Academic literature on the topic 'Monoaminy'
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Journal articles on the topic "Monoaminy"
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Zhou, Shi-Sheng, Yi-Ming Zhou, Da Li, and Qiang Ma. "Early Infant Exposure to Excess Multivitamin: A Risk Factor for Autism?" Autism Research and Treatment 2013 (2013): 1–8. http://dx.doi.org/10.1155/2013/963697.
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Autism, a neurodevelopmental disorder that affects boys more than girls, is often associated with altered levels of monoamines (serotonin and catecholamines), especially elevated serotonin levels. The monoamines act as both neurotransmitters and signaling molecules in the gastrointestinal and immune systems. The evidence related to monoamine metabolism may be summarized as follows: (i) monoamine neurotransmitters are enzymatically degraded/inactivated by three mechanisms: oxidative deamination, methylation, and sulfation. The latter two are limited by the supply of methyl groups and sulfate, respectively. (ii) A decrease in methylation- and sulfation-mediated monoamine inactivation can be compensated by an increase in the oxidative deamination catalyzed by monoamine oxidase, an X-linked enzyme exhibiting higher activity in females than in males. (iii) Vitamins can, on one hand, facilitate the synthesis of monoamine neurotransmitters and, on the other hand, inhibit their inactivation by competing for methylation and sulfation. Therefore, we postulate that excess multivitamin feeding in early infancy, which has become very popular over the past few decades, may be a potential risk factor for disturbed monoamine metabolism. In this paper, we will focus on the relationship between excess multivitamin exposure and the inactivation/degradation of monoamine neurotransmitters and its possible role in the development of autism.
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Murtazina, Alya R., Nadegda S. Bondarenko, Tatiana S. Pronina, et al. "A Comparative Analysis of CSF and the Blood Levels of Monoamines As Neurohormones in Rats during Ontogenesis." Acta Naturae 13, no. 4 (2021): 89–97. http://dx.doi.org/10.32607/actanaturae.11516.
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According to the literature, the cerebrospinal fluid (CSF) in the cerebral ventricles contains numerous neuron-derived physiologically active substances that can function as neurohormones and contribute to volume neurotransmission in the periventricular region of the brain. This study was aimed at carrying out a comparative analysis of CSF and the blood levels of monoamines in rats during ontogenesis as an indicator of age-related characteristics of monoamine transport to body fluids and their function as neurohormones in volume neurotransmission in the periventricular region of the brain. We have shown that CSF in the perinatal period and adulthood contains the most functionally significant monoamines: dopamine, noradrenaline, and serotonin. A comparison of the monoamine levels in the CSF and blood of animals of different age groups revealed that CSF contains monoamines of predominantly neuronal (cerebral) origin and almost no monoamines derived from the general circulation. We also established that monoamines are found in the CSF at physiologically active levels that allow them to act as neurohormones in both reversible volume neurotransmission in the adult brain and irreversible regulation of brain development in the perinatal period.
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Anlauf, Martin, Rolf Eissele, Martin K. H. Schäfer, et al. "Expression of the Two Isoforms of the Vesicular Monoamine Transporter (VMAT1 and VMAT2) in the Endocrine Pancreas and Pancreatic Endocrine Tumors." Journal of Histochemistry & Cytochemistry 51, no. 8 (2003): 1027–40. http://dx.doi.org/10.1177/002215540305100806.
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The uptake of monoamines into the secretory granules of monoamine-storing neuroendocrine cells is mediated by vesicular monoamine transporter protein 1 or 2 (VMAT1 or VMAT2). This study analyzed the expression of VMAT1 and VMAT2 in endocrine cells of normal human and monkey pancreas. The expression of VMAT1 and VMAT2 was also examined in infants with hyperinsulinemic hypoglycemia and in adults with pancreatic endocrine tumors (PETs). Using immunohistochemistry (IHC) and in situ hybridization (ISH), we demonstrated the mutually exclusive expression of VMAT1 in endocrine cells of the duct system and of VMAT2 in many cells of the islets of Langerhans. By confocal laser scanning microscopy, VMAT1-positive cells were identified as enterochromaffin (EC) cells and VMAT2-positive cells as β-cells. In PETs, VMAT1 was found exclusively in all serotonin-containing tumors. In contrast, VMAT2 expression was lost in many insulinomas, independent of their biological behavior. VMAT2 was expressed by some non-insulin-producing tumors. The mutually exclusive expression of VMAT1 in EC cells and of VMAT2 in β-cells suggests that both cell types store monoamines. Monoamine storage mediated by VMAT1 in EC cells is apparently maintained in EC cell tumors. In contrast, many insulinomas appear to lose their ability to accumulate monoamines via VMAT2.
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Mooslehner, Katrin A., Pok Man Chan, Weiming Xu, et al. "Mice with Very Low Expression of the Vesicular Monoamine Transporter 2 Gene Survive into Adulthood: Potential Mouse Model for Parkinsonism." Molecular and Cellular Biology 21, no. 16 (2001): 5321–31. http://dx.doi.org/10.1128/mcb.21.16.5321-5331.2001.
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ABSTRACT We have created a transgenic mouse with a hypomorphic allele of the vesicular monoamine transporter 2 (Vmat2) gene by gene targeting. These mice (KA1) have profound changes in monoamine metabolism and function and survive into adulthood. Specifically, these animals express very low levels of VMAT2, an endogenous protein which sequesters monoamines intracellularly into vesicles, a process that, in addition to being important in normal transmission, may also act to keep intracellular levels of the monoamine neurotransmitters below potentially toxic thresholds. Homozygous mice show large reductions in brain tissue monoamines, motor impairments, enhanced sensitivity to dopamine agonism, and changes in the chemical neuroanatomy of the striatum that are consistent with alterations in the balance of the striatonigral (direct) and striatopallidal (indirect) pathways. The VMAT2-deficient KA1 mice are also more vulnerable to the neurotoxic effects of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine in terms of nigral dopamine cell death. We suggest that the mice may be of value in examining, long term, the insidious damaging consequences of abnormal intracellular handling of monoamines. On the basis of our current findings, the mice are likely to prove of immediate interest to aspects of the symptomatology of parkinsonism. They may also, however, be of use in probing other aspects of monoaminergic function and dysfunction in the brain, the latter making important contributions to the pathogenesis of schizophrenia and addiction.
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Aksoz, Begum E., and Erkan Aksoz. "Vital Role of Monoamine Oxidases and Cholinesterases in Central Nervous System Drug Research: A Sharp Dissection of the Pathophysiology." Combinatorial Chemistry & High Throughput Screening 23, no. 9 (2020): 877–86. http://dx.doi.org/10.2174/1386207323666200220115154.
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Background: Monoamine oxidase and cholinesterase enzymes are very critical enzymes that regulate the level of neurotransmitters such as acetylcholine and monoamines. Monoamine neurotransmitters and acetylcholine play a very important role in many physiological events. An increase or decrease in the amount of these neurotransmitters is observed in a wide range of central nervous system pathologies. Balancing the amount of these neurotransmitters is important in improving the progression of these diseases. Inhibitors of monoamine oxidase and cholinesterase enzymes are important in symptomatic therapy and delaying progression of a group of central nervous system disease manifested with memory loss, cognitive decline and psychiatric disturbances like depression. Objective: In this article, the relationship between central nervous system diseases and the vital role of the enzymes, monoamine oxidase and cholinesterase, is discussed on the pathophysiologic basis, focusing on drug research. Conclusion: Monoamine oxidase and cholinesterase enzymes are still a good target for the development of novel drug active substances with optimized pharmacokinetic and pharmacodynamic properties, which can maximize the benefits of current therapy modalities.
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Boyle, Natalie, Sarah Betts, and Hui Lu. "Monoaminergic Modulation of Learning and Cognitive Function in the Prefrontal Cortex." Brain Sciences 14, no. 9 (2024): 902. http://dx.doi.org/10.3390/brainsci14090902.
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Extensive research has shed light on the cellular and functional underpinnings of higher cognition as influenced by the prefrontal cortex. Neurotransmitters act as key regulatory molecules within the PFC to assist with synchronizing cognitive state and arousal levels. The monoamine family of neurotransmitters, including dopamine, serotonin, and norepinephrine, play multifaceted roles in the cognitive processes behind learning and memory. The present review explores the organization and signaling patterns of monoamines within the PFC, as well as elucidates the numerous roles played by monoamines in learning and higher cognitive function.
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Nilsson, G. E., A. A. Alfaro, and P. L. Lutz. "Changes in turtle brain neurotransmitters and related substances during anoxia." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 259, no. 2 (1990): R376—R384. http://dx.doi.org/10.1152/ajpregu.1990.259.2.r376.
