Effects of mood stabilizers on hippocampus BDNF levels in an animal model of mania

Frey, Benício N.; Andreazza, Ana Cristina; Ceresér, Keila Maria Mendes; Martins, Márcio Rodrigo; Valvassori, Samira S.; Réus, Gislaine Z.; Quevedo, João; Kapczinski, Flávio

doi:10.1016/j.lfs.2006.01.002

Cited by 220 publications

(149 citation statements)

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“…One or a combination of these factors could contribute to increased depression and aggression scores reported in response to n-3 PUFA deprivation in rats. 15,39,[59][60][61][62] As CREB has been implicated in the pathophysiology of depression as well as of bipolar disorder, 33,63,64 n-3 PUFAs' ability to regulate CREB could be related to their effects in these diseases. CREB requires phosphorylation in order to transcribe CREB-regulated genes, including BDNF.…”

Section: Discussionmentioning

confidence: 99%

“…37 As well, drugs used to treat bipolar disorder (lithium and valproate) increase BDNF levels in rat brain. 38,39 Decreased BDNF levels are thought to contribute to bipolar disorder symptoms [40][41][42] while dietary n-3 PUFA supplementation improves symptoms, 13,14 and normalizes BDNF levels after traumatic brain injury in rats. 43 As a result of these observations, we hypothesized that dietary n-3 PUFA deprivation in rats would decrease frontal cortex BDNF levels and that this decrease would be related to changes in activity of CREB and of kinases that phosphorylate CREB.…”

Section: Introductionmentioning

confidence: 99%

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n-3 Polyunsaturated fatty acid deprivation in rats decreases frontal cortex BDNF via a p38 MAPK-dependent mechanism

et al. 2006

Mol Psychiatry

258

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Decreased docosahexaenoic acid (DHA) and brain-derived neurotrophic factor (BDNF) have been implicated in bipolar disorder. It also has been reported that dietary deprivation of n-3 polyunsaturated fatty acids (PUFAs) for 15 weeks in rats, increased their depression and aggression scores. Here, we show that n-3 PUFA deprivation for 15 weeks decreased the frontal cortex DHA level and reduced frontal cortex BDNF expression, cAMP response element binding protein (CREB) transcription factor activity and p38 mitogen-activated protein kinase (MAPK) activity. Activities of other CREB activating protein kinases were not significantly changed. The addition of DHA to rat primary cortical astrocytes in vitro, induced BDNF protein expression and this was blocked by a p38 MAPK inhibitor. DHA's ability to regulate BDNF via a p38 MAPK-dependent mechanism may contribute to its therapeutic efficacy in brain diseases having disordered cell survival and neuroplasticity.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

n-3 Polyunsaturated fatty acid deprivation in rats decreases frontal cortex BDNF via a p38 MAPK-dependent mechanism

et al. 2006

Mol Psychiatry

258

151

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“…It is interesting to remark that termination of a 6‐day AMPH exposure to rats (5.0 or 10.0 mg kg −1 day −1 ) has been associated with depressive‐like behavior and deficits in brain reward function, as indicated by increased intracranial self‐stimulation (Cryan et al., 2003). Also, repeated exposure to AMPH or MPH has been used to induce psychotic‐like states (Frey et al., 2006). We did not measure these variables, yet we cannot discard that similar alterations may have emerged in our study.…”

Section: Discussionmentioning

confidence: 99%

“…Males and females differentially react to drugs (Wille‐Bille et al., 2017), yet despite the increasing awareness of these differences and the explicit suggestion to have same‐sex representativeness (McCullough et al., 2014), women/female are still a neglected group in epidemiological and preclinical research. Last but not least, repeated MPH exposure and AMPH exposure are also used to model manic and bipolar conditions in laboratory animals (Frey et al., 2006), and there is some evidence suggesting exacerbated ethanol consumption in individuals with bipolar disorders (Strakowski & DelBello, 2000). …”

Section: Introductionmentioning

confidence: 99%

Amphetamine, but not methylphenidate, increases ethanol intake in adolescent male, but not in female, rats

et al. 2018

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IntroductionThere has been an increasing interest in analyzing the interactions between stimulants and ethanol during childhood and adolescence. Stimulants are used to treat attention‐deficit hyperactivity disorder (ADHD) in these developmental stages, during which ethanol initiation and escalation often occur.MethodsThis study assessed the effects of repeated d‐amphetamine (AMPH) or methylphenidate (MPH) treatment during adolescence [male and female Wistar rats, between postnatal day (PD) 28 to PD34, approximately] on the initiation of ethanol intake during a later section of adolescence (PD35 to PD40).ResultsAmphetamine and MPH exerted reliable acute motor stimulant effects, but there was no indication of sensitized motor or anxiety responses. MPH did not affect dopamine (DA) levels, whereas AMPH significantly reduced insular levels of DA in both sexes and norepinephrine levels in females only. Repeated treatment with AMPH, but not with MPH, enhanced ethanol intake during late adolescence in male, but not in female, rats.ConclusionA short treatment with AMPH during adolescence significantly altered DA levels in the insula, both in male and females, and significantly enhanced ethanol intake in males. The present results suggest that, in adolescent males, a very brief history of AMPH exposure can facilitate the initiation of ethanol intake.

