ABSTRACT
Se realiza una revisión de estudios de resonancia magnética integral y funcional, así como estudios bioquímicos en pacientes con y sin ideas suicidas. Estos estudios en pacientes con alto riesgo de suicidio presentan una disminución de volúmenes corticales en la corteza prefrontal dorso y ventrolateral. Lo importante de estos estudios es que resultan de la comparación con pacientes deprimidos con bajo riesgo de suicidio. Los estudios de resonancia magnética funcional mostraron una hipofuncionalidad del lóbulo prefrontal en los pacientes depresivos con ideas suicidas severas, que se observa como una disminución del flujo sanguíneo cerebral en las áreas lateral y ventral. Se observa una disminución del metabolismo de serotonina, en clara relación con la severidad de las ideas de muerte, también con un foco en la región lateroventral prefrontal. Dado que las funciones de la corteza prefrontal afirman al individuo en su perspectiva vital, disfunciones como las descritas debilitan la coordinación y organización del apego a la vida, quedando, por el contrario, la posibilidad de la búsqueda de la muerte. Se concluye que los pacientes depresivos con ideas suicidas tienen una alta vulnerabilidad para el intento de suicidio por la afectación de las zonas prefrontales.
A review of functional integral magnetic resonance and biochemical data from patients with and without suicidal ideation is presented. Patients with high suicidal risk show a decrease in cortical volume in ventrolateral and dorsal prefrontal cortex. These studies are compared to those of depressed patients with low suicidal risk. Functional magnetic resonance in depressed patients with severe suicidal ideation show an hypo functional prefrontal lobe, seen as a decrease in blood flow in lateral and ventral areas. There is a decrease in serotonin metabolism, clearly related to the severity of suicidal ideation, also in ventrolateral prefrontal cortex. As prefrontal cortex functions enhance vital perspectives, such dysfunctions weaken coordination and organization of attachment to life, making search for death a possibility. Authors conclude that depressed patients with suicidal ideation have a high vulnerability for suicidal intent due to changes in prefrontal areas.
Subject(s)
Humans , Suicide, Attempted , Prefrontal Cortex/physiopathology , Neurotransmitter Agents/metabolism , Depression/physiopathology , Suicidal Ideation , Magnetic Resonance Imaging , Prefrontal Cortex/metabolism , Prefrontal Cortex/diagnostic imaging , Depression/metabolismABSTRACT
La neuromodulación es una práctica médica implementada desde hace más de cuatro décadas. En lo que respecta a la Neurocirugía, cumple un papel en el tratamiento de diversas patologías (Parkinson, distonías, epilepsia, etc.) y con un gran potencial para aplicarlas en otras (trastorno obsesivo compulsivo [TOC], dolor pélvico). Es por ello que, en los últimos años, se cuadruplicaron las inversiones de empresas biotecnológicas en este campo por la demanda y aplicación de la terapia. La neuromodulación abarca también otras especialidades, como por ejemplo Otorrinolaringología (ORL) en implantes cocleares, Cardiología con diversos modelos de marcapasos cardíacos, Endocrinología con bombas de infusión de medicamentos, Uroginecología en incontinencia, etcétera. Nuestra institución aplica en su práctica clínica todas estas técnicas, y cumple una función jerárquica como centro de referencia en educación y políticas sanitarias. Por estos aspectos, sumados a su infraestructura, personal profesional y enfoque sanitario, puede ser considerada como un Centro de Neuromodulación referente en la región. (AU)