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Freshwater turtles (Pseudemys scripta elegans) were exposed to 0.5-13 h of anoxia at 25 degrees C, whereupon the brain concentrations of 14 amino acid and monoamine neurotransmitters and related substances were measured. Monoamines are of particular interest, because their synthesis and (in part) degradation require molecular oxygen. During anoxia, the level of the inhibitory transmitter gamma-aminobutyric acid (GABA) increased (2.3-fold after 13 h) and the level of the excitatory transmitter Glu fell. Furthermore, anoxia caused increases in the levels of Ala (14 times after 13 h), Tau, Gly, and Ser, whereas the Gln level fell. The increase in Ala is likely to inhibit pyruvate kinase, thereby mediating the decreased rate of glycolysis seen after prolonged anoxia. The increased level of Tau might protect the turtle brain against Ca2(+)-mediated anoxic damage. The monoamine metabolites almost vanished within a few hours of anoxia, indicating a halt in monoamine synthesis and breakdown, and the dopamine level fell. Nevertheless, serotonin, norepinephrine, and epinephrine levels were maintained during 13 h of anoxia, at levels extremely high compared with mammals, suggesting adaptive mechanisms such as stockpiling. It is hypothesized that the pattern of change in levels of amino acids (notably GABA and Glu) and monoamines is of functional significance, because it promotes the decrease in brain activity and energy consumption seen in anoxic turtles.
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Huang, Yu-Hong, Akio Ito, and Ryohachi Arai. "Immunohistochemical Localization of Monoamine Oxidase Type B in Pancreatic Islets of the Rat." Journal of Histochemistry & Cytochemistry 53, no. 9 (2005): 1149–58. http://dx.doi.org/10.1369/jhc.5a6658.2005.
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Monoamine oxidase (MAO) is regarded as a mitochondrial enzyme. This enzyme localizes on the outer membrane of mitochondria. There are two kinds of MAO isozymes, MAO type A (MAOA) and type B (MAOB). Previous studies have shown that MAOB activity is found in the pancreatic islets. This activity in the islets is increased by the fasting-induced decrease of plasma glucose level. Islet B cells contain monoamines in their secretory granules. These monoamines inhibit the secretion of insulin from the B cells. MAOB is active in degrading monoamines. Therefore, MAOB may influence the insulin-secretory process by regulating the stores of monoamines in the B cells. However, it has not been determined whether MAOB is localized on B cells or other cell types of the islets. In the present study, we used both double-labeling immunofluorescence histochemical and electron microscopic immunohistochemical methods to examine the subcellular localization of MAOB in rat pancreatic islets. MAOB was found in the mitochondrial outer membranes of glucagon-secreting cells (A cells), insulin-secreting cells (B cells), and some pancreatic polypeptide (PP)-secreting cells (PP cells), but no MAOB was found in somato-statin-secreting cells (D cells), nor in certain other PP cells. There were two kinds of mitochondria in pancreatic islet B cells: one contains MAOB on their outer membranes, but a substantial proportion of them lack this enzyme. Our findings indicate that pancreatic islet B cells contain MAOB on their mitochondrial outer membranes, and this enzyme may be involved in the regulation of monoamine levels and insulin secretion in the B cells.
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Martin-Iverson, Mathew T., and Bruce A. Lodge. "Effects of chronic treatment of rats with "designer" amphetamines on brain regional monoamines." Canadian Journal of Physiology and Pharmacology 69, no. 12 (1991): 1825–32. http://dx.doi.org/10.1139/y91-270.
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(+)-Amphetamine and two structurally related analogues, 4-methoxyamphetamine and a recent "designer drug," 4-ethoxy-amphetamine, were given to rats via subcutaneous osmotic minipumps for 1–14 days. Regional brain levels of the drugs as well as monoamine neurotransmitters and some of their major acidic metabolites were determined. Amphetamine produced depletions of dopamine in the striatum after at least 3 days of treatment but not in the nucleus accumbens or olfactory tubercle, even after 14 days of treatment. In contrast, the two ring-substituted amphetamine analogues increased levels of the monoamines and decreased levels of their acid metabolites. These data indicate that the two ring-substituted amphetamine analogues, at least one of which is a potent hallucinogen, have potent monoamine oxidase inhibition properties that are sustained during chronic treatment. Furthermore, these two compounds do not share amphetamine's regionally selective neurotoxic effects on dopamine-releasing terminals, even though brain and striatal drug levels are the same or higher than those of amphetamine.Key words: (+)-amphetamine, 4-methoxyamphetamine, 4-ethoxyamphetamine, designer amphetamines, monoamines, rats, chronic treatment.
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Harvey, P. J., X. Li, Y. Li, and D. J. Bennett. "Endogenous Monoamine Receptor Activation Is Essential for Enabling Persistent Sodium Currents and Repetitive Firing in Rat Spinal Motoneurons." Journal of Neurophysiology 96, no. 3 (2006): 1171–86. http://dx.doi.org/10.1152/jn.00341.2006.
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The spinal cord and spinal motoneurons are densely innervated by terminals of serotonin (5-HT) and norepinephrine (NE) neurons arising mostly from the brain stem, but also from intrinsic spinal neurons. Even after long-term spinal transection (chronic spinal), significant amounts (10%) of 5-HT and NE (monoamines) remain caudal to the injury. To determine the role of such endogenous monoamines, we blocked their action with monoamine receptor antagonists and measured changes in the sodium currents and firing in motoneurons. We focused on persistent sodium currents (Na PIC) and sodium spike properties because they are critical for enabling repetitive firing in motoneurons and are facilitated by monoamines. Intracellular recordings were made from motoneurons in the sacrocaudal spinal cord of normal and chronic spinal rats (2 mo postsacral transection) with the whole sacrocaudal cord acutely removed and maintained in vitro (cords from normal rats termed acute spinal). Acute and chronic spinal rats had TTX-sensitive Na PICs that were respectively 0.62 ± 0.76 and 1.60 ± 1.04 nA, with mean onset voltages of −63.0 ± 5.6 and −64.1 ± 5.4 mV, measured with slow voltage ramps. Application of 5-HT2A, 5-HT2C, and α1-NE receptor antagonists (ketanserin, RS 102221, and WB 4101, respectively) significantly reduced the Na PICs, and a combined application of these three monoamine antagonists completely eliminated the Na PIC, in both acute and chronic spinal rats. Likewise, reduction of presynaptic transmitter release (including 5-HT and NE) with long-term application of cadmium also eliminated the Na PIC. Associated with the elimination of the Na PIC in monoamine antagonists, the motoneurons lost their ability to fire during slow current ramps. At this point, the spike evoked by antidromic stimulation was not affected, suggesting that activation of the transient sodium current was not impaired. However, the spike evoked after a slow ramp depolarization was slightly reduced in height and rate-of-rise, suggesting decreased sodium channel availability as a result of increased channel inactivation. These results suggest that endogenous monoamine receptor activation is critical for enabling the Na PIC and decreasing sodium channel inactivation, ultimately enabling steady repetitive firing in both normal and chronic spinal rats.
Dissertations / Theses on the topic "Monoaminy"
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CitÃ, Maria do Carmo de Oliveira. "AlteraÃÃes comportamentais e neuroquÃmicas provocadas por diferentes perÃodos de retirada apÃs tratamento subcrÃnico com cocaÃna em ratos: envolvimento dos sistemas dopaminÃrgico, serotonÃrgico e noradrenÃrgico." Universidade Federal do CearÃ, 2009. http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=3986.
