Navegando por Palavras-chave "Central Nervous System"
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- ItemAcesso aberto (Open Access)Brazilian plants with possible action on the Central Nervous System: a study of historical sources from the 16th to 19th century(Sociedade Brasileira de Farmacognosia, 2011-06-01) Giorgetti, Melina [UNIFESP]; Rossi, Lucia; Rodrigues, Eliana [UNIFESP]; Universidade Federal de São Paulo (UNIFESP); Instituto de Botânica de São PauloEthnopharmacological research when grounded on historic literature has for its objective retrieving traditional knowledge compiled throughout history by early cultures. The current study has used literature from the 16th to the 19th centuries to assess reports that include accounts of Brazil's native plants, with possible reports of disorders of the Central Nervous System (CNS). Visits were paid to 27 institutions located in four Brazilian states. This resulted in raising 529 publications, out of which 65 were read, revealing that 33 of them contained reports of plants exerting effects on CNS ailments. These plants' scientific names underwent an updating process. The updating process resulted in 788 species names (129 correct scientific names and their 659 synonyms) out of which 66 hold current ethnopharmacology, pharmacology studies and/or patent application. Coincidences among past and present data have been observed in 46 cases. Only three of them carried applications for patents all of which coincided with past uses. There have hardly been any studies whatsoever throughout the centuries for many of the species currently being studied. Although of very seldom use, research in ethnopharmacology and historic literature can be promising tools for the selecting of new pharmaco products, further to contributing with retrieving traditional knowledge.
- ItemAcesso aberto (Open Access)Efeito da suplementação de lactato de cálcio no desempenho do passe de atletas de futsal em estado de fadiga mental(Universidade Federal de São Paulo, 2022-02-21) Thibana, Guilherme Tadashi Medoruma [UNIFESP]; Azevedo, Paulo Henrique Silva Marques de [UNIFESP]; http://lattes.cnpq.br/6559911217770194; http://lattes.cnpq.br/2703480565688457; Universidade Federal de São Paulo (UNIFESP)A fadiga mental (FM) é causada por uma atividade de alta demanda cognitiva realizada por longos períodos, e tem potencial para prejudicar a performance humana. Postula-se que uma das causas da FM é o baixo status energético neuronal que aumentaria a percepção subjetiva de esforço, sensação de fadiga e desengajamento do exercício. O objetivo do estudo é verificar se a suplementação com lactato de cálcio é capaz de diminuir a FM, e consequentemente manter a performance dos atletas de futsal. Diante disso, a amostra consistiu em 6 jogadores de futsal, que executaram um protocolo específico para indicar o desempenho do passe nas condições: 1) controle (sem FM); 2) FM; 3) FM e placebo; 4) FM e lactato, de forma randomizada, duplo-cega e contrabalanceada. A hipótese era a de que a administração de lactato de cálcio fosse capaz de reverter ou atenuar a FM, mantendo o desempenho do passe quando comparados ao controle.