Neuromodulation is a medical practice established for more than forty years. In the neurosurgical field it plays a role in the treatment of different diseases (Parkinson, Dystonia, Epilepsy, etc) and has a great potential to apply in other pathologies (Obsessive Compulsive Disorder, Pelvic pain). In the last years the biotechnological industry has quadrupled the investment in this field because of the demand and therapy application. Neuromodulation encompasses other specialities, for example otorhinolaryngology in cochlear implants, in cardiology with different models of pacemakers, endocrinology with implanted infusion pumps, urological gynecology in incontinence treatments, etc. Our institution applies all these techniques in its clinical practice, having a hierarchical role as a reference center in education and health policies. Due to these aspects, added to its infrastructure, professional staff and health approach, it can be considered as a reference Neuromodulation Center in the region. (AU)
Subject(s)
Humans , Parkinson Disease/therapy , Neurotransmitter Agents/therapeutic use , Deep Brain Stimulation , Chronic Pain/therapy , Drug Resistant Epilepsy/therapy , Pain Management/methods , Functional StatusABSTRACT
OBJECTIVE@#To investigate the therapeutic effect of Yixin Ningshen Tablet (YXNS) on comorbidity of myocardial infarction (MI) and depression in rats and explore the underlying mechanism.@*METHODS@#The Sprague-Dawley rats were randomly divided into 5 groups with 7 rats in each group according to their weights, including control, model, fluoxetine (FLXT, 10 mg/kg), low-dose YXNS (LYXNS, 100 mg/kg), and high-dose YXNS (HYXNS, 300 mg/kg) groups. All rats were pretreated with corresponding drugs for 12 weeks. The rat model of MI and depression was constructed by ligation of left anterior descending coronary artery and chronic mild stress stimulation. The echocardiography, sucrose preference test, open field test, and forced swim test were performed. Myocardial infarction (MI) area and myocardial apoptosis was also detected. Serum levels of interleukin (IL)-6, IL-1β, tumor necrosis factor-α (TNF-α), 5-hydroxytryptamine (5-HT), adrenocorticotrophic hormone (ACTH), corticosterone (CORT), and norepinephrine (NE) were determined by enzyme linked immunosorbent assay. The proteins of adenosine 5'-monophosphate -activated protein kinase (AMPK), p-AMPK, peroxisome proliferator-activated receptor gamma coactivator-1α (PGC-1α), and nuclear respiratory factor 1 (NRF1) in heart were detected by Western blot analysis. The expression levels of TNF-α, IL-6, indoleamine 2,3-dioxygenase (IDO1), kynurenine 3-monooxygenase (KMO), and kynureninase (KYNU) in hippocampus were detected by real-time quantitative polymerase chain reaction.@*RESULTS@#Compared with the model group, the cardiac function of rats treated with YXNS improved significantly (P<0.01). Meanwhile, YXNS effectively reduced MI size and cardiomyocytes apoptosis of rats (P<0.01 or P<0.05), promoted AMPK phosphorylation, and increased PGC-1α protein expression (P<0.01 or P<0.05). HYXNS significantly increased locomotor activity of rats, decreased the levels of TNF-α, IL-6 and IL-1β, and increased the serum levels of 5-HT, NE, ACTH, and CORT (all P<0.05). Moreover, HYXNS decreased the mRNA expressions of IDO1, KMO and KYNU (P<0.05).@*CONCLUSIONS@#YXNS can relieve MI by enhancing myocardial energy metabolism. Meanwhile, YXNS can alleviate depression by resisting inflammation and increasing availability of monoamine neurotransmitters. It may be used as a potential drug to treat comorbidity of MI and depression.