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CoordenaÃÃo de AperfeiÃoamento de Pessoal de NÃvel Superior<br>A cocaÃna à uma droga consumida mundialmente e considerada hoje como um problema de saÃde pÃblica. Uma das principais dificuldades enfrentadas no combate ao vÃcio da cocaÃna, na maioria dos casos, està relacionada aos sintomas de abstinÃncia da droga, como ansiedade, depressÃo, irritabilidade, fadiga e insÃnia, fazendo com que o indivÃduo volte a procurÃ-la. Para avaliar as alteraÃÃes comportamentais (ansiedade e depressÃo) e neuroquÃmicas, os ratos foram submetidos Ãs retiradas de 24 h, 7 d e 21 d apÃs o tratamento subcrÃnico por 7 dias com cocaÃna (20mg/kg), sendo realizados os modelos experimentais de Labirinto de Cruz Elevado (LCE), Campo Aberto (CA) e Nado ForÃado (NF). AlÃm disso, na abstinÃncia de 24h foram testados o propranolol (10mg/kg, i.p.), o ondansetrom (4mg/kg, i.p) e a buspirona (5 mg/kg, i.p.), no LCE e CA, bem como na abstinÃncia de 21 d foram testados a bupropiona (30mg/kg, i.p.) e paroxetina (10 mg/kg, i.p.) no NF, com o intuito de reverter tais alteraÃÃes comportamentais provocadas pela retirada forÃada do tratamento subcrÃnico com cocaÃna. Para o estudo neuroquÃmico (neuroadaptaÃÃo) foi utlizado o corpo estriado (CE) de ratos, avaliando-se os seguintes parÃmetros: nÃveis de monoaminas (NA, DA, 5-HT) e seus metabÃlitos (DOPAC, HVA e 5-HIAA) atravÃs do HPLC com detecÃÃo eletroquÃmica e a atividade da enzima catalase. Na avaliaÃÃo da ansiedade, os resultados mostraram que no LCE houve uma reduÃÃo do NEBA, PEBA, TPBA e PTBA na abstinÃncia de 24h e 7 d, apÃs 21d nÃo houve alteraÃÃo. No CA, as retiradas de 24h e 7 d promoveram um aumento da atividade locomotora do animal, no entanto na retirada de 21 d ocorreu uma diminuiÃÃo da atividade locomotora. Na abstinÃncia de 24h foram administrados propranolol, ondansetrom e buspirona. No LCE, o propranolol aumentou o NEBA e reduziu o PTBA, enquanto que o ondansetrom aumentou o NEBA, PEBA, TPBA e o PTBA em relaÃÃo ao grupo da cocaÃna. Jà a buspirona em relaÃÃo à cocaÃna aumentou o PTBA, TPBA e o PEBA, porÃm o NEBA foi reduzido. Enquanto que no CA, o propranolol, o ondansetrom e a buspirona reduziram a atividade locomotora em relaÃÃo ao grupo da cocaÃna. Para avaliar a atividade antidepressiva foi realizado o teste do nado forÃado, no qual as retiradas de 24h e 7 d reduziram o tempo de imobilidade, contudo na abstinÃncia de 21 d houve um aumento do parÃmetro avaliado. Na abstinÃncia de 21 d foram administrados paroxetina e bupropiona, verificando uma reduÃÃo do tempo de imobilidade em relaÃÃo ao grupo da cocaÃna. Para a realizaÃÃo dos estudos neuroquÃmicos, os animais foram dissecados para retirada do CE. No corpo estriado observou-se um aumento de dopamina (DA) e uma reduÃÃo de seus metabÃlitos (DOPAC e HVA) nas trÃs retiradas. A concentraÃÃo de serotonina aumentou nas trÃs retiradas, entretanto o seu metabÃlito (5HIAA) aumentou somente nas retiradas de 24h e 7d. Jà a noradrenalina reduziu apÃs as trÃs retiradas. Em relaÃÃo aos receptores, no corpo estriado D2 encontrava-se elevado em 24h e 7d, jà 5HT2 apÃs 7d e D1 nÃo foi alterado. Foi tambÃm avaliado no CE a atividade da catalase, enzima antioxidante, que mostrou uma reduÃÃo de sua atividade nas trÃs retiradas. Os resultados sugerem que diferentes perÃodos de retirada apÃs tratamento subcrÃnico com cocaÃna causam efeitos ansiogÃnicos e depressores sobre o SNC e tais efeitos foram revertidos por propranolol, ondansetrom, buspirona, bupropiona e paroxetina. O estudo neuroquÃmico mostrou que a abstinÃncia de cocaÃna sÃo eventos multimediados e que CE tem uma importante participaÃÃo, estando tambÃm a atividade da catalase envolvida neste processo. Estes achados sÃo importantes para a investigaÃÃo de novos tratamentos para a sÃndrome de abstinÃncia de cocaÃna.<br>Cocaine is world used and considered as a public health problem, being the relapse one of the hardly difficulties faced by cocaine users, that in the most cases, is related to abstinence symptoms, like anxiety, depression, irritability, fatigue and sleeplessness. To evaluate the behavioral alterations (anxiety and depression) and neurochemistry, rats were submitted to 24h, 7 d and 21 d withdrawal, after the subcronic treatment, for 7 days with cocaine (20mg/kg), being realized the experimental models of Elevated Plus Maze (EPM), Open Field (OF) and Forced Swimming (FS). Moreover, in the 24h abstinence, propranolol (10mg/kg, i.p.), ondansetrom (4mg/kg, i.p) and buspirone (5 mg/kg, i.p.) had been tested, in the EPM and OF, as wel as in the 21 d of abstinence bupropione (30mg/kg, i.p.) and paroxetine (10 mg/kg, i.p.) had been tested in the FS, aiming to revert the alterations caused by the abstinence of cocaine subcronic administration. For the neurochemistry study (neuroadaptation) was used striatum (ST) of rats, evaluating the following parameters: level of monoamines (NE, DA and 5HT) and its metabolites (DOPAC, HVA and 5HIAA), using the electrochemistry detection HPLC and the activity of the catalase enzyme. In the anxiety evaluation, results showed that in the EPM there was a reduction on NEOA, PEOA, TPOA and PTOA in the abstinence of 24h, 7 d and 21 d. In the OF, the withdrawal of 24 and 7 d promoted an increasing in the locomotor activity of animals, while the withdrawal of 21 d a decreasing in the locomotor activity was observed. In the 24h abstinence were administered propranolol, ondansetrom and buspirone. In the EPM, propranolol increased NEOA and reduced PTOA, while ondansetrom increased NEOA, PEOA, TPOA and PTOA, as compared to cocaine group. In addition buspirone as compared to cocaine group increased PTOA, TPOA, and PEOA, however NEOA was reduced. While in the OF, propranolol, ondansetron and buspirone reduced the locomotor activity as related to cocaine group. To evaluate the antidepressive effect the FS was performed, where the withdrawal of 24h and 7 d reduced the immobility time, although in the 21 d abstinence an increase of this parameter was observed. In the 21 d abstinence had been administered paroxetine and buproprione, verifying a reduction of the immobility time as related to cocaine group. To the performance of neurochemistry studies, animals were dissected to take off the ST. In the ST was observed an increasing of dopamine (DA) and a reduction of its metabolites (DOPAC and HVA) in the three withdrawals. The serotonine levels increased the three withdrawals, however its metabolite (5HIAA) increased only in the 24h and 7 d withdrawals. In addition norepinephrine reduced after the 24h, 7 d and 21 d withdrawal. In relation to the receptors, in the ST D2 24h and 7d met high in, already 5HT2 after 7d and D1 was not alteration. Were evaluated too in the ST the activity of catalase, antioxidant enzyme, that showed a reduction of your activity in the three withdrawal. Results suggests that different times of withdrawal after subcronic treatment with cocaine cause anxyogenic and depressive effects on the CNS and this effects were reverted by the administration of drugs (propranolol, ondansetrom, buspirone, bupropione and paroxetine). The neurochemistry study showed that the abstinence of cocaine were events multimediated and the brain area study ST has an important role, being the catalase activity involved in this process. These findings are important to the investigation of new treatments to the cocaine abstinence syndrome.
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Kaushal, Setu. "Characterization of Three Putative Monoamine Oxidase Genes in Caenorhabditis elegans." Ohio University / OhioLINK, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=ohiou1218747926.
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Aguiar, Lissiana Magna Vasconcelos. "Efeitos comportamentais e neuroquÃmicos da melatonina em ratos submetidos à lesÃo estriatal com 6-ohda." Universidade Federal do CearÃ, 2002. http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=19.