- ItemSomente MetadadadosImpacto Da Expressão Quantitativa Da Proteína P53 Nos Pacientes Portadores De Meduloblastoma Desmoplásico-Nodular(Universidade Federal de São Paulo (UNIFESP), 2018-06-28) Borges, Natalia Maria Tavares Ferreira [UNIFESP]; Petrilli, Antonio Sergio [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)Introduction: Brain Tumors Are The Second Most Common Pediatric Cancer Group, Accounting For 20% To 25% Of All Childhood Malignancies. Among The Cns Tumors, Medulloblastoma Accounts For About 20% Of All Brain Tumors In Childhood. Currently, Medulloblastoma Is Stratified According Chang"S Criteria, Histological Criteria And Biological Evaluation. In This Context, The Literature Suggest That Desmoplastic / Nodular Medulloblastoma (Mbdn) And Sonic-Hedgehog Molecular Subtype (Shh) Have A Better Prognosis In Children <3-5 Years. However, Some Of These Patients With Mutation In Tp53 Appear To Have A Poor Outcome. Some Studies Also Suggest The Correlation Of The P53 Protein With Tp53. The Present Study Aims To Evaluate The Quantitative Values Of The P53 Protein And To Correlate Its Results With The Survival Of Patients Diagnosed With Mbdn. Materials And Methods: Retrospective Analysis Of Medical Records Of Cases Of Mbdn Aged <5 Years, From January 2007 To December 2017, Analyzing Clinical And Epidemiological Profile
- ItemAcesso aberto (Open Access)Mecanismos Cardio-Respiratórios Integrados na Região Bulbar: Participação da Área Pressora Caudal, dos Núcleos do Trato Solitário e do Núcleo Retrotrapezóide(Universidade Federal de São Paulo (UNIFESP), 2009-01-28) Takakura, Ana Carolina Thomaz [UNIFESP]; Colombari, Eduardo [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)Cardiovascular responses are integrated at different levels of the central nervous system (CNS). In the brainstem, there are different areas related to the cardiovascular control. It is well known that in the ventrolateral medulla there are, at least, three important regions involved with cardiovascular control: the rostral ventrolateral medulla (RVLM), the caudal ventrolateral medulla (CVLM) and the caudal pressor area (CPA). The RVLM is the main source of excitatory input to sympathetic preganglionic neurons playing a crucial role for tonic and reflex control of the cardiovascular system. The caudal ventrolateral medulla (CVLM) contains the GABAergic sympathoinhibitory neurons that project to RVLM. Besides these two regions, the NTS is the site of the first synapse of the viscerosensory afferent fibers in the brainstem including those related to cardiovascular and respiratory afferents. Besides the circuitry described above, more recent studies have also shown a new site, the CPA, located in the caudal end of the ventrolateral medulla, which provides excitatory signals that affect sympathetic activity to the cardiovascular system in rats. Therefore, the aim of the present study was to investigate the involvement of the NTS (commissural and/or intermediate regions) on the stimulation or inhibition of the CPA. Male Holtzman rats (280-350 g; n = 6-8) anesthetized with urethane (1.2 g/kg, i.v.) were used. Unilateral microinjection of L-glutamate (1 mM - 100 nL) into the CPA resulted in an increase in mean arterial pressure (MAP, D = +28 ± 3 mmHg, vs. controle: D = +2 ± 2 mmHg, p<0.05) and heart rate (HR, D = +20 ± 1 bpm, vs. controle: D = +3 ± 3 bpm, p<0.05). Electrolytic lesions of the commissural NTS (commNTS) (1 mA x 10s) abolished the pressor and tachycardic responses at 10 (D = +5 ± 7 mmHg and D = +4 ± 3 bpm), 30 (D = +7 ± 3 mmHg and D = +6 ± 3 bpm) and 60 minutes (D = +11 ± 3 mmHg and D = +5 ± 1 bpm) produced by injection of L-glutamate into the CPA. In the same way, muscimol (GABA-A receptor agonist) (2 mM - 60 nL) injected into the commNTS abolished the pressor and