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

Js, Rao; Rn, Ertley; Hj, Lee; Jc, DeMar; Jt, Arnold; Si, Rapoport; Rp, Bazinet

doi:10.1038/sj.mp.4001888

Cited by 258 publications

(169 citation statements)

References 91 publications

(108 reference statements)

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“…Our previous study has indicated possible involvement of intracellular PLA 2 s (probably iPLA 2 ) and release of long chain fatty acids in the mouse prefrontal cortex after chronic antidepressant treatment (Lee et al 2009). It is possible that treatment modalities of depression may involve the induction of PLA 2 isoforms to endogenously release long chain fatty acids such as DHA, which have antidepressant effects (DeMar et al 2006;Rao et al 2007). Interestingly, many of the lipid changes in the striatum were opposite to that of the prefrontal cortex.…”

Section: Discussionmentioning

confidence: 99%

Brain lipid changes after repetitive transcranial magnetic stimulation: potential links to therapeutic effects?

Lee

Tan

et al. 2011

Metabolomics

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Repetitive transcranial magnetic stimulation (rTMS) is increasingly used in the management of neurologic disorders such as depression and chronic pain, but little is known about how it could affect brain lipids, which play important roles in membrane structure and cellular functions. The present study was carried out to examine the effects of rTMS on brain lipids at the individual molecular species level using the novel technique of lipidomics. Rats were subjected to high frequency (15 Hz) stimulation of the left hemisphere with different intensities and pulses of rTMS. The prefrontal cortex, hippocampus and striatum were harvested 1 week after rTMS and lipid profiles analyzed by tandem mass spectrometry. rTMS resulted in changes mainly in the prefrontal cortex. There were significant alterations in plasmalogen phosphatidylethanolamines, phosphatidylcholines, and increases in sulfated galactosylceramides or sulfatides. Plasmalogen species with long chain polyunsaturated fatty acids (PUFAs) showed decrease in abundance together with corresponding increase in lysophospholipid species suggesting endogenous release of long chain fatty acids such as docosahexaenoic acid (DHA) in brain tissue. The hippocampus showed no significant changes, whilst changes in the striatum were often opposite to that of the prefrontal cortex. It is postulated that changes in brain lipids may underlie some of the clinical effects of rTMS.

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Section: Discussionmentioning

confidence: 99%

Brain lipid changes after repetitive transcranial magnetic stimulation: potential links to therapeutic effects?

Lee

Tan

et al. 2011

Metabolomics

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“…As ERKs also play a role in cytoskeletal polymerisation, these findings may be related to structural hippocampal differences between SAL and LAL such as the intra-and infrapyramidal mossy fibres [42]. Also relevant are findings from Rao et al (2007) who showed that in rats dietary deprivation of certain polyunsaturated fatty acids led to increases in aggression and depression together with, among others, reductions in frontal cortex BDNF expression and p38 MAPK activity [43].…”

Section: Identification Of Biological Pathways Associated With Aggresmentioning

confidence: 93%

Genes and Gene Networks Implicated in Aggression Related Behaviour

et al. 2014

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Aggressive behaviour is a major cause of mortality and morbidity. Despite of moderate heritability estimates, progress in identifying the genetic factors underlying aggressive behaviour has been limited. There are currently three genetic mouse models of high and low aggression created using selective breeding. This is the first study to offer a global transcriptomic characterization of the prefrontal cortex across all three genetic mouse models of aggression. A systems biology approach has been applied to transcriptomic data across the three pairs of selected inbred mouse strains (Turku Aggressive (TA) and Turku Non-Aggressive (TNA), Short Attack Latency (SAL) and Long Attack Latency (LAL) mice and North Carolina Aggressive (NC900) and North Carolina Non-Aggressive (NC100)), providing novel insight into the neurobiological mechanisms and genetics underlying aggression. First, weighted gene co-expression network analysis (WGCNA) was performed to identify modules of highly correlated genes associated with aggression. Probe sets belonging to gene modules uncovered by WGCNA were carried forward for network analysis using ingenuity pathway analysis (IPA). The RankProd non-parametric algorithm was then used to statistically evaluate expression differences across the genes belonging to modules significantly associated with aggression. IPA uncovered two pathways, involving NF-kB and MAPKs. The secondary RankProd analysis yielded 14 differentially expressed genes, some of which have previously been implicated in pathways associated with aggressive behaviour, such as Adrbk2. The results highlighted plausible candidate genes and gene networks implicated in aggression-related behaviour.

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“…There are numerous studies indicating that ROS induced neuronal damage has an important role in the pathophysiology of depression, probably via membrane omega 3 polyunsaturated fatty acids (PUFAs) pathology [8,9], decreasing activity of GSH-Px, catalase and superoxide dismutase (SOD) [3], and antioxidant vitamin [10], suggesting oxidative damage. Although most of the oxygen used in brain tissue is converted to CO 2 and water, small amounts of oxygen forms ROS.…”

Section: Introductionmentioning

confidence: 99%

Protective Effects of Lamotrigine, Aripiprazole and Escitalopram on Depression-induced Oxidative Stress in Rat Brain

2007

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We investigated the effects of lamotrigine, aripiprazole and escitalopram administration and experimental depression on lipid peroxidation (LP) and antioxidant levels in cortex of the brain in rats. Forty male wistar rats were randomly divided into five groups. First group was used as control although second group was depression-induced group. Aripiprazole, lamotrigine and escitalopram per day were orally supplemented to chronic mild stress (CMS) depression-induced rats constituting the third, fourth and fifth groups for 28 days, respectively. Depression resulted in significant decrease in the glutathione peroxidase (GSH-Px) activity, reduced glutathione and vitamin C of cortex of the brain although their levels and beta-carotene concentrations were increased by the three drugs administrations to the animals of CMS induced depression group. The LP levels in the cortex of the brain and plasma of depression group were elevated although their levels were decreased by the administrations. The increases of antioxidant values in lamotrigine group were higher according to aripiprazole and escitalopram supplemented groups. Vitamin A level did not change in the five groups. In conclusion, the experimental depression is associated with elevated oxidative stress although treatment with lamotrigine has most protective effects on the oxidative stress within three medicines.

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

Cited by 258 publications

References 91 publications

Brain lipid changes after repetitive transcranial magnetic stimulation: potential links to therapeutic effects?

Brain lipid changes after repetitive transcranial magnetic stimulation: potential links to therapeutic effects?

Genes and Gene Networks Implicated in Aggression Related Behaviour

Protective Effects of Lamotrigine, Aripiprazole and Escitalopram on Depression-induced Oxidative Stress in Rat Brain

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