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Conselho Nacional de Desenvolvimento CientÃfico e TecnolÃgico<br>Os efeitos da melatonina (Mel) in vivo foram estudados no sistema dopaminÃrgico nigroestriatal de ratos, utilizando um modelo experimental da doenÃa de Parkinson que consiste na injeÃÃo intraestriatal da neurotoxina 6-hidroxidopamina (6-OHDA). Ratos Wistar, machos (200-250g) foram submetidos a lesÃo unilateral com 6-OHDA, tratados com melatonina nas doses de 2, 5, 10 e 25 mg/kg, i.p. 1 hora apÃs a lesÃo e depois, diariamente durante 7 dias, quatro semanas apÃs a lesÃo, foi realizado o teste rotacional e 24 horas depois os animais foram sacrificados, os seus cÃrebros dissecados e os estriados direito (ipsilateral â lado lesionado) e esquerdo (contralateral â lado nÃo lesionado) utilizados para dosagens de monoaminas em HPLC e ensaios de binding dopaminÃrgico. Para as dosagens de malonildialdeÃdo (MDA), os animais foram sacrificados no oitavo dia apÃs a lesÃo. Os resultados demonstraram que a injeÃÃo intraestriatal de 6-OHDA diminuiu cerca de 77 à 85% os conteÃdos das monoaminas e dos seus metabÃlitos no lado ipsilateral quando comparado com o lado contralateral nos controles. O tratamento com melatonina, nas doses estudadas, reverteu parcialmente as diminuiÃÃes causadas pela lesÃo com 6-OHDA nos nÃveis destes neurotransmissores, e os conteÃdos se aproximaram de 50% daqueles observados nos lados contralaterais dos controles ou dos grupos tratados com melatonina. A Mel foi mais eficiente na dose de 5 mg/kg, i.p., e os efeitos foram similares entre as doses mais baixas e as mais altas, caracterÃstica de um tipo de resposta com a curva em forma de sino. O prÃ-tratamento e o tratamento crÃnico com melatonina na dose que obteve o melhor efeito tambÃm foram estudados, o tratamento crÃnico promoveu uma melhor recuperaÃÃo dos nÃveis de monoaminas enquanto os efeitos do prÃ-tratamento foram similares aos do grupo Mel 5 mg/kg, durante 7dias. O comportamento rotacional induzido pela apomorfina (3 mg/kg) foi bloqueado em cerca de 60, 89, 78 e 47% nos grupos tratados com melatonina nas doses de 2, 5, 10 e 25 mg/kg, i.p., respectivamente. O tratamento crÃnico bloqueou o comportamento rotacional em cerca de 96% e o prÃ-tratamento 86%. A melatonina (5 mg/kg) produziu uma upregulation dos receptores D1 (Bmax: 277,8+/-25,8) associada com uma diminuiÃÃo nos valores do Kd (1,5+/-0,1) quando comparado ao controle (Bmax:194,8+/-19,0; Kd:2,9+/-0,38). Um efeito similar foi observado com o tratamento com NAS (Bmax: 245,3+/-27,6; Kd: 1,1+/-0,28), precursor da melatonina. Foi verificado um aumento nos nÃveis de MDA, nos controles (127%), quando comparado com o grupo falso operado (104%), o tratamento com melatonina (106%) recuperou esses nÃveis à valores prÃximos do normal, sugerindo uma aÃÃo antioxidante da melatonina in vivo. Os resultados apresentados podem indicar uma aÃÃo neuroprotetora da melatonina e sugerem um possÃvel papel no tratamento de doenÃas neurodegenerativas causadas pelo estresse oxidativo, como a doenÃa de Parkinson.<br>The present work studied the neuroprotective effects of melatonin In vivo on the nigrostriatal dopaminergic system in rats after a unilateral 6-hydroxydopamine (6-OHDA) lesions in rat striatum. Results showed that the intrastriatal injection of 6-OHDA significantly decreases DA, DOPAC and HVA levels. Although there is also a decrease in 5-HT levels no changes were observed in 5-HIAA levels as compared to controls. On the other hand, melatonin (2, 5, 10 and 25 mg/kg, i.p., daily for 7 days) treatment starting 1 h after 6-OHDA lesions, partially reverses the decreases caused by 6-OHDA lesions on these neurotransmitter levels, and contents were brought to approximately 50% of that observed in the contralateral sides of controls or the melatonin treated group. Melatonin was more efficient at the doses of 5 and 10 mg/kg, i.p., and effects were similar between the lowest and highest doses characteristic of a bell-shaped type of response. Pretreatment and cronic treatment with melatonin at the 5mg/kg dose were also tested, cronic treatment promoted a recovey of monoamines levels more efficiently while the pretreatment effects were similar to the melatonin treatment at the dose of the 5mg/kg for 7 days. The apomorphine-induced rotational behavior (3 mg/kg, i.p.) was blocked by 60, 89, 78 and 47% after the doses of 2, 5, 10 and 25 mg/kg, i.p., respectively. Similarly, in this case the doses of 5 and 10 mg/kg were also more efficient. The cronic treatment blocked the rotational behavior by 86%. Melatonin (5mg/kg) produced an upregulation of D1 receptors associated with a decrease in Kd value. While no change was observed in maximum density of D2 receptors, the Kd value was also decreased, a similar effect was observed with its precursor N-acetylserotonin. Compared with sham-operated and expressed as a ratio relative to the contralateral side, there was an increase in the lipid peroxidation product malondialdehyde (MDA, 127%) on controls which was restored to normal levels on the melatonin treated group, suggesting the in vivo action of melatonin as an antioxidant. The present results may indicate a neuroprotective action of melatonin and suggest a possible role in the treatment of oxidative stress-induced neurodegenerative disease such as Parkinsonâs disease.
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Figueira, Fernanda Hernandes. "EFEITO DO DISSELENETO DE DIFENILA SOBRE ALTERAÇÕES COMPORTAMENTAIS E BIOQUÍMICAS INDUZIDAS POR ANFETAMINA EM CAMUNDONGOS." Universidade Federal de Santa Maria, 2012. http://repositorio.ufsm.br/handle/1/11225.
Full textAbstract:
Selenium is an element that can modulate the dopaminergic neurotransmission.
Studies show that diphenyl diselenide, an organic compound of selenium, has
antioxidant activity improves depressive-like behavior and reduce the activity of the
enzyme monoamine oxidase (MAO). However, there are few studies concerning
about possible alterations of diphenyl diselenide in dopaminergic system. Thus, the
purpose of the present study was to evaluate the effects of acute and sub-chronic
treatment of diphenyl diselenide on amphetamine-induced behavioral and
biochemical alterations in mice. In the acute treatment, the mice were treated with
diphenyl diselenide (5 and 10 mg/kg, s.c.) or vehicle (10% Tween 80, s.c.) 30 min
before administration of amphetamine (1.25 mg/kg, i.p.). After 25 min, locomotor
activity was assessed with an open field and, also, the time of stereotypy and
immobility was assessed in a glass cage. Sub-chronic treatment was conducted with
seven administrations of diphenyl diselenide (5 and 10 mg/kg, s.c.), or its vehicle
being one administration per day. On the eighth day, amphetamine (1.25 mg/kg, i.p.)
was administered and the behavioral tests were conducted after 25 min. In both
treatments ex vivo tests were performed: isoform activity MAO-A and MAO-B, and
measurement of total protein and non-protein thiol levels, oxidation of
diclorofluorescein. Amphetamine increased the number of crossing and rearing in the
open field test and diphenyl diselenide prevented only the increase in the number of
crossings when acutely administered to mice. Furthermore, amphetamine increased the time of immobility and stereotypy in mice. Diphenyl diselenide did not prevent
these effects. By contrary, at 10 mg/kg, sub-chronic administration of diphenyl
diselenide increased per se the time of immobility and stereotypy. It was also found
a positive correlation between immobility and stereotypy in acute and sub-chronic
treatment with diphenyl diselenide. It was also detected a decrease in brain MAO-B
activity caused by sub-chronic treatment with diphenyl diselenide either alone or in
combination of amphetamine. Any change was detected in oxidative stress
parameters. In conclusion, sub-chronic administration of diphenyl diselenide can
promote a behavioral sensitization that seems to be, at least in part, dependent of
MAO-B inhibition.<br>O selênio é um elemento químico capaz importante para o funcionamento
celular, envolvido também na modulação do sistema dopaminérgico. Estudos
mostram que o disseleneto de difenila, um composto orgânico de selênio, possui
atividade antioxidante, melhora o comportamento tipo-depressivo relacionado à
inibição da atividade da enzima monoamino oxidase (MAO). No entanto, existem
poucos estudos acerca dos efeitos do disseleneto de difenila sobre o sistema
dopaminérgico. Desta forma, o objetivo do presente estudo foi avaliar os efeitos do
tratamento agudo e sub-crônico do disseleneto de difenila sobre as alterações
bioquímicas e comportamentais induzidas por anfetamina em camundongos. No
tratamento agudo, os camundongos foram tratados com disseleneto de difenila (5 e
10 mg/kg, s.c.) ou veículo (10% de tween 80, s.c.) 30 minutos antes da
administração de anfetamina (1,25 mg/kg, i.p.). Após 25 minutos, foram avaliados a
atividade locomotora através do teste de campo aberto, além do tempo de
estereotipia e imobilidade, avaliado em caixa espelhada. O tratamento subcrônico foi
realizado com sete administrações de disseleneto de difenila ou veículo (5 e 10
mg/kg, s.c.) sendo uma administração por dia. No oitavo dia foi administrada a
anfetamina (1,25 mg/kg, i.p.) e realizados os testes comportamentais 25 minutos
após. Em ambos os tratamentos os testes ex-vivo realizados foram: atividade das
isoformas MAO-A e MAO-B, níveis de tióis totais e não-protéico, oxidação da diclorofluoresceína. O tratamento com anfetamina aumentou o número de
cruzamentos e de levantadas no teste do campo aberto e o disseleneto de difenila
preveniu somente o número de cruzamentos quando administrado agudamente aos
camundongos. Além disso, o tratamento com anfetamina aumentou o tempo de
imobilidade e estereotipia em camundongos. O disseleneto de difenila não preveniu
estes efeitos. Pelo contrário, na dose de 10 mg/kg, a administração subcrônica de
disseleneto de difenila aumentou per se o tempo de imobilidade e de estereotipia.