tachycardic responses at 10 (D = +5 ± 5 mmHg and D = +5 ± 3 bpm), 30 (D = +8 ± 5 mmHg and D = +7 ± 2 bpm) and 60 minutes (D = +11 ± 6 mmHg and D = +5 ± 2 bpm) produced by injection of L-glutamate into the CPA. On the other hand, the injection of Lglutamate unilaterally into the CPA 10, 30 and 60 minutes after the injection of muscimol into the intermediate NTS produced no change on MAP increase (D = +11± 2, +27 ± 4 and +24 ± 7 mmHg, respectively) and HR (D = +30 ± 12, +32 ± 15 and +24 ± 8 bpm, respectively). It seems that the activation of the CPA depends on the integrity of the commNTS neurons. Does the CPA integrity depend on NTS activation? Bilateral injection of muscimol (GABA-A agonist, 2 mM – 60 nl) into the CPA produced a decrease in MAP (D = -18 ± 2 mmHg, p<0.05) and HR (D = -21 ± 6 bpm, p<0.05). The depressor and bradycardia responses produced by L-glutamate into the commNTS was abolished at 10 (D = -5 ± 3 mmHg and D = +8 ± 9 bpm), 30 (D = -5 ± 2 mmHg and D = +7 ± 4 bpm) and 60 minutes (D = -6 ± 4 mmHg and D = +10 ± 6 bpm) after muscimol injection into the CPA. On the other hand, the depressor and bradicardic responses produced by L-glutamate into the intermediate NTS was not changed at 10 (D = -41 ± 9 mmHg and D = -67 ± 26 bpm), 30 (D = -31 ± 12 mmHg and D = -23 ± 4 bpm) and 60 minutes (D = -32 ± 8 mmHg and D = -21 ± 3 bpm) after muscimol injection into the CPA. Our next question was to know if the inhibition of the CPA will change the cardiovascular reflexes. Baroreflex curves were generated by lowering MAP with sodium nitroprusside (30 mg/kg) and increasing MAP by constricting an abdominal aortic snare. The relationship between MAP and sympathetic nerve discharge (SND) (baroreflex curves) revealed no change after muscimol injection into the CPA. After inhibition of the CPA, the baroreflex operated around a comparable MAP (MAP50) in all groups of rats. The lower and upper plateau, as well the baroreflex range was not different from the control group. The chemoreflex was actvated by i.v. injections of sodium cyanide (NaCN – 50 mg/kg). The activation of chemoreflex with NaCN produced a rise in MAP (D = +16 ± 4 mmHg, vs. saline D = +2 ± 2 mmHg, p<0.05), an increase in SND (D = +236 ± 11% of resting, p<0.01) and an increase in phrenic nerve discharge (PND). Muscimol injection into the CPA reduced the pressor (D = +9 ± 2 mmHg, vs. saline D = +18 ± 4 mmHg, p<0.05), sympathoexcitatory (D = +88 ± 18%, vs. saline D = +217 ± 33 %, p<0.01) and the increase in PND produced by chemoreflex activation with NaCN. Carotid chemoreceptor afferents terminate predominantly in commNTS. The next experiment was designed to test and to confirm the interaction between the commNTS and the CPA neurons by anatomical approaches. We tested whether glutamatergic or GABAergic. The rats were exposed to hypoxia (8% O2, n = 5) or to normal air (n = 4). Fos-immunoreactivity was used to identify commNTS neurons that were activated by hypoxia. NTS or CPA neurons were classified as glutamatergic or GABAergic based on whether they contained VGLUT2 mRNA or GAD67 mRNA. The vast majority of the commNTS (64 ± 13%), intermediate NTS (41 ± 9%) and CPA (26 ± 9%) neurons that were immunoreactive for Fos contained VGLUT2 mRNA, whereas only a small proportion of the same class of neurons contained GAD-67 mRNA (commNTS: 7 ± 4%; intermediate NTS: 16 ± 9% and CPA: 5 ± 3%). Therefore, our results are the first to show the existence of an interaction between the commNTS and CPA in terms of cardiovascular control. However we know that commNTS neurons receive inputs from peripheral chemoreceptors and the stimulation of commNTS depends on CPA integrity. These data suggest that CPA contributes to resting MAP, sSND and to the sympathoexcitatory effect during stimulation of peripheral chemoreceptors.