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“…Mesmo com diferentes graus de validade, modelos animais são relevantes, já que permitem manipulações não factíveis em estudos clínicos 49 . No momento, há modelos animais de mania com validade suficiente utilizando a anfetamina e a ouabaína [50][51][52] . Ambos os modelos estão associados a uma diminuição do BDNF hipocampal, que é revertida com lítio.…”

Section: Neuroplasticidadeunclassified

Marcadores periféricos e a fisiopatologia do transtorno bipolar

Magalhães¹,

Fries²,

Kapczinski³

2012

Rev. psiquiatr. clín.

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Introdução: O entendimento da fisiopatologia do transtorno bipolar vem tendo avanços consistentes nos últimos anos. Um enfoque na relação entre carga alostática e alterações sistêmicas vem tomando corpo, com o objetivo de se entender a frequente progressão da doença. Proeminentes entre os mediadores periféricos têm sido as moléculas que poderiam ser amplamente agrupadas em neurotrofinas, marcadores de estresse oxidativo e marcadores inflamatórios. Objetivo: Descrever achados recentes em relação à fisiopatologia sistêmica do transtorno bipolar, com enfoque especial em estudos brasileiros, tentando articular uma visão coerente do conhecimento atual do campo. Método: Revisão narrativa da literatura relacionada a neurotrofinas, estresse oxidativo e marcadores inflamatórios no transtorno bipolar. Resultados: Diversas fontes de evidência, provenientes tanto de estudos pré-clínicos quanto clínicos, revelam consistentemente alterações sistêmicas no transtorno bipolar. Os achados são especialmente robustos em pacientes com múltiplos episódios. Nesses, alterações relacionadas a episódios de mania e depressão são notáveis em neurotrofinas e dano oxidativo a lipídeos. Um número menor de estudos mostra alterações no sistema imune, em particular estados pró-inflamatórios. Conclusão: Alterações sistêmicas que correlacionam o transtorno bipolar a comorbidade clínica, disfunção cognitiva, incapacidade e mortalidade precoce começam a ser traçadas. Estudos envolvendo desenhos longitudinais, amostras populacionais e ensaios clínicos envolvendo marcadores periféricos devem ser incorporados no futuro próximo e reforçar a validade de uma noção de envolvimento multissistêmico no transtorno bipolar.Magalhães PVS, et al. / Rev Psiq Clín. 2012;39(2):60-7 Palavras-chave: Transtorno bipolar, inflamação, estresse oxidativo, neurotrofinas, fator neurotrófico derivado do cérebro, fisiopatologia, biomarcadores. ABSTRACT Introduction:The understanding of the pathophysiology of bipolar disorder has steadily advanced in the past few years. Thereby, a focus on allostatic load and systemic changes has appeared, with the aim to understand illness progression. Amongst the peripheral markers, molecules that can be widely classified into neurotrophins, oxidadive stress markers, and inflammation markers have been elevated. Objective: To describe recent findings regarding the systemic pathophysiology of bipolar disorder, with a special focus on Brazilian studies and to create a coherent view of the current knowledge in the field. Method: Narrative review of the literature regarding neurotrophins, oxidative stress, and inflammatory markers in bipolar disorder. Results: A diverse body of evidence, based on both pre-clinical and clinical studies, reveals consistent systemic changes in bipolar disorder. The findings are particularly robust in patients after multiple episodes. Thereby, remarkable changes related to manic and depressive episodes were found in neurotrophins and oxidative damage to lipids. Regarding to immune system alterations, in particular pro...

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Effects of mood stabilizers on hippocampus BDNF levels in an animal model of mania

Cited by 220 publications

References 39 publications

n-3 Polyunsaturated fatty acid deprivation in rats decreases frontal cortex BDNF via a p38 MAPK-dependent mechanism

n-3 Polyunsaturated fatty acid deprivation in rats decreases frontal cortex BDNF via a p38 MAPK-dependent mechanism

Amphetamine, but not methylphenidate, increases ethanol intake in adolescent male, but not in female, rats

Marcadores periféricos e a fisiopatologia do transtorno bipolar

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