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1.
Ciênc. cogn ; 26(2): 266-276, 31 dez. 2021. ilus
Article in Portuguese | LILACS | ID: biblio-1353869

ABSTRACT

O fenômeno de aceleração social, intimamente ligado a nossa modernização tecnológica e os sistemas políticos e sociais que adotamos, vem sendo alvo de questionamentos por parte da teoria crítica por diversos filósofos e sociólogos, principalmente em relação a se tal "aceleração" seja algo que, possa ser justificável pelo bem comum da sociedade. De fato, as rápidas mudanças que ocorreram no último século causaram uma tremenda mudança em nossos estilos-de-vida, e na maneira como experienciamos o mundo. Que a nossa sociedade mudou e continua a mudar é um fato evidente quando olhamos criticamente para o passado e presente, e comparamos diferentes épocas da história humana. Neste ensaio tentaremos explorar algumas possíveis hipóteses que fundamentem o comportamento aceleracionista em certos fatores e mecanismo biológicos que caracterizam os sistemas de motivação e saciação humanos. Também tentaremos mostrar como certos fenômenos sociais podem auxiliar em fortalecer este tipo de comportamento, e suas possíveis origens evolutivas. Este estudo tem como objetivo principal fundamentar a Tese Aceleracionista em evidências neurofisiológicas, cognitivo-comportamentais, evolutivas e sociais.


The phenomenon of social acceleration is closely linked to our technological modernization and the political and social systems we have adopted, and it has been questioned by several philosophers and sociologists, especially in relation to whether such acceleration is something that can be justified for the common good of society. In fact, the rapid changes that have occurred in the last century have caused a tremendous change in our lifestyles, and in the way we experience the world. That society have changed and continues to change is an evident fact when we look critically to the past and our present and compare different times in human history. In this essay we will try to explore some possible hypotheses that underpin accelerated behavior, in certain biological factors and mechanisms that characterize human motivation and satiation systems. We will also try to show how certain social phenomena can help to strengthen this type of behavior, and its possible evolutionary origins. The main objective of this study is to base the Accelerationist Thesis on neurophysiological, cognitive-behavioral, evolutionary and also social evidence.


Subject(s)
Humans , Reward , Satiation/physiology , Social Change , Cognition/physiology , Neurotransmitter Agents/physiology , Motivation/physiology
2.
Fisioter. Bras ; 22(5): 733-757, Nov 11, 2021.
Article in Portuguese | LILACS | ID: biblio-1353562

ABSTRACT

A estimulação elétrica transcraniana (EET) é uma técnica de neuromodulação não invasiva, que tem sido utilizada como coadjuvante no tratamento de transtornos depressivos devido à sua capacidade de modificar a excitabilidade cortical. Objetivo: Analisar os efeitos da EET nos transtornos depressivos e propor parâmetros para a prática clínica. Métodos: Estudo de revisão sistemática no qual foram incluídos ensaios clínicos randomizados que utilizaram a EET no tratamento dos transtornos depressivos, publicados entre 2010 e junho de 2018, nas línguas inglesa e portuguesa. Resultados: Foram encontrados 14.775 estudos, sendo selecionados para a amostra apenas 15 trabalhos. Todos os estudos selecionados utilizaram a EET por corrente contínua e apresentaram semelhanças em relação aos demais parâmetros elétricos de tratamento e locais de aplicação dos eletrodos. Em 12 dos 15 estudos avaliados foi observada melhora significativa (p < 0,05) dos sintomas depressivos e, em relação aos efeitos adversos, constatou-se que são inferiores aos tratamentos convencionais. Conclusão: A EET apresenta eficácia no tratamento dos transtornos depressivos e que isto está diretamente relacionado ao uso adequado dos parâmetros e técnicas de aplicação da corrente elétrica. (AU)


Subject(s)
Depression , Depressive Disorder , Transcranial Direct Current Stimulation , Neurotransmitter Agents , Electric Stimulation
3.
Rev. cuba. invest. bioméd ; 40(1): e842, ene.-mar. 2021. tab
Article in Spanish | LILACS, CUMED | ID: biblio-1289454