Uma correlação positiva entre o tempo de estereotipia e de imobilidade foi também
encontrada tanto para o tratamento agudo como subcrônico com disseleneto de
difenila. Também foi detectada uma diminuição na atividade cerebral da MAO-B
causada pelo tratamento subcrônico com disseleneto de difenila tanto per se quanto
em combinação com a anfetamina. Não foram encontradas alterações em
parâmetros de estresse oxidativo. Em conclusão, o tratamento subcrônico com
disseleneto de difenila pode promover uma sensibilização comportamental que
parece ser, pelo menos em parte, dependente da inibição da MAO-B.
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Mullan, Elaine L. "Inhibitors of monoamine oxidase." Thesis, Queen's University Belfast, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.337116.
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VenÃncio, Edith Teles. "Estudo dos efeitos comportamentais e neuroquÃmicos do extrato padronizado de Justicia pectoralis (chambÃ) em camundongos." Universidade Federal do CearÃ, 2009. http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=3935.
Full textAbstract:
CoordenaÃÃo de AperfeiÃoamento de Pessoal de NÃvel Superior<br>O extrato padronizado de chambÃ, preparado a partir das partes aÃreas da Justicia pectoralis Jacq. var stenophylla Leonard, foi avaliado em modelos animais clÃssicos para screening de drogas com atividade em ansiedade, depressÃo, sedaÃÃo e convulsÃo, tais como, labirinto em cruz elevado (LCE), claro/escuro, campo aberto, rota rod, nado forÃado, suspensÃo da cauda, tempo de sono induzido por pentobarbital e convulsÃo induzida por pentilenotetrazol, e em estudo neuroquÃmico, atravÃs da concentraÃÃo de monoaminas e seus metabÃlitos, tais como dopamina (DA), Ãcido diidrofenil acÃtico (DOPAC), Ãcido homovalÃnico (HVA), noradrenalina (NE), 5-hidroxitriptamina (5-HT) e Ãcido 5-hidroxindolacÃtico (5-HIAA). O chambà foi administrado de forma aguda em todos os testes, nas doses de 50, 100 e 200 mg/kg, atravÃs da via oral (v.o.) Os resultados mostraram que o extrato apresentou efeito ansiolÃtico nos modelos LCE e claro/escuro, pois aumentou todos os parÃmetros analisados no LCE, como NEBA, PEBA, TPBA e PTBA, assim como o tempo de permanÃncia no box claro no claro/escuro. Este efeito està possivelmente relacionado com o sistema gabaÃrgico jà que o flumazenil, antagonista dos receptores GABAA/BenzodiazepÃnico, reverteu o efeito ansiolÃtico do chambà no LCE. No teste do campo aberto, nÃo foi observado nenhuma alteraÃÃo na atividade locomotora, bem como no nÃmero de grooming e rearing. O chambà apresentou efeito depressor do Sistema Nervoso Central (SNC), pois nos testes nado forÃado e suspensÃo da cauda, aumentou o tempo de imobilidade dos animais. A avaliaÃÃo sedativa/hipnÃtica do chambÃ, no teste do tempo de sono induzido por pentobarbital, mostrou que nÃo houve alteraÃÃo na duraÃÃo do sono dos animais, descartando efeito sedativo. No teste da convulsÃo induzida por pentilenotetrazol, o chambà nÃo alterou a latÃncia de convulsÃo, bem como a latÃncia de morte. Esse resultado sugeriu que o chambà nÃo possui efeito anticonvulsivante. A avaliaÃÃo neuroquÃmica comprovou o efeito depressor do extrato, pois foi verificada uma reduÃÃo da concentraÃÃo das monoaminas. Em conclusÃo, esses efeitos mostraram que o chambà apresenta efeito ansiolÃtico, provavelmente relacionado com o sistema gabaÃrgico e efeito depressor, desprovido de atividade anticonvulsivante e sedativa.<br>The standardized extract of chamba, prepared from the aerial parts of Justicia pectoralis Jacq. var stenophylla Leonard, was evaluated in classical animal models to the screening of drugs with activity in axiety, depression, sedation and convulsion, such as elevated plus maze (EPM), light/dark, open field, rota rod, forced swimming, tail suspension, pentobarbital-induced sleep time and pentilenotetrazole-induced seizures and a neurochemistry study, through the level of monoamines and its metabolites, such as dopamine (DA), 3,4-dihydroxyphenyl acetic acid (DOPAC), homovanilic acid (HVA), norepinephrine (NE), 5-hydroxytryptamine (5HT) and 5-hydroxyindoleacetic acis (5HIAA). Chambà was administered acutely in all tests, in the doses of 50, 100 and 200 mg/kg, through the oral via (p.o.). Results showed that the extract presented an anxiolytic effect in the models of EPM and light/dark, since increased all the parameters analyzed in the EPM, such as NEOA, PEOA, TPOA, PTOA, as well as the permanence time in the light compartment. This effect is probably related with the GABAergic system since Flumazenil, an antagonist of GABAA/benzodiazepinic, reversed the anxiolytic effect of chamba in the EPM. In the open field, it was not observed any alteration in the locomotor activity, as well as the number of grooming and rearing. Chamba presented depressor effect of Central Nervous System (CNS), since in the forced swimming and tail suspension, increased the immobility time of animals. The sedative/hypnotic evaluation of chamba, in pentobarbital-induced sleep time showed that it has no alteration in the duration of sleep of animals, discarding sedative effect. In the pentilenotetrazole-induced seizures, chamba did not change the convulsion latency, as well the death latency. This result suggests that chamba did not have anticonvulsivant effect. The neurochemistry evaluation comproved the depressor effect of the extract, since it was verified a reduction in the level of monoamine levels, involved in the depression. In conclusion, these effects showed that chamba presented anxiolytic effect, probably related with the GABAergic system and depressor effect disproved anticonvulsant and sedative effects.
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Moura, Brinell Arcanjo. "AlteraÃÃes comportamentais, neuroquÃmicas e glicolipÃdicas em ratos tratados com Hoodia gordonii, um supressor natural do apetite." Universidade Federal do CearÃ, 2012. http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=8886.