- ItemSomente MetadadadosPoluição do ar de São Paulo (mp2,5) como fator de risco para o desenvolvimento de distúrbios comportamentais e alterações moleculares no cérebro de ratos(Universidade Federal de São Paulo (UNIFESP), 2020-07-15) Carletti, Carla De Oliveira [UNIFESP]; Fernandes, Maria Jose Da Silva [UNIFESP]; Universidade Federal de São PauloIntroduction: Air pollution is a public health problem and it can cause neurological pathologies and behavioral disorders such as anxiety, depression, aggression, cognitive disorders and delayed psychomotor development. Pre-clinical studies have shown behavioral changes and neuroinflammation associated to exposure to pollution in the gestational and postnatal period, but the mechanisms involved are little known. Objectives: The aim of the study was to evaluate the impact of exposure to PM2,5 during the initial period of postnatal development, on the behavioral and neurobiological parameters of adult male and female rats. Methods: Rats were exposed to a polluted air chamber, once a day, in order to inhale a dose of ˜600 μg / m³ of PM2,5. The exposure was done for 30 days and started on the 7th postnatal day. The control group was exposed to a filtered air chamber, once a day and during the same period. After exposure, the animals were subjected to behavioral tests and assessment of neuronal excitability using Pentylenetetrazol (PTZ). At the end of the behavioral tests, the animals were euthanized and the hippocampus were used for the analysis of neuroinflammation (TNF-α, IL-1β, IL-6, IL-10, P2X7, NLRP3), markers of inhibitory neurotransmission (GABA-B , GAD-67, Parvalbumin), excitatory (mGluR2/3, GluR5-7, NMDA1, NMDA2B), monoamines (D2 and 5-HT2A), and the anti-aging protein klotho. The expression of astrocyte and neuron markers was performed by western blot. Results: The data showed that male rats, exposed to PM2.5, had depression, anxiety and short and long-term memory deficit, with little social interaction, while females had increased social interaction with manifestation of aggression. The males showed neuronal hyperexcitability, since subconvulsant doses of PTZ was needed to induce severe seizures, while the females, in contrast, only presented seizures with high doses of PTZ. Biochemical analyzes showed that males exposed to PM2,5, showed an imbalance between inhibitory and excitatory neurotransmission, with increased excitatory factors (cytokines and GluR5-7), and reduced GABAergic neurotransmission (GABA-B, parvalbumina). In females, there was a decrease in GABAergic neurotransmission and in neuroinflammation, with decreased level of NLRP3 and IL-10. Regarding the monoamine markers, D2 decreased in the hippocampus of males and increased in females, whereas 5-HT2A reduced only in females. The klotho protein had a significant reduction only in the hippocampus of females in the pollution group. Conclusion: The present study showed that exposure to PM2,5 for 30 days, initiated in the first postnatal week, is sufficient to cause long-term changes in the hippocampus of rats, resulting in behavioral disorders such as depression and anxiety, accompanied by neuroinflammation and neuronal hyperexcitability in males, and aggressiveness, with reduced GABAergic neurotransmission, monoamine disorder and reduced klotho protein in females.
- ItemAcesso aberto (Open Access)Possíveis correlações entre o hormônio tireoidiano e depressão do tipo ansiosa em ratos obesos(Universidade Federal de São Paulo (UNIFESP), 2017-01-31) Lorena, Fernanda Beraldo [UNIFESP]; Ribeiro, Miriam Oliveira [UNIFESP]; http://lattes.cnpq.br/7069953370349465; http://lattes.cnpq.br/2138429278346904; Universidade Federal de São Paulo (UNIFESP)Obesity is related to memory and learning processes impairment, as well as the depressive and anxious behavior. The thyroid hormone (TH) modulates the development and functioning of the CNS by regulating the expression of genes related to brain plasticity. The same genes regulated by T3 are changed in obesity. The literature describes the relationship between thyroid hormone and mood changes such as depression and anxiety that may generally be reversed by treatment with T3. Thus, our working hypothesis is based on the possibility that changes in T3 signaling in the brain of obese rats may be involved with changes in the functioning of the CNS observed in obesity. To test our hypothesis we treat male Wistar rats with high fat diet (40%) by 32 weeks. At the end of this period, the animals were subjected to behavioral testing to assess the acquisition memory capacity and the presence of anxious and depressive behavior in obese animals. We also evaluated changes in the expression of genes involved in depression, genes involved in the availability of T3 in the brain and genes regulated by T3. Through behavioral tests, we found that obesity induces a depressive and anxious behavior, but does not lead to memory impairment. The gene expression analysis showed that obesity leads to increased expression of TH transporters, receptors for TH (TRs) and lower expression of genes positively regulated by T3, Aldh1a1 and RBM3, and increased Halpln1, a gene negatively regulated . It is possible that obese individuals show a lower availability of T3 in the brain, which induces a local moderate hypothyroidism and possibly changes in the pathway signaling of this hormone are a compensatory mechanism. Furthermore, we observed a significant increase in the expression of genes related to inflammation, which may also be associated with the phenotype found in these animals. In summary, our results suggest that there is a change in TH signaling in the brain that may be involved in the development of a depressed and anxious phenotype induced by obesity.