Subject(s)
AMP-Activated Protein Kinases/metabolism , Adrenocorticotropic Hormone , Animals , Comorbidity , Depression/drug therapy , Energy Metabolism , Interleukin-6/metabolism , Myocardial Infarction/pathology , Neurotransmitter Agents , Rats , Rats, Sprague-Dawley , Serotonin/metabolism , Tablets , Tumor Necrosis Factor-alpha/metabolismABSTRACT
Objective: To investigate the effects of PM2.5 exposure at different stages of early life on the prefrontal cortex of offspring rats. Methods: Twelve pregnant SD rats were randomly divided into four groups: Control group (CG), Maternal pregnancy exposure group (MG), Early postnatal exposure group (EP) and Perinatal period exposure group (PP), 3 rats in each group. The pregnant and offspring rats were exposed to clean air or 8-fold concentrated PM2.5. MG was exposed from gestational day (GD) 1 to GD21. EP was exposed from postnatal day (PND) 1 to PND21, and PP was exposed from GD1 to PND21. After exposure, the prefrontal cortex of 6 offspring rats in each group was analyzed. HE staining was used to observe the pathological damage in the prefrontal cortex. ELISA was employed to detect neuroinflammatory factors, and HPLC/MSC was applied to determine neurotransmitter content. Western blot and colorimetry were applied for detecting astrocyte markers and oxidative stress markers, respectively. Results: Compared with MG and CG, the pathological changes of prefrontal cortex in PP and EP were more obvious. Compared with MG and CG, the neuroinflammatory factors (IL-1, IL-6, TNF-α) in PP and EP were increased significantly (P＜0.01), the level of MT were decreased significantly (P＜0.05), and the level of oxytocin (OT) showed a downward trend; the level of neurotransmitter ACh was also increased significantly (P＜0.01). Compared with MG and CG, the GFAP level of PP and EP showed an upward trend, the level of oxidative stress index SOD in PP and EP was decreased significantly (P＜0.01), and the level of ROS was increased significantly (P＜0.01). Compared with the offspring rats of CG and MG, the CAT level of PP was decreased significantly (P＜0.01, P＜0.05). Compared with the offspring rats of CG, the CAT level of EP was decreased significantly (P＜0.05). There was no significant difference in IL-1, IL-6, TNF-α, MT, OT, ACh, GFAP, SOD, ROS and CAT levels between PP and EP, or MG and CG. Conclusion: PM2.5 exposure in early life has adverse effects on the prefrontal cortex of offspring male rats, and early birth exposure may be more sensitive.
Subject(s)
Animals , Female , Interleukin-1/pharmacology , Interleukin-6 , Male , Neurotransmitter Agents , Particulate Matter/toxicity , Prefrontal Cortex , Pregnancy , Rats , Rats, Sprague-Dawley , Reactive Oxygen Species , Superoxide Dismutase , Tumor Necrosis Factor-alpha/pharmacologyABSTRACT
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/physiologyABSTRACT
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 StimulationABSTRACT
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 AgentsABSTRACT
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 , NeurotoxinsABSTRACT
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 , RatsABSTRACT
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 TechniquesABSTRACT
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 OutcomeABSTRACT
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 , HyperalgesiaABSTRACT
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 , FishesABSTRACT
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 SpectrometryABSTRACT
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 , MetabolismABSTRACT
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, É2 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 É2-adrenergic receptors.
El danÌo a las ceÌlulas neuronales a menudo es causado por el uso prolongado de metilfenidato (MPH). El topiramato (TPM) tiene propiedades neuroprotectoras, pero su mecanismo de accioÌn no es claro. El presente estudio evaluÌa 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 aÌcido domoico (DOM), bicuculina (BIC), ketamina (KET), yohimbina (YOH) y haloperidol (HAL), asiÌ como antagonistas AMPA/kainato, GABAA, NMDA, É2-adreneÌrgico y D2 dopamineÌrgicos, respectivamente. Se utilizaron las pruebas de campo abierto (OFT), elevacioÌn de laberinto (EPM) y natacioÌn forzada (FST) para estudiar la actividad motora, la ansiedad y el nivel de depresioÌn. El TPM (100 y 120 mg/kg) redujo el aumento inducido por MPH e inhibioÌ la promocioÌn inducida por MPH en la alteracioÌn de la actividad motora, la ansiedad y la depresioÌn. El tratamiento previo de animales con KET, HAL, YOH y BIC inhibioÌ el TPM, mejora la ansiedad y la depresioÌn a traveÌs de la interaccioÌn con los receptores dopamineÌrgicos, GABAA, NMDA y É2-adreneÌrgico.