Full textAbstract:
Conselho Nacional de Desenvolvimento CientÃfico e TecnolÃgico<br>Hoodia gordonii à uma planta da famÃlia das apocinÃceas. OriginÃria do sudeste da Ãfrica, onde tem sido historicamente usada para suprimir o apetite durante longas jornadas de caÃa, sendo utilizada em diversos paÃses com o objetivo de emagrecer. No Brasil foi retirada do mercado devido à falta de estudos que comprovem sua eficÃcia e seguranÃa para o uso. O objetivo deste trabalho foi avaliar as alteraÃÃes comportamentais, neuroquÃmicas e glicolipÃdicas em ratos tratados com Hoodia gordonii. Para a realizaÃÃo deste estudo H. gordonii foi administrada por via oral nas doses de 25 e 50 mg/Kg durante oito dias consecutivos em ratos Wistar machos (160-200g), D-anfetamina 2 mg/Kg foi administrada intraperitonealmente de forma aguda e usada como padrÃo positivo. Os testes aconteceram 60 minutos apÃs o ultimo dia de tratamento com a Hoodia e 30 minutos apÃs o tratamento com D-anfetamina. Foram avaliados a variaÃÃo de peso dos animais durante o tratamento, bem como o consumo de Ãgua e comida. Para os testes comportamentais foram feitos os testes de labirinto em cruz elevado, campo aberto e placa perfurada. Para os estudos neuroquÃmicos foi feito HPLC com detecÃÃo eletroquÃmica. Para os testes glicolipÃdicos foi feita dosagem de Glicose, HDL, LDL, TG, colesterol total, ALT e AST. Os resultados mostraram que H. gordonii à capaz de reduzir o ganho de massa corpÃrea, bem como reduzir o consumo de comida e Ãgua. Os resultados dos testes comportamentais mostraram que ela à capaz de reduzir os parÃmetros observados no teste do labirinto em cruz e placa perfurada sem mostrar alteraÃÃo significante no campo aberto. Os resultados dos experimentos neuroquÃmicos evidenciaram um aumento do conteÃdo de noradrenalina e dopamina em corpo estriado de ratos, detectados eletroquimicamente pelo HPLC. Nos testes bioquÃmicos foi visto que ela tem a capacidade de reduzir os nÃveis de glicose, bem como a concentraÃÃo de triglicerÃdeos e colesterol total em soro de ratos, sem mostrar alteraÃÃo significante da ALT e AST. Foi possÃvel concluir que H. gordonii à capaz de reduzir a ingestÃo de alimentos e que este efeito pode estar de alguma forma ligado à neurotransmissÃo noradrenÃrgica e dopaminÃrgica, possuindo tambÃm atividade ansiogÃnica evidenciada pelos estudos comportamentais.<br>Hoodia gordonii is a plant of the family apocinaceae. Originally from southeastern Africa, where it has historically been used to suppress appetite during long hunting trips, being used in several countries in order to lose weight. In Brazil was withdrawn from the market due to lack of studies proving its efficacy and safety for use. The aim of this study was to evaluate the behavioral changes and neurochemical glicolipÃdicas in rats treated with Hoodia gordonii. For this study H. gordonii was administered orally at doses of 25 and 50 mg/kg for eight consecutive days in male Wistar rats (160-200g), D-amphetamine 2 mg/kg was intraperitoneally administered acutely and used as a positive standard. The tests took place 60 minutes after the last day of treatment with the Hoodia and 30 minutes after treatment with D-amphetamine. We evaluated the weight change of the animals during treatment, as well as the consumption of water and food. For behavioral tests were performed tests elevated plus-maze, open field and hole board. For neurochemical studies was done HPLC with electrochemical detection. For testing was done glycolipid glucose, HDL, LDL and TG, total cholesterol, ALT and AST. The results showed that H. gordonii is capable of reducing body mass gain and reduce the consumption of food and water. The results of behavioral tests showed that it is able to reduce the parameters observed in the plus-maze test and hole board showing no significant change in the open field. The results of experiments showed an increase in the neurochemical content of noradrenaline and dopamine in the striatum of rats electrochemically detected by HPLC. In biochemical tests it was seen that it has the ability to lower blood glucose levels as well as the concentration of triglycerides and total cholesterol in serum from mice, showing no significant change in ALT and AST. It was concluded that H. gordonii is able to reduce food intake, and this effect may be somehow linked to the dopaminergic and noradrenergic neurotransmission, having also anxiogenic activity evidenced by behavioral studies.
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Linhares, Maria Isabel. "Estudo da Ritalina (Cloridrato de Metilfenidato) sobre o sistema nervoso central de animais jovens e adultos: aspectos comportamentais e neuroquÃmicos." Universidade Federal do CearÃ, 2012. http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=9347.
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CoordenaÃÃo de AperfeiÃoamento de Pessoal de NÃvel Superior<br>O Transtorno de DÃficit de AtenÃÃo/ Hiperatividade (TDAH) Ã um transtorno prevalente e debilitante, diagnosticado com base em persistentes nÃveis de hiperatividade, desatenÃÃo e impulsividade. FÃrmacos estimulantes tÃm sido eficazes no tratamento desse transtorno, sendo que o metilfenidato (MFD) Ã o agente terapÃutico mais prescrito e seu uso aumentou significativamente nos Ãltimos anos, entretanto, as conseqÃÃncias da sua utilizaÃÃo ainda sÃo pouco conhecidas. O MFD foi avaliado em modelos animais clÃssicos para screening de drogas com atividade em ansiedade, depressÃo e convulsÃo, tais como, labirinto em cruz elevado (LCE), campo aberto, rota rod, nado forÃado e convulsÃo induzida por pilocarpina, e em estudo neuroquÃmico, atravÃs da concentraÃÃo de monoaminas, tais como dopamina (DA), noradrenalina (NE) e 5-hidroxitriptamina (5-HT), alÃm da atividade da enzima Acetilcolinesterase (AChE). O MFD foi administrado de forma aguda em todos os testes, nas doses de 2,5; 5; 10 e 20 mg/Kg, atravÃs da via oral (v.o.) em camundongos jovens (21 dias) e adultos. Os resultados mostraram que o MFD apresentou efeito ansiolÃtico nos modelos LCE, pois aumentou todos os parÃmetros analisados no LCE, como NEBA, PEBA, TPBA e PTBA nas doses de 10 e 20mg/Kg nos animais jovens e apenas na de 20mg/Kg nos animais adultos. No teste do campo aberto, foi observado aumento na atividade locomotora em todas as doses nos animais jovens e apenas nas doses maiores (10 e 20mg/Kg) nos animais adultos. NÃo alterou o nÃmero de grooming e rearing. O MFD apresentou efeito antidepressivo no Sistema Nervoso Central (SNC), pois no teste do nado forÃado diminuiu o tempo de imobilidade nas doses de 10 e 20 mg/Kg nos animais jovens e apenas na dose de 20mg/Kg nos animais adultos. A avaliaÃÃo neuroquÃmica comprovou o efeito antidepressivo do MFD, pois se verificou um aumento da concentraÃÃo das monoaminas. No teste da convulsÃo induzida por pilocarpina, o metilfenidato diminuiu a latÃncia de convulsÃo, bem como a latÃncia de morte nos animais jovens e adultos, sugerindo que o MFD apresenta atividade proconvulsivante. O estudo sobre os efeitos sobre o sistema de neurotransmissÃo colinÃrgica demonstrou que o prÃ-tratamento com MFD reduziu a atividade da AChE apenas no corpo estriado. Em conclusÃo, esses efeitos mostraram que o MFD apresenta efeito ansiolÃtico, efeito antidepressivo e atividade proconvulsivante.<br>Attention-deficit hyperactivity disorder (ADHD) is a prevalent and debilitating disorder diagnosed on the basis in persistent levels of overactivity, inattention and impulsivity. Stimulant drugs have been effective in treating this disorder, and methylphenidate (MPH) is the most widely prescribed therapeutic agent and its use has increased significantly in recent years, however, the consequences of its use are still poorly known. The MFD was assessed in classical animal models to the screening of drugs with activity in anxiety, depression and convulsion, such as elevated plus maze (EPM), open field, rota rod, forced swimming and pilocarpine-induced seizures and a neurochemistry study, through the level of monoamines, such as dopamine (DA), norepinephrine (NE) and 5-hidroxytriptamine (5-HT) but the activity of the enzyme acetylcholinesterase (AChE). The MPH was administered acutely in all tests at doses of 2,5; 5; 10 e 20 mg/Kg, through the oral via (p.o.) in young mice (21 days) and adults. Results showed that the MPH presented an anxyolitic effects in the models of EPM, since increased all the parameters analyzed in the EPM, such as NEOA, PEOA, TPOA, PTOA, at doses of 10 and 20 mg/Kg in young animals, and only in animals of 20 mg/Kg in adults. In the open field, we observed an increase in locomotor activity at all doses in young animals and only at higher doses (10 e 20 mg/Kg) in adult animals. Not was observed no alteration the number of rearing and grooming. MPH presented antidepressant effect of Central Nervous System (CNS), since in the forced swimming, decreases the time of immobility in doses of 10 and 20 mg/Kg in young animals and only at a dose of 20 mg/Kg in adult animals. The neurochemistry evaluation comproved the antidepressant effect do MPH, because there was an increased concentration of monoamines. The test of the seizure by pilocarpine, MPH did decrease the latency of convulsion and latency of death in young and adult animals, suggesting that the MPH has proconvulsivante activity. The study of the effects of the cholinergic neurotransmission system has show that pretreatment with MPH reduced AChE activity only in the striatum. In conclusion, these effects showed that MPH presented anxiolitic effect, antidepressant effect and proconvulsivante activity.
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Meschin, Pierre. "Régulations monoaminergiques AMPc-dépendantes du coeur sain et pathologique." Thesis, Montpellier 1, 2014. http://www.theses.fr/2014MON1T010.