ABSTRACT

Introducción: La etiología de las enfermedades autoinmunes aún se desconoce, aunque se plantean diferentes causas. Objetivo: Describir el rol de factores como las hormonas, alimentación, estrés, enfermedades infecciosas y cáncer en las enfermedades autoinmunes. Métodos: Se realizó una revisión bibliográfica empleando Google Académico y artículos de libre acceso en la base de datos PubMed y SciELO, publicados entre enero del 2014 y junio del 2020. Se consultó la bibliografía nacional e internacional relevante y actualizada, con un total de 51 referencias, de estas, tres libros básicos de la especialidad de Inmunología y 48 artículos (12 en idioma español y 36 en inglés). Se utilizaron los términos de búsqueda según los descriptores del DeCS y MeSH. Resultados: Las hormonas femeninas incrementan el riesgo de las enfermedades autoinmunes. Un desbalance en la neurohormona melatonina puede generar linfocitos autorreactivos. El estrés puede mantener respuestas inflamatorias crónicas que causen daño tisular. Una adecuada alimentación permite que los comensales de la microbiota intestinal mantengan la homeostasis del sistema inmune. Las infecciones en ocasiones desarrollan respuestas autoinmunitarias. La causalidad entre el cáncer y la autoinmunidad es bidireccional producto de procesos inflamatorios. Conclusiones: Las enfermedades autoinmunes son más frecuentes en las mujeres. Una alimentación adecuada permite que la microbiota intestinal no se altere y que mantenga la homeostasis inmunológica. Situaciones de estrés e infecciones pueden iniciar respuestas autoinmunes. El cáncer puede favorecer el desarrollo de manifestaciones autoinmunes, y estas últimas por el predominio inflamatorio, favorecen la tumorogénesis(AU)


Introduction: The etiology of autoimmune diseases is still unknown, though several causes have been suggested. Objective: Describe the role of hormones, eating, stress, infectious diseases and cancer in immune diseases. Methods: A bibliographic review was conducted using Google Scholar and open access papers published in the databases Pubmed and SciELO from January 2014 to June 2020. Relevant updated national and international bibliography was consulted, for a total 51 references: three basic books from the specialty of immunology and 48 papers (12 in Spanish and 36 in English). The search terms used were obtained from the descriptors DeCS and MeSH. Results: Feminine hormones increase the risk of autoimmune diseases. Imbalance in the neurohormone melatonin may generate autoreactive lymphocytes. Stress may maintain chronic inflammatory responses causing tissue damage. Appropriate eating habits allow gut microbiota commensals to maintain the homeostasis of the immune system. Infections occasionally develop autoimmune responses. Causality between cancer and autoimmunity is bidirectional, due to the presence of inflammatory processes. Conclusions: Autoimmune diseases are more common among women. Appropriate eating habits prevent alterations of the gut microbiota, allowing it to maintain immune homeostasis. Stress situations and infections may trigger autoimmune responses. Cancer may foster the development of autoimmune manifestations, and these, due to the inflammatory predominance, may foster tumorigenesis(AU)


Subject(s)
Humans , Autoimmune Diseases , Autoimmunity , Eating , Allergy and Immunology , Gastrointestinal Microbiome , Immune System , Immune System Diseases , Neurotransmitter Agents
4.
J. venom. anim. toxins incl. trop. dis ; 27: e20210009, 2021. tab, graf, ilus, mapas
Article in English | LILACS, VETINDEX | ID: biblio-1279406

ABSTRACT

Spider venom is a rich cocktail of neuroactive compounds designed to prey capture and defense against predators that act on neuronal membrane proteins, in particular, acetylcholinesterases (AChE) that regulate synaptic transmission through acetylcholine (ACh) hydrolysis - an excitatory neurotransmitter - and beta-secretases (BACE) that primarily cleave amyloid precursor proteins (APP), which are, in turn, relevant in the structural integrity of neurons. The present study provides preliminary evidence on the therapeutic potential of Phlogiellus bundokalbo venom against neurodegenerative diseases. Methods Spider venom was extracted by electrostimulation and fractionated by reverse-phase high-performance liquid chromatography (RP-HPLC) and characterized by matrix-assisted laser desorption ionization-time flight mass spectrometry (MALDI-TOF-MS). Neuroactivity of the whole venom was observed by a neurobehavioral response from Terebrio molitor larvae in vivo and fractions were screened for their inhibitory activities against AChE and BACE in vitro. Results The whole venom from P. bundokalbo demonstrated neuroactivity by inducing excitatory movements from T. molitor for 15 min. Sixteen fractions collected produced diverse mass fragments from MALDI-TOF-MS ranging from 900-4500 Da. Eleven of sixteen fractions demonstrated AChE inhibitory activities with 14.34% (± 2.60e-4) to 62.05% (± 6.40e-5) compared with donepezil which has 86.34% (± 3.90e-5) inhibition (p > 0.05), while none of the fractions were observed to exhibit BACE inhibition. Furthermore, three potent fractions against AChE, F1, F3, and F16 displayed competitive and uncompetitive inhibitions compared to donepezil as the positive control. Conclusion The venom of P. bundokalbo contains compounds that demonstrate neuroactivity and anti-AChE activities in vitro, which could comprise possible therapeutic leads for the development of cholinergic compounds against neurological diseases.(AU)


Subject(s)
Animals , Acetylcholinesterase , Spider Venoms/toxicity , Neurotransmitter Agents , Neurodegenerative Diseases , In Vitro Techniques
5.
Article in Chinese | WPRIM | ID: wpr-887477

