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La depresión es una de las patologías más abordadas actualmente, la presencia de síntomas característicos provoca gran precaución y requiere de alto cuidado personal, además, el padecimiento de esta enfermedad se enlaza directamente a los aspectos neurobiológicos que explica los procesos dentro del sistema nervioso central. Objetivo. El objetivo del presente estudio es describir las siguientes teorías de la neurología de la depresión mayor: teoría de la monoaminas, teoría neurotrófica y teoría inflamatoria junto con su relación con la depresión. Metodología. Se realizó una revisión bibliográfica de la literatura científica relacionados a la neurobiología de la depresión mayor, incluyendo estudios; experimentales, originales, metaanálisis y paginas oficiales. Se utilizó la base de datos PubMed, y Google scholar, cuyos documentos fueron publicados entre 2015 a 2022 en idioma español e inglés; se utilizaron los términos MESH y DeCs: "depresión" "inflamación" "neurobiología" "monoaminas biogénicas". Conclusión: Se concluye que, a pesar de los nuevos descubrimientos en cuanto a diferentes mecanismos de la neurobiología de la depresión, aún existen vacíos por descubrir que impiden desarrollar una teoría unificada de la etiología.
Depression is currently one of the most frequently addressed pathologies, the presence of characteristic symptoms causes great caution and requires high personal care, in addition, the suffering of this disease is directly linked to the neurobiological aspects that explain the processes within the central nervous system. Objective. The aim of the present study is to describe the following theories of the neurology of major depression: monoamine theory, neurotrophic theory and inflammatory theory together with their relation to depression. Methodology. A bibliographic review of the scientific literature related to the neurobiology of major depression was carried out, including experimental studies, original studies, meta-analysis and official pages. The PubMed database was used, and Google scholar, whose documents were published between 2015 to 2022 in Spanish and English language; the terms MESH and DeCs were used: "depression" "inflammation" "neurobiology" "biogenic monoamines". Conclusion: It is concluded that, despite new discoveries regarding different mechanisms of the neurobiology of depression, there are still undiscovered gaps that prevent the development of a unified theory of etiology.
A depressão é uma das patologias mais freqüentemente abordadas atualmente, a presença de sintomas característicos causa grande cautela e requer um alto cuidado pessoal, além disso, o sofrimento desta doença está diretamente ligado aos aspectos neurobiológicos que explicam os processos dentro do sistema nervoso central. Objetivo. O objetivo do presente estudo é descrever as seguintes teorias da neurologia da depressão grave: teoria monoamina, teoria neurotrófica e teoria inflamatória, juntamente com sua relação com a depressão. Metodologia. Foi realizada uma revisão bibliográfica da literatura científica relacionada à neurobiologia da depressão grave, incluindo estudos experimentais, estudos originais, meta-análises e páginas oficiais. Utilizamos o banco de dados PubMed e Google scholar, cujos documentos foram publicados entre 2015 e 2022 em espanhol e inglês; usamos os termos MESH e DeCs: "depressão" "inflamação" "neurobiologia" "monoaminas biogênicas". Conclusão: Conclui-se que, apesar das novas descobertas sobre diferentes mecanismos da neurobiologia da depressão, ainda existem lacunas ainda não descobertas que impedem o desenvolvimento de uma teoria unificada da etiologia.