Full textAbstract:
La fonction cardiaque est finement régulée par des hormones de type monoamines qui constituent des régulateurs cruciaux de l’activité cardiaque (chronotropie et inotropie). Ces hormones dérivées d’acides aminés aromatiques comprenant les catécholamines et la sérotonine maintiennent l’activité du myocarde dans un cadre physiologique tout en lui permettant de s’adapter aux contraintes environnementales. Les récepteurs cellulaires des monoamines sont couplés à des voies de signalisation qui impliquent un nucléotide cyclique, l’AMPc, et modulent la contractilité des cardiomyocytes par l’intermédiaire de multiples phosphorylations des protéines régulatrices du cycle du calcium (canal calcique de type L, RyR2 ou phospholamban) par la protéine kinase A AMPc-dépendante. Lorsque les monoamines voient leurs activités dérégulées en contextes pathologiques tels que l’insuffisance cardiaque (IC) ou un lors d'un traitement antidépresseur, elles conduisent à une hyperstimulation de leurs récepteurs spécifiques. Cette dernière altère alors les voies impliquant l’AMPc et les flux calciques engendrant des évènements ectopiques proarythmogéniques nommés post-dépolarisations. Ces dysfonctions de la contractilité cellulaire et de l'homéostasie calcique peuvent être à l’origine d’arythmies tissulaires et de morts subites cardiaques. Les altérations de l’homéostasie calcique subsistent en dépit des approches thérapeutiques actuelles (!-bloquants, inhibiteurs de l’enzyme de conversion de l’angiotensine) qui vise à freiner le remodelage myocardique post-ischémique et constituent donc une cible active de la recherche cardiovasculaire. Les Rycals, stabilisateurs pharmacologiques du RyR2, représentent une nouvelle approche visant à remédier à ces altérations. Au sein de ces travaux de recherche, nous avons axé nos études sur les deux voies monoaminergiques AMPc cardiaques majeures, les voies adrénergiques et sérotoninergiques. Un premier axe d’étude a consisté en l’évaluation des bénéfices potentiels d’un nouveau Rycal, le S44121, sur la survenue d’arythmies cellulaires et tissulaires en comparaison d’un !-bloquant de référence, le métoprolol, dans un contexte d’IC post-infarctus chez le rat. L’étude n’a cependant pas mise en évidence de bénéfices du S44121 mais a confirmé la cardioprotection exercée par le métoprolol. Un deuxième axe d’étude a évalué l’implication potentielle au niveau cardiaque de la protéine S100A10 dans la modulation de la voie du récepteur à la sérotonine de type 4 (5-HT4R) en conditions physiologiques ou en contexte d’IC. Cette étude originale a mis en avant pour la première fois dans le coeur sain un rôle de la S100A10 dans l’apparition d’une voie 5-HT4R proarythmogène lorsque son expression est induite par une neurotrophine (Brain-derived neurotrophic factor) ou un antidépresseur (imipramine). En revanche, le rôle de la S100A10 dans la modulation de la voie 5-HT4R en contexte d’IC n’a pas été déterminé de façon certaine<br>Cardiac function is tightly regulated by hormones such as monoamines which are substantial modulators of cardiac activity (chronotropy and inotropy). These hormones, derived from aromatic amino acids, maintain myocardial activity in a physiological range and allow the cardiac adaptation to environmental conditions. The cellular receptors to monoamines are coupled to signaling pathways involving a cyclic nucleotide, cAMP, and modulate cardiac activity by phosphorylating several key proteins of calcium handling (L-type calcium channel, RyR2 or phospholamban) by the cAMP-dependent protein kinase A. Deregulation of monoamines in pathological conditions such as heart failure (HF) or during antidepressanttreatment leads to a hyperstimulation of their specific receptors. It therefore induces alterations of the cAMP signaling pathway and calcium handling leading to the occurrence of proarrhythmogenic ectopic cellular events known as afterdepolarizations. These dysfunctions in cellular contractility and calcium handling may cause tissue arrhythmias andeven sudden cardiac death. Calcium handling alterations leading to cardiac arrhythmias remain a clinically relevant issue despite the current therapeutical approaches (!-blockers, angiotensin-converting-enzyme inhibitors) which slow the post-ischemic myocardial remodeling and thus represent an active target in the cardiovascular research field. Rycals, RyR2 pharmacological stabilisers, are a new approach to prevent these alterations. In this work, we focused on the two major monoaminergic cAMP-dependent pathways in the heart, the adrenergic and serotoninergic pathways. In the first part of this work, we aimed to evaluate the potential benefits of a new Rycal, S44121, on cellular and tissue arrhythmias occurrence in post-myocardial infarction rat model. These effects were compared to those of the well-known !-blocker, metoprolol. This study failed to show any strong benefit of S44121 but confirmed the cardioprotection associated with the metoprolol use. In a second part of the work presented here, we aimed to evaluate the potential involvement of the S100A10 protein in the modulation of the cardiac serotonin receptor 4 pathway (5-HT4R) in physiological conditions or during HF. This original study unraveled for the first time a new role for S100A10 in the healthy heart by revealing a functional 5-HT4R pathway when S100A10 expression is induced by neurotrophins such as brain-derived neurotrophic factor or by antidepressant drugs such as imipramine. However, we failed to conclude on a direct evidence for a role of S100A10 in the modulation of the 5-HT4R pathway in the failingheart
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Vacher, Claire-Marie. "Régulation par les monoamines de l'expression de la vasopressine dans l'hypothalamus neuroendocrine : étude cytophysiologique chez la souris Tg8, knock-out pour la monoamine oxydase A (MAO-A)." Paris 6, 2002. http://www.theses.fr/2002PA066359.
Full textBooks on the topic "Monoaminy"
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Sergienko, N. G. Biogennye monoaminy i vozbudimostʹ golovnogo mozga. Nauk. dumka, 1992.
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Binda, Claudia, ed. Monoamine Oxidase. Springer US, 2023. http://dx.doi.org/10.1007/978-1-0716-2643-6.
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Oreland, Lars, and Brian A. Callingham, eds. Monoamine Oxidase Enzymes. Springer Vienna, 1987. http://dx.doi.org/10.1007/978-3-7091-8901-6.
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National Institutes of Health (U.S.), ed. Low monoamine (LMA) diet. U.S. Dept. of Health and Human Services, Public Health Service, National Institutes of Health, 1989.
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1939-, Oreland L., Callingham B. A, and Workshop on Amine Oxidases (2nd : 1986 : Biomedical Center, Uppsala University), eds. Monoamine oxidase enzymes: Review and overview. Springer-Verlag, 1987.
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Szelenyi, I., ed. Inhibitors of Monoamine Oxidase B. Birkhäuser Basel, 1993. http://dx.doi.org/10.1007/978-3-0348-6348-3.
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F, Tipton Keith, ed. Amine oxidases: Function and dysfunction : proceedings of the 5th International Amine Oxidase Workshop, Galway, Ireland, August 22-25, 1992. Springer-Verlag, 1994.
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1938-, Lieberman A. N., ed. Monoamine oxidase inhibitors in neurological diseases. M. Dekker, 1994.
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Ebrahimi, Soltan Ahmed. Characterisation of guinea pig liver monoamine oxidase. University of Portsmouth, School of Pharmacy and Biomedical Science, 1995.
Find full textBook chapters on the topic "Monoaminy"
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Salman, Baris Can, and Mehmet Gunes. "Depression: Definition, Epidemiology, Etiology, Symptoms, Diagnosis, Classification and Prognosis." In Depression Treatment Updates. Nobel Tip Kitabevleri, 2024. http://dx.doi.org/10.69860/nobel.9786053359456.1.
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This section contains information about the definition, epidemiology, etiology, symptoms, diagnosis, classification, and prognosis of depression. Depression is a psychiatric condition characterized by depressed or anhedonic mood for at least two weeks, as well as symptoms and loss of functionality in many areas. The concepts of "melancholia" and "black bile", which also include the symptoms of depression, were formed during the Hippocratic period and were shaped throughout the historical process. With the formation of the DSM and ICD diagnostic systems in the twentieth century, the diagnostic criteria and classification of depression took their final form. According to the current data from the World Health Organization, the 1-year prevalence of unipolar depression is 6.6%, and the lifetime prevalence of depression is 16.2%. Genetic factors such as polymorphism in MAO-A and BDNF genes, inadequate functioning of monoamines, monoamine receptor up-regulation, endocrine system irregularities such as HPA anomaly, psychosocial factors such as loss of parents in early childhood, self-perception and hopeless schemas about the future are involved in the etiology of depression.
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Morgan, Michael M., MacDonald J. Christie, Thomas Steckler, et al. "Monoamine Depletion." In Encyclopedia of Psychopharmacology. Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-68706-1_3405.
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Morgan, Michael M., MacDonald J. Christie, Thomas Steckler, et al. "Monoamine Hypotheses." In Encyclopedia of Psychopharmacology. Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-68706-1_3406.
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Rey, Jose A. "Monoamine Oxidase." In Encyclopedia of Clinical Neuropsychology. Springer New York, 2011. http://dx.doi.org/10.1007/978-0-387-79948-3_1742.