ABSTRACT

OBJECTIVE@#To observe the effect of @*METHODS@#A total of 60 children with intellectual disability were randomly divided into an observation group (30 cases, 2 cases dropped off) and a control group (30 cases, 2 cases dropped off). In the control group, rehabilitation training and routine acupuncture were adopted, 30 min each time, once a day, 6 times a week for 3 months. On the base of the treatment as the control group, @*RESULTS@#Compared before treatment, the scores of DQ and ADL and the serum levels of DA, NE, 5-HT after treatment were increased (@*CONCLUSION@#On the base of rehabilitation training and routine acupuncture,


Subject(s)
Activities of Daily Living , Acupuncture Points , Acupuncture Therapy , Child , Humans , Intellectual Disability , Needles , Neurotransmitter Agents , Treatment Outcome
6.
Article in Chinese | WPRIM | ID: wpr-921648

ABSTRACT

The rats were exposed to chronic unpredictable mild stress(CUMS) and kept in separate cages for inducing depressive disorder, which was judged by behavioral indicators. The number and morphology of neurons in hippocampal CA3 area and prefrontal cortex were observed by hematoxylin-eosin(HE) staining. The levels of brain-derived neurotrophic factor(BDNF), 5-hydroxytryptamine(5-HT), 5-hydroxyindoleacetic acid(5-HIAA), dopamine(DA), norepinephrine(NE), glutamic acid(GLU), interleukin-1β(IL-1β), interleukin-18(IL-18), and tumor necrosis factor-α(TNF-α) were detected by enzyme-linked immunosorbent assay(ELISA). Real-time polymerase chain reaction(RT-PCR) and Western blot were conducted to determine the mRNA and protein expression levels of related molecules in NLRP3 pathway. The results showed that compared with the model group, acidic polysaccharides from Poria at the low-, medium-, and high-doses(0.1, 0.3 and 0.5 g·kg~(-1)·d~(-1)) all improved the depression-like behavior of rats, increased the number of neurons and the levels of BDNF, 5-HT, 5-HIAA, DA, and NE in the hippocampus, and reduced GLU and serum IL-1β, IL-18, and TNF-α levels. The mRNA expression levels of ASC, caspase-1, IL-1β, and IL-18 and the protein expression levels of NLRP3, ASC, caspase-1, IL-1β, and IL-18 in each medication group were down-regulated, whereas the protein expression levels of pro-caspase-1, pro-IL-1β, and pro-IL-18 were up-regulated. All these have indicated that acidic polysaccharides from Poria exerted the antidepressant effect possibly by regulating neurotransmitters and NLRP3 inflammasome signaling pathway.


Subject(s)
Animals , Antidepressive Agents , Depression/drug therapy , Interleukin-1beta , NLR Family, Pyrin Domain-Containing 3 Protein/genetics , Neurotransmitter Agents , Polysaccharides/pharmacology , Poria , Rats
7.
Rev. méd. Minas Gerais ; 31: 31205, 2021.
Article in English, Portuguese | LILACS | ID: biblio-1291276

ABSTRACT

A Esclerose Lateral Amiotrófica (ELA), uma doença neurodegenerativa fatal, que afeta neurônios motores superiores e inferiores, tem como fisiopatologia mais aceita a excitotoxicidade mediada por glutamato. O atual estudo tem como objetivo estabelecer a relação entre esse neurotransmissor e a ELA, a partir de uma revisão de literatura nas bases de dados Pubmed e Medline. O glutamato é o principal neurotransmissor do Sistema Nervoso Central (SNC) e a excitotoxicidade gerada pelo seu acúmulo nas fendas sinápticas é tida como um dos principais mecanismos envolvidos na fisiopatologia da ELA. Os indivíduos afetados pela ELA apresentam diminuição da expressão de determinados grupos de receptores metabotrópicos de glutamato (mGlu) nos neurônios e nas células da glia desses pacientes. Os mGlu possuem um papel de destaque na modulação da excitotoxicidade por glutamato e são subdivididos em três grupos. Os mGlus do grupo 1 amplificam as transmissões sinápticas excitatórias rápidas, e os dos grupos 2 e 3 atuam como neuroprotetores inibindo a liberação do glutamato na fenda sináptica. Os mGlus são, portanto, considerados alvos terapêuticos para a atuação de drogas que combatem a excitotoxicidade e induzem a produção de fatores neurotróficos, constituindo importante atuação no combate à ELA.


Amyotrophic Lateral Sclerosis (ALS), a fatal neurodegenerative disease that affects upper and lower motor neurons, has as the most accepted pathophysiology the glutamate-mediated excitotoxicity. The present study aims to establish the relationship between this neurotransmitter and ALS, based on a literature review in the PubMed and Medline databases. Glutamate is the main neurotransmitter of the central nervous system (CNS) and the excitotoxicity generated by its accumulation in the synaptic clefts is considered one of the main mechanisms involved in the pathophysiology of ALS. People affected by ALS present a decrease in expression of certain metabotropic glutamate receptor (mGlu) groups in neurons and glial cells of these patients. mGlu has a prominent role in modulating glutamate excitotoxicity and are subdivided into three groups. Group 1 mGlu amplifies rapid excitatory synaptic transmissions, while groups 2 and 3 act as neuroprotective agents, since among other functions they inhibit glutamate release into the synaptic cleft. Finally, mGlu are considered therapeutic targets for the action of drugs that fight excitotoxicity and induce the production of neurotrophic factors, constituting an important action in the fight against ALS.