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 effectsABSTRACT
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/metabolismABSTRACT
Los trastornos de ansiedad constituyen un grupo de alteraciones psicológicas y neurológicas que representan varias formas de miedo y ansiedad anormales o patológicas (Orozco & Baldares, 2012). Aun cuando alrededor del 14% de la población del planeta ha sufrido algún trastorno de ansiedad, las causas que desencadenan el mismo no son del todo claras (Posada, 2013). La aproximación clásica de los estudios para la identificación de los factores de predisposición de estos trastornos neuropsiquiátricos se ha orientado a las teorías de la personalidad como la Teoría de Eysenck (Mitchell & Kumari, 2016) y la Teoría Bio-Psicológica de la personalidad (Knyazev, Pylkova, Slobodskoj-Plusnin, Bocharov, & Ushakov, 2015). Sin embargo, a partir de estos estudios, han surgido nuevas propuestas involucrando los aspectos neuroanatómicos y neurofuncionales. La transmisión eléctrica y química de la información y como esta se asocia a distintas conductas demuestran la relevación de la regulación de la producción y recaptación de neurotransmisores en sistema nervioso central (SNC). Aunque esta regulación se encuentra directamente relacionada con la expresión genética, em tanto se han identificado ciertos genes candidatos que aportan un porcentaje a esta predisposición, estos no son totalmente determinantes. Actualmente, dado a este vacío, se ha comenzado a investigar la influencia de factores epigenéticos que en conjunto con los factores genéticos permitirían ampliar la explicación de los factores de predisposición de ciertos trastornos neuropsiquiátricos que anteriormente eran considerados de etiología ambiental
Anxiety disorders are a group of psychological and neurological disorders that represent various forms of abnormal or pathological fear and anxiety (Orozco & Baldares, 2012). Even though around 14% of the planet's population has suffered from an anxiety disorder, the causes that trigger it are not entirely clear (Posada, 2013). The classical approach of studies for the identification of the predisposing factors of these neuropsychiatric disorders has been oriented to personality theories such as the Eysenck Theory (Mitchell & Kumari, 2016) and the Bio-Psychological Theory of Personality (Knyazev, Pylkova, Slobodskoj-Plusnin, Bocharov, & Ushakov, 2015). However, from these studies, new proposals involving neuroanatomical and neurofunctional aspects have emerged. The electrical and chemical transmission of the information and how it is associated with different behaviors demonstrate the relief of the regulation of the production and reuptake of neurotransmitters in the central nervous system (CNS). This regulation is directly related to genetic expression, however, although certain candidate genes that contribute a percentage to this predisposition have been identified, these are not totally determinant (Montag, Reuter, Newport, Elger & Weber, 2008). Currently, given this gap, we have begun to investigate the influence of epigenetic factors that, together with genetic factors, would allow us to expand the explanation of the predisposing factors of certain neuropsychiatric disorders that were previously considered to be of environmental etiology
Subject(s)
Humans , Anxiety Disorders , Psychological Theory , Neurotransmitter Agents , Nervous System Diseases , Anxiety , Personality , Vacuum , Behavior , Causality , Fear , Epigenomics , Genes , GeneticsABSTRACT
Functional chest pain accounts for about a third of the patients with noncardiac chest pain. It is a very common functional esophageal disorder that remains even today a management challenge to the practicing physician. Based on the definition offered by the Rome IV criteria, diagnosis of functional chest pain requires a negative workup of noncardiac chest pain patients that includes, proton pump inhibitor test or empirical proton pump inhibitor trial, endoscopy with esophageal mucosal biopsies, reflux testing, and esophageal manometry. The mainstay of treatment are neuromodulators that are primarily composed of anti-depressants. Alternative medicine and psychological interventions may be provided alone or in combination with other therapeutic modalities.