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Rey, Jose A. "Monoamine Oxidase." In Encyclopedia of Clinical Neuropsychology. Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-56782-2_1742-2.
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Edmondson, Dale E., and Claudia Binda. "Monoamine Oxidases." In Subcellular Biochemistry. Springer Singapore, 2018. http://dx.doi.org/10.1007/978-981-10-7757-9_5.
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Rey, Jose A. "Monoamine Oxidase." In Encyclopedia of Clinical Neuropsychology. Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-57111-9_1742.
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Gainetdinov, Raul R., and Marc G. Caron. "Monoamine Transporters." In Neurotransmitter Transporters. Humana Press, 2002. https://doi.org/10.1007/978-1-59259-158-9_5.
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Singer, T. P. "Perspectives in MAO: past, present, and future." In Monoamine Oxidase Enzymes. Springer Vienna, 1987. http://dx.doi.org/10.1007/978-3-7091-8901-6_1.
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Tipton, K. F., Anne-Marie O’Carroll, and J. M. McCrodden. "The catalytic behaviour of monoamine oxidase." In Monoamine Oxidase Enzymes. Springer Vienna, 1987. http://dx.doi.org/10.1007/978-3-7091-8901-6_2.
Full textConference papers on the topic "Monoaminy"
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Verlinden, Heleen. "Monoamine receptors and swarming behaviour in locusts." In 2016 International Congress of Entomology. Entomological Society of America, 2016. http://dx.doi.org/10.1603/ice.2016.95192.
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Serra, Silvia, Eugenio Uriarte, Lourdes Santana, Giovanna Delogu, and Maria Matos. "Synthesis of New Possible Monoamine Oxidase Inhibitors." In The 14th International Electronic Conference on Synthetic Organic Chemistry. MDPI, 2010. http://dx.doi.org/10.3390/ecsoc-14-00378.
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Serra, Silvia, Eugenio Uriarte, Lourdes Santana, Giovanna Delogu, and Maria Matos. "Synthesis of new possible monoamine oxidase inhibitors." In The 14th International Electronic Conference on Synthetic Organic Chemistry. MDPI, 2010. http://dx.doi.org/10.3390/ecsoc-14-00474.
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Ma, Peixiang, Shanshan Wang, Feng Qu, and Yulin Deng. "Determination of Monoamine Oxidase Activity by Capillary Electrophoresis Method." In 2007 IEEE/ICME International Conference on Complex Medical Engineering. IEEE, 2007. http://dx.doi.org/10.1109/iccme.2007.4382056.
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"Monoamine signaling gene networks unraveled in mouse social stress model." In Bioinformatics of Genome Regulation and Structure/ Systems Biology. institute of cytology and genetics siberian branch of the russian academy of science, Novosibirsk State University, 2020. http://dx.doi.org/10.18699/bgrs/sb-2020-172.
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Yurttas, Leyla, Asaf Evren, Demokrat Nuha, Sam Dawbaa, and Begüm Sağlık. "New thiazolylhydrazone derivatives as potent monoamine oxidase and aromatase inhibitors." In 7th International Electronic Conference on Medicinal Chemistry. MDPI, 2021. http://dx.doi.org/10.3390/ecmc2021-11582.
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Bayer, A., E. Zrenner, H. J. Thiel, S. Ried, and D. Schmidt. "Early detection of anticonvulsant drug toxicity by colour vision tests." In Noninvasive Assessment of the Visual System. Optica Publishing Group, 1991. http://dx.doi.org/10.1364/navs.1991.md10.
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Phenytoin and Carbamazepine, especially in combination or after repeated exposure to toxic blood concentrations, can produce neurological and mental syndroms. Possible mechanisms of impaired neurological and mental function include neuronal damage, or disturbance of folic acid, monoamine or hormonal metabolism. Phenytoin and Carbamazepine may also impair the ocular system. The most common symptoms are diplopia, nystagmus and blurred vision. Cerebellar or vestibulo-ocular dysfunction is suspected as mechanism of these ocular adverse effects.
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Yan, Shaomin, and Guang Wu. "Distributions of amino acids in the primary structure of monoamine oxidase family." In International Conference on Biomedical and Intelligent Systems (IC-BIS 2022), edited by Ahmed El-Hashash. SPIE, 2022. http://dx.doi.org/10.1117/12.2660263.
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Kamruzzaman, A. S. M. "Integration of midgut-fat body-gonadal axis inPeriplaneta americana: Monoamine and peptide regulation." In 2016 International Congress of Entomology. Entomological Society of America, 2016. http://dx.doi.org/10.1603/ice.2016.94434.
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Khidiyatova, Irina, Gulnara Akhmadeeva, Irina Gilyazova, et al. "THE ROLE OF MONOAMINE METABOLISM SYSTEM GENES IN NEUROPSYCHOLOGICAL MANIFESTATIONS OF PARKINSON'S DISEASE." In XVI International interdisciplinary congress "Neuroscience for Medicine and Psychology". LLC MAKS Press, 2020. http://dx.doi.org/10.29003/m1317.sudak.ns2020-16/494-495.
Full textReports on the topic "Monoaminy"
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Jacobs, Barry L. Central Postsynaptic Actions of Monoamine Neurotransmitters in Behaving Animals. Defense Technical Information Center, 1997. http://dx.doi.org/10.21236/ada325701.
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Gluck, Martin R. Parkinson's Disease: The Link Between Monoamine Oxidase and Mitochondrial Respiration. Defense Technical Information Center, 2004. http://dx.doi.org/10.21236/ada612171.
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Shih, Jean C., and Bogdan Z. Olenyuk. Monoamine Oxidase A: A Novel Target for Progression and Metastasis of Prostate Cancer. Defense Technical Information Center, 2014. http://dx.doi.org/10.21236/ada612725.
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Shih, Jean C., and Bogdan Z. Olenyuk. Monoamine Oxidase A: A Novel Target for Progression and Metastasis of Prostate Cancer. Defense Technical Information Center, 2013. http://dx.doi.org/10.21236/ada593309.
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Mincher, Bruce Jay. Radiation chemistry of the branched-chain monoamide di-ethylhexyl-isobutyramide. Office of Scientific and Technical Information (OSTI), 2016. http://dx.doi.org/10.2172/1406976.
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Yin, Ziqian, Haoyang Xue, Youjia Qiu, et al. Safety and efficacy of vesicular monoamine transporter 2 inhibitors for the treatment of Huntington's disease: a review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, 2023. http://dx.doi.org/10.37766/inplasy2023.10.0004.
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Arias Quiroz, Kevin Josué, and Ariel Enrique Pastrana Arias. Efectos en el sistema nervioso de recién nacidos por consumo de cocaína en la vida intrauterina. Universidad de Cartagena, 2023. https://doi.org/10.32997/11227/18440.
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Si bien en la actualidad no es que ese vean muchos casos de niños afectados por el consumo de la droga durante la vida intra uterina, pero cada vez se es más frecuente por lo cual es un tema de investigación importante. Para que se hagan de cuanto está aumentando el consumo en mujeres en edad fértil algún tipo de sustancia en Colombia, el Observatorio de Drogas de Colombia (ODC) reportó un aumentó en un 3,5% en el consumo de sustancias como marihuana, pasta básica de coca, éxtasis o heroína en las personas entre los 15 y 65 años. Desde hace muchos años se han descrito numerosos efectos secundarios, aunque la inconsistencia de los hallazgos y los problemas metodológicos unidos a los problemas de seguimiento a largo plazo de los estudios realizados hacen que la evidencia no sea convincente y que sean precisos nuevos estudios que tengan en cuenta otros factores del entorno fetal. Se identificaron 6 artículos de interés basados en la toxicidad de la cocaína en los hijos de madres consumidoras, con el fin de identificar los efectos y secuelas neurológicas que se producen tanto en la vida uterina como en el recién nacido y su desarrollo en la vida. La cocaína tiene diferentes efectos en el sistema nervioso central a consecuencia de su mecanismo, inhibiendo la recaptación y estimulando la liberación de dopamina y otras monoaminas endógenas: adrenalina, noradrenalina y en menor grado serotonina. La estimulación del Sistema Nervioso Simpático explica la presentación clínica en la intoxicación aguda: síndrome simpáticomimético (excitación psicomotriz, midriasis o dilatación de pupilas, aumento de la frecuencia cardíaca y de la presión arterial, arritmias cardíacas, convulsiones, isquemia miocárdica, cerebral y menos frecuentemente en otros órganos, por vasoespasmo arterial). Por ende, esta sustancia es una de las mas adictivas y su consumo se ha incrementado con los años, así cada día se ven más paciente consumidores crónicos que requieren de un tratamiento.