Subject(s)
Humans , Receptors, Metabotropic Glutamate , Amyotrophic Lateral Sclerosis , Motor Neuron Disease , Neurotransmitter Agents , Neurodegenerative Diseases , Superoxide Dismutase-1 , Neurotoxins
9.
Neotrop. ichthyol ; 18(2): e190120, 2020. tab, graf
Article in English | LILACS, VETINDEX | ID: biblio-1135376

ABSTRACT

Organisms with source-populations restricted to the subterranean biotope (troglobites) are excellent models for comparative evolutionary studies, due to their specialization to permanent absence of light. Eye and dark pigment regression are characteristics of most troglobites. In spite of the advance in knowledge on the mechanisms behind eye regression in cave fishes, very little is known about pigmentation changes. Studies were focused on three species of the genus Pimelodella. Exemplars of the troglobitic P. spelaea and P. kronei were compared with the epigean (surface) P. transitoria, putative sister-species of the latter. Melanophore areas and densities are significantly lower in the troglobitic species. Evaluating the in vitro response of these cells to adrenaline, acetylcholine and MCH, we observed a reduced response in both troglobites to adrenaline. The same trend was observed with MCH, but not statistically significant. No response to acetilcholine was detected in all the three. Contrary to expectations, even though eye-regression in P. spelaea was much lower than in P. kronei, pigmentation regression was more advanced. Multiple mechanisms of loss showing a mosaic of traits in troglobitic fishes are discussed here.(AU)


Organismos com populações-fonte restritas ao biótopo subterrâneo (troglóbios) são excelentes modelos para estudos evolutivos comparativos, devido à especialização resultante do isolamento sob um regime seletivo particular, com ênfase na permanente falta de luz. A regressão do olho e da pigmentação são características dos troglobites. Apesar do avanço do conhecimento sobre os mecanismos subjacentes à regressão ocular em peixes de caverna, pouco se sabe sobre mudanças de pigmentação. Os estudos foram focados em três espécies do gênero Pimelodella. Exemplares das espécies troglóbias P. spelaea e P. kronei foram comparados com a epígea P. transitoria, provável espécie-irmã dessa última. As áreas e densidades dos melanóforos são significativamente menores nas espécies troglóbias. Avaliando a resposta in vitro dessas células à adrenalina, acetilcolina e MCH, observamos uma resposta reduzida em ambos os troglóbios à adrenalina. A mesma tendência foi observado com o MCH, mas não estatisticamente. Nenhuma resposta à acetilcolina foi detectada três. Contrariamente às expectativas, embora a regressão ocular em P. spelaea seja bem menor do que em P. kronei, a regressão na pigmentação foi mais acentuada. Múltiplos mecanismos de regressão, mostrando um mosaico de características em peixes troglóbios, são discutidos aqui.(AU)


Subject(s)
Animals , Catfishes/physiology , Pigmentation , Color , Neurotransmitter Agents , Hormones , Fishes
10.
Article in Chinese | WPRIM | ID: wpr-827965

ABSTRACT

To explore the pathogenesis of heart and kidney imbalance insomnia and the regulatory effect of Jiaotai Pills, in order to study the changes of central and peripheral neurotransmitters in rat. Insomnia rats with heart and kidney imbalance were induced through intraperitoneal injection with p-chlorophenylalanine(PCPA, 400 mg·kg~(-1)·d~(-1)), and the model rats were intragastrically administrated with Jiaotai Pills(3.3 g·kg~(-1)·d~(-1)) for 7 days. Nine neurotransmitters were determined by UPLC-MS/MS and principal component analysis(PCA) method in serum, urine, brain, heart, liver, kidney and adrenal gland of rats. The results showed that the ratio of 5-HT and 5-HIAA in platelet of insomnia rats was significantly lower than that in the normal group, and Jiaotai Pills had a significant up-regulatory or down-regulatory effect. Compared with the normal group, the changed neurotransmitters in blood of insomnia rats were 5-HIAA, E, NE, DA, Glu and ACH, and except ACH, the changes of 7 kinds of neurotransmitters in urine were more significant, Jiaotai Pills had a significant up-regulatory or down-regulatory effect. Compared with the normal group, all of the 8 neurotransmitters in insomnia rats except HVA were changed. Jiaotai Pills could regulate the neurotransmitters in each tissue of insomnia rats, especially in brain, liver and adrenal gland. In conclusion, insomnia is caused by not only a change of neurotransmitters in brain, but also a series of changes in peripheral tissues. It indicates that insomnia is a systematic imbalance of neurotransmitters. Jiaotai Pills not only regulates the central nervous system, but also has a certain protective effect on other organs, reflecting the multi-target and systematic effect of Jiaotai Pills in the treatment of insomnia.


