Activation of phosphatidylinositol bisphosphate signal transduction pathway after experimental brain injury: a lipid study

Dhillon, Harbhajan S.; Carbary, Timothy J.; Dose, John M.; Dempsey, Robert J.; Prasad, M. R. N.

doi:10.1016/0006-8993(95)00840-m

Cited by 51 publications

(35 citation statements)

References 31 publications

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“…Others have shown that free fatty acids (FFAs) and diacylglycerols (DAGs) are increased in the sensorimotor cortex and cerebellum following CCI TBI in rats (21). Similar findings were noted in another rat model of FPI where phosphatidylinositol 4,5-bisphosphate levels were decreased but FFA and DAG levels were increased in injured animals compared to controls (22). Collectively, these studies suggest that brain PL composition and metabolism is perturbed following TBI.…”

supporting

confidence: 81%

“…Post hoc analyses showed that differences between the injury groups were only significant for the hippocampi (PϽ0.01). For SM, component 1 explaining 48% of the variance was associated with injury (F (5,22) ϭ18.4, PϽ0.01). Post hoc comparisons showed that differences between injury and control mice were significant for all of the brain regions (PϽ0.05).…”

Section: Individual Molecular Species Of Pc Sm Pe and Pi Have Distmentioning

confidence: 99%

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Lipidomic analyses identify injury‐specific phospholipid changes 3 mo after traumatic brain injury

et al. 2014

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Phospholipid (PL) abnormalities are observed in the cerebrospinal fluid of patients with traumatic brain injury (TBI), suggesting their role in TBI pathology. Therefore, PL levels were examined in a TBI mouse model that received 1.8 mm deep controlled cortical impact injury or craniectomy only (control). The rotarod and Barnes maze acquisition and probe tests were performed within 2 wk after injury, with another probe test performed 3 mo postinjury. Liquid chromatography/mass spectrometry analyses were performed on lipid extracts from several brain regions and plasma from injured and control mice collected at 3 mo postinjury. Compared to controls, injured mice with sensorimotor and learning deficits had decreased levels of cortical and cerebellar phosphatidylcholine (PC) and phosphatidylethanolamine (PE) levels, while hippocampal PC, sphingomyelin and PE levels were elevated. Ether PE levels were lower in the cortices and plasma of injured animals. Polyunsaturated fatty acid-containing PC and PE species, particularly ratios of docosahexaenoic acid (DHA) to arachidonic acid, were lower in the hippocampi and cortices and plasma of injured mice. Given the importance of DHA in maintaining neuronal function and resolving inflammation and of peroxisomes in synthesis of ether PLs, normalizing these PLs may be a useful strategy for treating the chronic pathology of TBI.-Abdullah, L., Evans, J. E., Ferguson, S., Mouzon, B., Montague, H., Reed, J., Crynen, G., Emmerich, T., Crocker, M., Pelot, R., Mullan, M., Crawford, F. Lipidomic analyses identify injury-specific phospholipid changes 3 months after traumatic brain injury. FASEB J. 28, 5311-5321 (2014). www.fasebj.org Key Words: controlled cortical impact ⅐ mass spectrometry ⅐ phosphatidylcholine ⅐ phosphatidylethanolamine ⅐ phosphatidylinositol ⅐ sphingomyelin Traumatic brain injury (TBI) is a significant cause of morbidity and mortality in the United States among adults from both the civilian and military populations. Due to the improvements made in military body armor and combat helmets over the past 2 decades, the rate of severe TBI associated with Iraq and Afghanistan deployments has decreased to 1% of the total TBI sustained by military personnel, a rate that is lower than those reported for previous deployments (1-3). Estimates from the U.S. Centers for Disease Control and Prevention suggest that severe TBI remains an important issue in the civilian population. In 2010, 2.5 million admissions to emergency departments were due to TBI (4) contributing to about a third of injury related deaths in the United States. The annual U.S. costs associated with TBI are estimated to be $75 billion, largely attributed to medical care, loss of productivity, and long-term disability (5). Although mild TBI occurs more frequently than severe TBI, the latter has the largest adverse effect on the activities of daily living of injured individuals and accounts for 90% of the total TBI-related medical costs (5). The primary injury is caused by the immediate force of the trauma a...

