions. In this article, we report on cortical wiring organization after pre- and postnatal exposure to the SSRI citalopram. We show that manipulation of 5-HT during early development in both in vitro and in vivo models disturbs characteristic chemoarchitectural and electrophysiological brain features, including changes in raphe and callosal connections, sensory processing, and myelin sheath formation. Also, drug-exposed rat pups exhibit neophobia and disrupted juvenile play behavior. These findings indicate that 5-HT homeostasis is required for proper brain maturation and that fetal/infant exposure to SSRIs should be examined in humans, particularly those with developmental dysfunction, such as autism.