Subject(s)
Animals , Chromatography, Liquid , Drugs, Chinese Herbal , Neurotransmitter Agents , Rats , Sleep Initiation and Maintenance Disorders , Tandem Mass Spectrometry
11.
Chinese Journal of Biotechnology ; (12): 1051-1059, 2020.
Article in Chinese | WPRIM | ID: wpr-826871

ABSTRACT

Neurotransmitters play an important role in nervous system. Temporal and spatial changes of neurotransmitter distribution are crucial to information processing in neural networks. Biosensors that can visually monitor neurotransmitters are one of the vital tools to explore a variety of physiological and pathological activities. This article reviews recent advances in monitoring neurotransmitters with high temporal and spatial resolution, and introduces the latest fluorescent imaging methods for typical neurotransmitters, including glutamate, dopamine, γ-aminobutyric acid and acetylcholine. The article also summarizes the basic principles, advantages and disadvantages of various visually detection methods, and provides systematic suggestions for designing neurotransmitter sensors with high temporal and spatial resolution.


Subject(s)
Animals , Biosensing Techniques , Fluorescence , Humans , Neurotransmitter Agents , Metabolism
12.
Biol. Res ; 53: 36, 2020. tab, graf
Article in English | LILACS | ID: biblio-1131882

ABSTRACT

BACKGROUND: To investigate the thalamic neurotransmitters and functional connections in the development of chronic constriction injury (CCI)-induced neuropathic pain. METHODS: The paw withdrawal threshold was measured by mechanical stimulation the right hind paw with the von frey hair in the rats of CCI-induced neuropathic pain. The N-acetylaspartate (NAA) and Glutamate (Glu) in thalamus were detected by magnetic resonance spectrum (MRS) process. The thalamic functional connectivity with other brain regions was scanned by functional magnetic resonance image (fMRI). RESULTS: The paw withdrawal threshold of the ipsilateral side showed a noticeable decline during the pathological process. Increased concentrations of Glu and decreased levels of NAA in the thalamus were significantly correlated with mechanical allodynia in the neuropathic pain states. The thalamic regional homogeneity (ReHo) decreased during the process of neuropathic pain. The functional connectivity among the thalamus with the insula and somatosensory cortex were significantly increased at different time points (7, 14, 21 days) after CCI surgery. CONCLUSION: Our study suggests that dynamic changes in thalamic NAA and Glu levels contribute to the thalamic functional connection hyper-excitation during CCI-induced neuropathic pain. Enhanced thalamus-insula functional connection might have a significant effect on the occurrence of neuropathic pain.


Subject(s)
Animals , Rats , Thalamus/metabolism , Wounds and Injuries/physiopathology , Neurotransmitter Agents/metabolism , Neuralgia , Thalamus/physiopathology , Aspartic Acid/analogs & derivatives , Aspartic Acid/metabolism , Glutamic Acid/metabolism , Constriction , Hyperalgesia
13.
Bol. latinoam. Caribe plantas med. aromát ; 18(5): 459-479, sept. 2019. ilus
Article in English | LILACS | ID: biblio-1008268

ABSTRACT

Neuronal cell damage is often caused by prolonged misuse of Methylphenidate (MPH). Topiramate (TPM) carries neuroprotective properties but its assumed mechanism remains unclear. The present study evaluates in vivo role of various doses of TPM and its mechanism against MPH-induced motor activity and related behavior disorder. Thus, we used domoic acid (DOM), bicuculline (BIC), Ketamine (KET), Yohimibine (YOH) and Haloperidole (HAL) as AMPA/kainite, GABAA, NMDA, ɑ2 adrenergic and D2 of dopamine receptor antagonists respectively. Open Field Test (OFT), Elevated Plus Maze (EPM) and Forced Swim Test (FST) were used to study motor activity, anxiety and depression level. TPM (100 and 120 mg/kg) reduced MPH-induced rise and inhibited MPH-induced promotion in motor activity disturbance, anxiety and depression. Pretreatment of animals with KET, HAL, YOH and BIC inhibited TPM- improves anxiety and depression through the interacting with Dopaminergic, GABAA, NMDA and ɑ2-adrenergic receptors.