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supporting

confidence: 81%

Section: Individual Molecular Species Of Pc Sm Pe and Pi Have Distmentioning

confidence: 99%

Lipidomic analyses identify injury‐specific phospholipid changes 3 mo after traumatic brain injury

et al. 2014

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“…Most studies suggested that PLA2 plays a potentially deleterious role in TBI by producing of inflammatory mediators and other second messengers (Stephenson et al, 1999;Sapirstein and Bonventre, 2000). PLA2 can hydrolyze membrane phospholipids and liberate free fatty acids including arachidonic acid, diacylglycerol (DAG), and precursor platelet activating factor (PAF), all of which are important components in immune and inflammatory responses (Dhillon et al, 1995;Bazan, 1998;Uhl et al, 1999).…”

Section: Inflammation-associated Genesmentioning

confidence: 99%

Altered expression of randomly selected genes in mouse hippocampus after traumatic brain injury

Long

Zou

et al. 2002

J of Neuroscience Research

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Using a cDNA microarray method, we analyzed gene expression profiles in mouse hippocampus after traumatic brain injury (TBI). Of 6,400 randomly selected arrayed genes and expressed sequence tags from a mouse cDNA library, 253 were found to be differentially expressed (106 increased and 147 decreased). Genes involved in cell homeostasis and calcium signaling were primarily up-regulated while those encoding mitochondrial enzymes, metabolic molecules, and structural proteins were predominantly down-regulated. Equal numbers of genes related to inflammatory reactions showed increased or decreased expression. Importantly, a large proportion of the dysregulated genes we identified have not been reported as differentially expressed in TBI models. Semiquantitative reverse-transcriptase polymerase chain reaction (RT-PCR) analyses of representative genes confirmed the validity of the corresponding microarray findings. Thus, our microarray-based evaluation of gene expression in traumatically injured hippocampus identified both known and novel genes that respond to TBI. Further investigation of these candidate molecules may suggest new ways to attenuate the traumatic effects of brain injury.

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“…It is also possible that the amphetamine-mediated increase in norepinephrine decreased the excitotoxicity of amino acids through al-and a2-adrenergic receptors (Crowder and Bradford, 1987;Delangen and Mulder, 1980;Lynch and Bliss, 1986;Feeney, 1991;Sutton and Feeney, 1992;Prasad et al, 1995). This reduction of excitotoxicity by amphetamine may include neurotransmitter-linked early secondary injury processes, such as lactic acidosis (Hovda et al, 1992;Prasad et al, 1994a,b), cytoskeletal changes (Taft et al, 1992;Posmantur et al, 1994;Hicks e al., 1995), membrane phospholipid breakdown (Dhillon et al, 1994(Dhillon et al, , 1995a, altered cyclic nucleotide and protein kinase C-mediated phosphorylations (Dhillon et al, 1995a,b;Padmaperuma et al, 1995Padmaperuma et al, , 1996, and other processes Lyeth and Hayes, 1992;Mclntosh, 1993). It is also likely that irreversible axonal changes (Pettus et al, 1994) contributed to incomplete improvement of behavioral function by amphetamine in that particular study .…”

Section: Effect Of Drugs On Spatial Learningmentioning

confidence: 99%

Lack of Delayed Effects of Amphetamine, Methoxamine, and Prazosin (Adrenergic Drugs) on Behavioral Outcome after Lateral Fluid Percussion Brain Injury in the Rat

Dose¹,

Dhillon²,

Maki³

et al. 1997

Journal of Neurotrauma

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This study examined the delayed effects of the administration of d-amphetamine, methoxamine (an alpha1-adrenergic receptor agonist), and prazosin (an alpha1-adrenergic receptor antagonist) on the behavioral outcome of lateral fluid-percussion (FP) brain injury. Rats trained to perform a beam-walking task were subjected to brain injury of moderate severity (2.1 to 2.2 atm). Twenty-four hours after injury, rats were treated with amphetamine, methoxamine, or prazosin at two or three different dose levels. Amphetamine-treated animals displayed no significant improvement in beam-walking ability either during or after drug intoxication (from days 3 to 5 after brain injury). Similarly, neither methoxamine nor prazosin significantly affected beam-walking ability during or after drug intoxication. Neither amphetamine treatment at three different doses nor treatment with methoxamine or prazosin at two different doses affected the spatial learning disabilities of brain-injured animals. These results suggest that (1) unlike amphetamine administration after sensorimotor cortex (SMC) ablation or contusion brain injury models, amphetamine administration at 24 h after concussive FP brain injury does not improve beam-walking performance; (2) unlike amphetamine administration 10 min after concussive FP brain injury amphetamine administration 24 h after injury does not improve cognitive function; and (3) unlike prazosin administration after SMC ablation brain injury, prazosin administration 24 h after concussive FP brain injury does not effect beam-walking performance.

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Activation of phosphatidylinositol bisphosphate signal transduction pathway after experimental brain injury: a lipid study

Cited by 51 publications

References 31 publications

Lipidomic analyses identify injury‐specific phospholipid changes 3 mo after traumatic brain injury

Lipidomic analyses identify injury‐specific phospholipid changes 3 mo after traumatic brain injury

Altered expression of randomly selected genes in mouse hippocampus after traumatic brain injury

Lack of Delayed Effects of Amphetamine, Methoxamine, and Prazosin (Adrenergic Drugs) on Behavioral Outcome after Lateral Fluid Percussion Brain Injury in the Rat

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