Assuntos
DepressãoRESUMO
Objective To investigate the effects of nicergoline on expressions of 5-hydroxytryptamine 1A receptor (5-HT1AR), D2 dopamine receptor (D2DR),α2A adrenaline receptor (α2AAR) in the hippocampal CA1 region and the serum level of apolipoprotein E4 (ApoE4) in a rat model of vascular depression (VD) . Methods Forty-eight male Sprague-Daw ley rats w ere randomly al ocated into a normal control group, a model group, fluoxetine group, a low-dose nicergoline group, a medium-dose nicergoline group, and a nicergoline high-dose group ( n=8 in each group). A rat model of VD w as induced by the ligation of bilateral common carotid arteries combined w ith chronic unpredictable mild stress (CUMS) plus single housing. The rats did not conduct CUMS or single housing in the normal control group, and the rats in the model group conducted CUMS and single housing. The rats in the fluoxetine group w ere given fluoxetine 1.3 mg/(kg· d) for gastric lavage for 3 w eeks at the beginning of CUMS and single housing. The rats in the low -, medium-and high-dose nicergoline groups w ere given nicergoline 0.9, 1.9 and 3.8 mg/(kg· d), respectively for gastric lavage for 3 w eeks at the beginning of CUMS and single housing. The normal control group and the model group w ere given equal volume of distil ed w ater for gastric lavage, once a day for 3 w eeks. Depression-like behavior w as evaluated using sucrose solution consumption and open-field test. Immunohistochemical staining and Western blot were used to detect the expressions of 5-HT1AR, D2DR, andα2AAR in the hippocampal CA1 region. Enzyme linked immunosorbent assay w as used to detect serum ApoE4 level. Results Before CUMS, the scores of horizontal and vertical movement and sucrose solution consumption in the model group, the fluoxetine group and each nicergoline group w ere decreased significantly compared w ith the normal control group (al P<0.01);w hile at 21 days after CUMS, those in the fluoxetine group and the nicergoline medium-and high-dose groups w ere significantly higher than those in the model group (al P<0.05). There w ere no significant differences betw een the fluoxetine group and each nicergoline group. The expression levels of 5-HT1A R, D2DR, α2A AR, and the serum ApoE4 in the model group, the fluoxetine group, and each nicergoline group w ere significantly higher than those in the normal control group. Those of the fluoxetine group and the nicergoline medium -and high-dose groups were significantly lower than the model group (al P<0.01), while there were no significant differences betw een the fluoxetine group and each nicergoline group. Conclusions Nicergoline can improve the depression-like behavior in VD rats. Its mechanism may be associated w ith the dow nregulation of 5-HT1AR, D2DR, α2AAR expressions and serum ApoE4 level.
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Objective To observe the effect of Zhuang Jing mixture (ZJM ) on behavior of primary senile rat and monoamine neurotransmitters in it′s brain ,and to study its mechanism of anti‐aging .Methods Fifty senile female rates which average weight was(300 ± 20)g were randomized divided into 5 groups :blank control group ,low‐,mid‐and high‐dose group of ZJM ,positive control group ,with 10 rats in each group .After medication for 8 weeks ,Morris water maze test was used to evaluate the spatial learning and memory ability of primary senile rats .High performance liquid chromatography with fluorescence detection (HPLC‐FD) was used to detect the monoamine neurotransmitter content in rat′s cerebral cortex and hippocampus .Results Compared with blank control group ,high‐,middle‐dose group of ZJM and positive control group were improved the ability of learning and memory of pri‐mary senile rat ,as well as the cerebral cortex and hippocampus monoamine neurotransmitters levels .High‐dose group of ZJM had significant difference compared with positive control group in improving the ability of learning and memory(P<0 .05) ,and in im‐proving the cerebral cortex and hippocampus monoamine neurotransmitters(P<0 .05) .Conclusion ZJM could significantly improve the learning and memory abilities of primary senile rats ,and its mechanism may be related to adjust the monoamine neurotransmitter in brain .
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Objective To investigate the effects of sodium cyanide(NaCN) and /or acute hypobaric hypoxia on the contents of monoamine neurotransmitters in rats' brain.Methods 128 adult male SD rats were divided into normoxic group and acute hypoxia group with 64 animals for each group.An artificial hypobaric hypoxia chamber was used to simulate a 4 000m altitude situation.The acute hypoxic exposure models were established by exposing rats to the hypobaric chamber for 3 days.All the rats were then injected intra-peritoneally with NaCN in a dosage of 3.6mg/kg at sea level and at simulated high altitude at 0,0.5,2 and 6h time points.The rats were sacrificed and the brains were isolated.The brain tissues of hippocampus and striatum corpora were then dissected on ice.Proteins of the brain tissue were extracted by centrifugation.Contents of dopamine(DA),epinephrine(NE) and 5-hydroxytryptamine(5-HT) in the brain tissues were analyzed by HPLC.Results NaCN intoxication did not affect the contents of DA,NE and 5-HT at 0.5h,2h and 6h in the selected brain tissues of the normoxic group.Compared with non-intoxication group,however,NaCN intoxication for 2h or 6h significantly decreased the levels of NE and 5-HT in the hippocampus tissues and the contents of DA,NE and 5-HT in striatum corpora in acute hypobaric hypoxia group.The contents of DA,NE and 5-HT in striatum corpora and the contents of NE and 5-HT in acute hypoxia group were significantly decreased compared with that in normoxic group(P