El daño a las células neuronales a menudo es causado por el uso prolongado de metilfenidato (MPH). El topiramato (TPM) tiene propiedades neuroprotectoras, pero su mecanismo de acción no es claro. El presente estudio evalúa el papel in vivo de varias dosis de TPM y su mecanismo contra la actividad motora inducida por MPH y el trastorno de comportamiento relacionado. Utilizamos ácido domoico (DOM), bicuculina (BIC), ketamina (KET), yohimbina (YOH) y haloperidol (HAL), así como antagonistas AMPA/kainato, GABAA, NMDA, ɑ2-adrenérgico y D2 dopaminérgicos, respectivamente. Se utilizaron las pruebas de campo abierto (OFT), elevación de laberinto (EPM) y natación forzada (FST) para estudiar la actividad motora, la ansiedad y el nivel de depresión. El TPM (100 y 120 mg/kg) redujo el aumento inducido por MPH e inhibió la promoción inducida por MPH en la alteración de la actividad motora, la ansiedad y la depresión. El tratamiento previo de animales con KET, HAL, YOH y BIC inhibió el TPM, mejora la ansiedad y la depresión a través de la interacción con los receptores dopaminérgicos, GABAA, NMDA y ɑ2-adrenérgico.


Subject(s)
Animals , Male , Rats , Behavior, Animal/drug effects , Neuroprotective Agents/pharmacology , Topiramate/pharmacology , Mental Disorders/prevention & control , Methylphenidate/adverse effects , Rats, Wistar , Neurotransmitter Agents/metabolism , Mental Disorders/chemically induced , Motor Activity/drug effects
14.
Rev. Assoc. Med. Bras. (1992) ; 65(5): 706-713, May 2019. tab
Article in English | LILACS | ID: biblio-1012947

ABSTRACT

SUMMARY The term meditation can be used in many different ways, according to the technique to which it refers. Transcendental Meditation (MT) is one of these techniques. TM could serve as a model for research on spiritual meditation, unlike the meditation techniques based on secular knowledge. The purpose of the present study is to conduct a bibliographic review to organize scientific evidence on the effects of TM on neurophysiology, neurochemistry, and cognitive and behavioral aspects of its practitioners. To conduct this critical narrative review of the literature, we searched for scientific papers on the PubMed database of the National Center for Biotechnology Information. The keywords used in the search were Transcendental Meditation, Neuroscience of meditation e Meditation and behavior. We selected 21 papers that analyzed different aspects that could be altered through meditation practice. We concluded that TM has positive and significant documentable neurochemical, neurophysiological, and cognitive-behavioral effects. Among the main effects are the reduction of anxiety and stress (due to the reduction of cortisol and norepinephrine levels), increase of the feeling of pleasure and well-being (due to the increase of the synthesis and release of dopamine and serotonin), and influence on memory recall and possible consolidation. Further studies are needed using creative and innovative methodological designs that analyze different neural circuitry and verify the clinical impact on practitioners.


RESUMO O termo meditação pode ser utilizado de diversas formas, de acordo com a técnica a que se refere. A meditação transcendental (MT) é uma dessas técnicas meditativas. A MT pode ser um modelo para pesquisas de meditação espiritual, diferentemente de técnicas de meditação baseadas em uma compreensão secular. O presente estudo objetiva realizar uma revisão bibliográfica para organizar as evidências científicas sobre os efeitos da MT sobre a neurofisiologia, neuroquímica e aspectos cognitivos e comportamentais dos seus praticantes. Para a realização desta revisão narrativa crítica da literatura, foi realizado um levantamento dos artigos científicos presentes na base de dados PubMed do National Center for Biotechnology Information. As palavras-chave utilizadas na busca foram Transcendental Meditation, Neuroscience of meditation e Meditation and behavior. Foram selecionados 21 artigos que analisavam diferentes aspectos que poderiam ser alterados pela prática meditativa. Conclui-se que a MT produz efeitos neuroquímicos, neurofisiológicos e cognitivo-comportamentais documentáveis em seus praticantes, de caráter positivo e significativo. Entre os principais efeitos estão a diminuição da ansiedade e do estresse (via diminuição nos níveis de cortisol e noradrenalina), aumento na sensação de prazer e bem-estar (em decorrência ao aumento na síntese e liberação de dopamina e serotonina) e influência na evocação e possível consolidação da memória. São necessários mais estudos utilizando desenhos metodológicos inovadores e criativos, analisando diferentes circuitos neurais e verificando o impacto clínico sobre os praticantes.


Subject(s)
Humans , Cognition/physiology , Meditation/psychology , Nervous System/chemistry , Nervous System Physiological Phenomena , Neurotransmitter Agents/analysis , Neurotransmitter Agents/metabolism
16.
Neuroscience Bulletin ; (6): 301-314, 2019.
Article in English | WPRIM | ID: wpr-775476

