Herefore, CL (along with its naphthalene derivative) represents a new valuable tool to localize and monitor unpaired structures in a DNA double helix context.Author ContributionsConceived and designed the experiments: SNR. Performed the experiments: MN. Analyzed the data: MN SNR. Contributed reagents/ materials/analysis tools: GP MP. Wrote the paper: SNR.Clerocidin Dissects DNA Secondary Structure
Although deficit in motor function is a common Peptide M supplier consequence of traumatic brain injury (TBI), not much is known about the influence of brain injury on motor centers in the spinal cord. We are starting to understand that TBI reduces the expression of molecules important for synaptic plasticity in the spinal cord [1], and are thus arguing for the need of broad therapeutic strategies to influence the brain and spinal cord. Here we have studied the capacity of foods to promote increased spinal cord resilience to the type of diffuse injury caused by brain trauma, in particular, the essential omega-3 (n-3) poly-unsaturated fatty acid (PUFA) docosahexaenoic acid (DHA, 22:6n-3), which is gaining recognition for supporting neuronal function and plasticity. Inadequate consumption of dietary DHA during CNS development results in aberrations in neuronal function, and learning ability [2,3], while dietary DHA supplementation in the adult brain aids recovery after brain injury [4,5]. In the present study, we seek to determine whether dietary supplementation of DHA could influence the capacity of the spinal cord to cope with the effects of injury to the brain. We used fluid-percussion injury (FPI) as an animal model of TBI since this injury promotes circuit dysfunction without extensive neuronal death [6]. Specifically, FPI results in significant reductions of brain-derived neurotrophic factor (BDNF) and its downstream effectors. BDNF is important for many aspects of neuronal function and plasticity, influencing adult neurogenesis, and providing protection after neuronal injury [7]. As we know that TBI promotes oxidative damage of the plasma membrane [8], likely influencing the membrane’s phospholipid composition, suchas DHA, we used the lipid peroxidation marker 4-HNE to assess the status of the plasma membrane in response to TBI and DHA interventions [8]. We have also assessed syntaxin-3 based on its role as a modulator of neuronal membrane expansion, especially during synaptic growth [9], and assessed calcium-independent phospholipase A-2 (iPLA-2) based on its influence on membrane phospholipid biosynthesis and turnover [10].Results Synaptic Proteins (Fig. 1)BDNF levels were significantly reduced in the animals fed the n3 AVP cost deficient diet (n-3 def/sham, 74 , p,0.01, n = 5) as compared to the animals fed adequate n-3 (n-3 adq/sham, n = 6) (Fig. 1A). FPI reduced levels of BDNF in the n-3 deficient group (n-3 def/ FPI, p,0.01, n = 5). Although FPI reduced BDNF levels in the n-3 adq rats (p,0.02, n = 7), these levels were still higher than the n-3 def group (p,0.05, Fig. 1A). The n-3 deficient diet reduced the levels of pTrkB/TrkB when compared to the n-3 11967625 adq/sham group (p,0.01, Fig. 1B). Although FPI reduced levels of pTrkB/TrkB in the group receiving adequate levels of n-3, pTrkB/TrkB levels were still higher than the n-3 def group (n-3 adq/FPI vs. n-3 def/ FPI, p,0.05, Fig. 1B). Levels of pCREB/CREB were reduced in the animals exposed to the n-3 deficient diet (n-3 def/sham vs. n-3 adq/sham, p,0.05, Fig. 1C) and FPI had a tendency to reduce pCREB/CREB levels ev.Herefore, CL (along with its naphthalene derivative) represents a new valuable tool to localize and monitor unpaired structures in a DNA double helix context.Author ContributionsConceived and designed the experiments: SNR. Performed the experiments: MN. Analyzed the data: MN SNR. Contributed reagents/ materials/analysis tools: GP MP. Wrote the paper: SNR.Clerocidin Dissects DNA Secondary Structure
Although deficit in motor function is a common consequence of traumatic brain injury (TBI), not much is known about the influence of brain injury on motor centers in the spinal cord. We are starting to understand that TBI reduces the expression of molecules important for synaptic plasticity in the spinal cord [1], and are thus arguing for the need of broad therapeutic strategies to influence the brain and spinal cord. Here we have studied the capacity of foods to promote increased spinal cord resilience to the type of diffuse injury caused by brain trauma, in particular, the essential omega-3 (n-3) poly-unsaturated fatty acid (PUFA) docosahexaenoic acid (DHA, 22:6n-3), which is gaining recognition for supporting neuronal function and plasticity. Inadequate consumption of dietary DHA during CNS development results in aberrations in neuronal function, and learning ability [2,3], while dietary DHA supplementation in the adult brain aids recovery after brain injury [4,5]. In the present study, we seek to determine whether dietary supplementation of DHA could influence the capacity of the spinal cord to cope with the effects of injury to the brain. We used fluid-percussion injury (FPI) as an animal model of TBI since this injury promotes circuit dysfunction without extensive neuronal death [6]. Specifically, FPI results in significant reductions of brain-derived neurotrophic factor (BDNF) and its downstream effectors. BDNF is important for many aspects of neuronal function and plasticity, influencing adult neurogenesis, and providing protection after neuronal injury [7]. As we know that TBI promotes oxidative damage of the plasma membrane [8], likely influencing the membrane’s phospholipid composition, suchas DHA, we used the lipid peroxidation marker 4-HNE to assess the status of the plasma membrane in response to TBI and DHA interventions [8]. We have also assessed syntaxin-3 based on its role as a modulator of neuronal membrane expansion, especially during synaptic growth [9], and assessed calcium-independent phospholipase A-2 (iPLA-2) based on its influence on membrane phospholipid biosynthesis and turnover [10].Results Synaptic Proteins (Fig. 1)BDNF levels were significantly reduced in the animals fed the n3 deficient diet (n-3 def/sham, 74 , p,0.01, n = 5) as compared to the animals fed adequate n-3 (n-3 adq/sham, n = 6) (Fig. 1A). FPI reduced levels of BDNF in the n-3 deficient group (n-3 def/ FPI, p,0.01, n = 5). Although FPI reduced BDNF levels in the n-3 adq rats (p,0.02, n = 7), these levels were still higher than the n-3 def group (p,0.05, Fig. 1A). The n-3 deficient diet reduced the levels of pTrkB/TrkB when compared to the n-3 11967625 adq/sham group (p,0.01, Fig. 1B). Although FPI reduced levels of pTrkB/TrkB in the group receiving adequate levels of n-3, pTrkB/TrkB levels were still higher than the n-3 def group (n-3 adq/FPI vs. n-3 def/ FPI, p,0.05, Fig. 1B). Levels of pCREB/CREB were reduced in the animals exposed to the n-3 deficient diet (n-3 def/sham vs. n-3 adq/sham, p,0.05, Fig. 1C) and FPI had a tendency to reduce pCREB/CREB levels ev.