ABSTRACT

Neuropathic pain is a chronic debilitating symptom characterized by spontaneous pain and mechanical allodynia. It occurs in distinct forms, including brush-evoked dynamic and filament-evoked punctate mechanical allodynia. Potassium channel 2.1 (Kir2.1), which exhibits strong inward rectification, is and regulates the activity of lamina I projection neurons. However, the relationship between Kir2.1 channels and mechanical allodynia is still unclear. In this study, we first found that pretreatment with ML133, a selective Kir2.1 inhibitor, by intrathecal administration, preferentially inhibited dynamic, but not punctate, allodynia in mice with spared nerve injury (SNI). Intrathecal injection of low doses of strychnine, a glycine receptor inhibitor, selectively induced dynamic, but not punctate allodynia, not only in naïve but also in ML133-pretreated mice. In contrast, bicuculline, a GABA receptor antagonist, induced only punctate, but not dynamic, allodynia. These results indicated the involvement of glycinergic transmission in the development of dynamic allodynia. We further found that SNI significantly suppressed the frequency, but not the amplitude, of the glycinergic spontaneous inhibitory postsynaptic currents (gly-sIPSCs) in neurons on the lamina II-III border of the spinal dorsal horn, and pretreatment with ML133 prevented the SNI-induced gly-sIPSC reduction. Furthermore, 5 days after SNI, ML133, either by intrathecal administration or acute bath perfusion, and strychnine sensitively reversed the SNI-induced dynamic, but not punctate, allodynia and the gly-sIPSC reduction in lamina IIi neurons, respectively. In conclusion, our results suggest that blockade of Kir2.1 channels in the spinal dorsal horn selectively inhibits dynamic, but not punctate, mechanical allodynia by enhancing glycinergic inhibitory transmission.


Subject(s)
Animals , Bicuculline , Pharmacology , Disease Models, Animal , Glycine , Metabolism , Hyperalgesia , Drug Therapy , Metabolism , Imidazoles , Pharmacology , Inhibitory Postsynaptic Potentials , Physiology , Male , Mice, Inbred C57BL , Neurons , Metabolism , Neurotransmitter Agents , Pharmacology , Peripheral Nerve Injuries , Drug Therapy , Metabolism , Phenanthrolines , Pharmacology , Potassium Channels, Inwardly Rectifying , Metabolism , Receptors, GABA-A , Metabolism , Receptors, Glycine , Metabolism , Strychnine , Pharmacology , Synaptic Transmission , Physiology , Tissue Culture Techniques , Touch
17.
Neuroscience Bulletin ; (6): 57-66, 2019.
Article in English | WPRIM | ID: wpr-775452

ABSTRACT

Metformin (MET), an antidiabetic agent, also has antioxidative effects in metabolic-related hypertension. This study was designed to determine whether MET has anti-hypertensive effects in salt-sensitive hypertensive rats by inhibiting oxidative stress in the hypothalamic paraventricular nucleus (PVN). Salt-sensitive rats received a high-salt (HS) diet to induce hypertension, or a normal-salt (NS) diet as control. At the same time, they received intracerebroventricular (ICV) infusion of MET or vehicle for 6 weeks. We found that HS rats had higher oxidative stress levels and mean arterial pressure (MAP) than NS rats. ICV infusion of MET attenuated MAP and reduced plasma norepinephrine levels in HS rats. It also decreased reactive oxygen species and the expression of subunits of NAD(P)H oxidase, improved the superoxide dismutase activity, reduced components of the renin-angiotensin system, and altered neurotransmitters in the PVN. Our findings suggest that central MET administration lowers MAP in salt-sensitive hypertension via attenuating oxidative stress, inhibiting the renin-angiotensin system, and restoring the balance between excitatory and inhibitory neurotransmitters in the PVN.


Subject(s)
Animals , Antioxidants , Therapeutic Uses , Arterial Pressure , Hypertension , Drug Therapy , Infusions, Intraventricular , Male , Metformin , Pharmacology , Neurotransmitter Agents , Metabolism , Oxidative Stress , Paraventricular Hypothalamic Nucleus , Rats , Reactive Oxygen Species , Metabolism , Sodium Chloride, Dietary , Pharmacology
18.
Article in English | WPRIM | ID: wpr-741923

ABSTRACT

To conceptualize a novel bio-psychosocial-behavioral treatment model of panic disorder (PD), it is necessary to completely integrate behavioral, psychophysiological, neurobiological, and genetic data. Molecular genetic research on PD is specifically focused on neurotransmitters, including serotonin, neuropeptides, glucocorticoids, and neurotrophins. Although pharmacological interventions for PD are currently available, the need for more effective, faster-acting, and more tolerable pharmacological interventions is unmet. Thus, glutamatergic receptor modulators, orexin receptor antagonists, corticotrophin-releasing factor 1 receptor antagonists, and other novel mechanism-based anti-panic therapeutics have been proposed. Research on the neural correlates of PD is focused on the dysfunctional “cross-talk” between emotional drive (limbic structure) and cognitive inhibition (prefrontal cortex) and the fear circuit, which includes the amygdala-hippocampus-prefrontal axis. The neural perspective regarding PD supports the idea that cognitive-behavioral therapy normalizes alterations in top-down cognitive processing, including increased threat expectancy and attention to threat. Consistent with the concept of “personalized medicine,” it is speculated that Research Domain Criteria can enlighten further treatments targeting dysfunctions underlying PD more precisely and provide us with better definitions of moderators used to identify subgroups according to different responses to treatment. Structuring of the “negative valence systems” domain, which includes fear/anxiety, is required to define PD. Therefore, targeting glutamate- and orexin-related molecular mechanisms associated with the fear circuit, which includes the amygdala-hippocampus-prefrontal cortex axis, is required to define a novel bio-psychosocial-behavioral treatment model of PD.


Subject(s)
Glucocorticoids , Molecular Biology , Nerve Growth Factors , Neuropeptides , Neurotransmitter Agents , Orexin Receptor Antagonists , Panic Disorder , Panic , Serotonin
19.
Article in English | WPRIM | ID: wpr-741922

ABSTRACT

The core concept for pathophysiology in panic disorder (PD) is the fear network model (FNM). The alterations in FNM might be linked with disturbances in the autonomic nervous system (ANS), which is a common phenomenon in PD. The traditional FNM included the frontal and limbic regions, which were dysregulated in the feedback mechanism for cognitive control of frontal lobe over the primitive response of limbic system. The exaggerated responses of limbic system are also associated with dysregulation in the neurotransmitter system. The neuroimaging studies also corresponded to FNM concept. However, more extended areas of FNM have been discovered in recent imaging studies, such as sensory regions of occipital, parietal cortex and temporal cortex and insula. The insula might integrate the filtered sensory information via thalamus from the visuospatial and other sensory modalities related to occipital, parietal and temporal lobes. In this review article, the traditional and advanced FNM would be discussed. I would also focus on the current evidences of insula, temporal, parietal and occipital lobes in the pathophysiology. In addition, the white matter and functional connectome studies would be reviewed to support the concept of advanced FNM. An emerging dysregulation model of fronto-limbic-insula and temporooccipito-parietal areas might be revealed according to the combined results of recent neuroimaging studies. The future delineation of advanced FNM model can be beneficial from more extensive and advanced studies focusing on the additional sensory regions of occipital, parietal and temporal cortex to confirm the role of advanced FNM in the pathophysiology of PD.


Subject(s)
Autonomic Nervous System , Connectome , Frontal Lobe , Limbic System , Neuroimaging , Neurotransmitter Agents , Occipital Lobe , Panic Disorder , Panic , Parietal Lobe , Rabeprazole , Temporal Lobe , Thalamus , White Matter
20.
J. venom. anim. toxins incl. trop. dis ; 25: e148818, 2019. graf, ilus
Article in English | LILACS, VETINDEX | ID: biblio-1002502

ABSTRACT

L-Glutamate (L-Glu), the major excitatory neurotransmitter in the mammalian Central Nervous System (CNS), is essential to cognitive functions. However, when L-Glu is accumulated in large concentrations at the synaptic cleft, it can induce excitotoxicity that results in secondary damage implicated in many neurological disorders. Current therapies for the treatment of neurological disorders are ineffective and have side effects associated with their use; therefore, there is a need to develop novel treatments. In this regard, previous studies have shown that neuroactive compounds obtained from the venom of the spider Parawixia bistriata have neuroprotective effects in vitro and in vivo. In this sense, this work aimed to evaluate potential neuroprotective effects of fraction RT10, obtained from this spider venom, on primary cultures of neuron and glial cells subjected to glutamate excitotoxicity insults. Methods: Primary cultures of neurons and glia were obtained from the cerebral tissue of 1-day-old postnatal Wistar rats. After 7 days in vitro (DIV), the cultures were incubated with fraction RT10 (0.002; 0.02; 0.2 and 2 µg/µL) or riluzole (100 µM) for 3-hours before application of 5 mM L-Glu. After 12 hours, the resazurin sodium salt (RSS) test was applied to measure metabolic activity and proliferation of living cells, whereas immunocytochemistry for MAP2 was performed to measure neuronal survival. In addition, the cells were immunolabeled with NeuN and GFAP in baseline conditions. Results: In the RSS tests, we observed that pre-incubation with RT10 before the excitotoxic insults from L-Glu resulted in neuroprotection, shown by a 10% reduction in the cell death level. RT10 was more effective than riluzole, which resulted in a cell-death reduction of 5%. Moreover, qualitative analysis of neuronal morphology (by MAP2 staining, expressed as fluorescence intensity (FI), an indirect measure of neuronal survival) indicate that RT10 reduced the toxic effects of L-Glu, as shown by a 38 % increase in MAP2 fluorescence when compared to L-Glu insult. On the other hand, the riluzole treatment resulted in 17% increase of MAP2 fluorescence; therefore, the neuroprotection from RT10 was more efficacious. Conclusion: RT10 fraction exhibits neuroprotective effects against L-Glu excitotoxicity in neuron-glia cultured in vitro.(AU)


Subject(s)
Spider Venoms , Neuroprotection , Neurotransmitter Agents , Excitatory Amino Acid Agonists , Evaluation Studies as Topic
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