Proteomic identification of brainstem cytosolic proteins in a neuropathic pain model

Álzate, Óscar; Hussain, Syed-Rehan A.; Goettl, Virginia M.; Tewari, Arun K.; Madiai, Francesca; Stephens, Robert L.; Hackshaw, Kevin V.

doi:10.1016/j.molbrainres.2004.06.037

Cited by 34 publications

(16 citation statements)

References 30 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…These dysfunctions can be observed either immediately or some time after an injury. They include chronic neuropathic pain that is characterized by allodynia, a painful response to innocuous stimulus, hyperalgesia, and increased sensitivity to nociceptive stimulus (Alzate et al 2004). Recent evidence has revealed that the chronic pain occurring after a sciatic nerve injury could possibly be attributed to a combination of factors such as anatomical, neurochemical, excitotoxic, and inflammatory alterations and ion channel expression in the CNS (Hains et al 2001(Hains et al , 2003aFinnerup and Jensen 2004;Waxman and Hains 2006).…”

Section: Introductionmentioning

confidence: 99%

Effect of Memantine on the Levels of Neuropeptides and Microglial Cells in the Brain Regions of Rats with Neuropathic Pain

et al. 2009

View full text Add to dashboard Cite

Neuropathic pain induced by sciatic nerve injury not only causes peripheral dysfunctions but also affects the cortical and subcortical regions of the brain. It is still unknown whether neuropathic pain could relate to behavioral and neurochemical alterations in the central nervous system. This paper deals with the effect of peripheral neuropathic pain on mechanical allodynia, neuropeptide levels, neuropeptide-degrading enzyme activities, and microglial cells in the brain regions of rats by applying chronic constriction injury, a partial sciatic nerve injury. We examined the possible protection effect on the allodynia and changes in levels of neuropeptides and microglial activation in chronic constriction injury of the rat brain by memantine. On 4 days after chronic constriction injury, the induction of mechanical allodynia was suppressed by memantine treatment. Reductions in the substance P in the hypothalamus and somatostatin in the periaqueductal gray of chronic constriction injury rat brain were reversed by memantine. This suggests the role of these neuropeptides in pain information processing in the brain. Immunohistochemical experiments revealed that the expression of CD11b, a marker protein of microglia, was increased in the hypothalamus and periaqueductal gray in the chronic constriction injury rat brain as compared with the controls, and memantine treatment could suppress the activation of microglia, suggesting the involvement of microglia in pain mechanism. The present behavioral, biochemical, and immunohistochemical studies demonstrated that peripheral neuropathic pain affects the neuropeptide levels and microglial activation in the brain regions, and these events described above may play an important role in neuropathic pain pathogenesis.

show abstract

Section: Introductionmentioning

confidence: 99%

Effect of Memantine on the Levels of Neuropeptides and Microglial Cells in the Brain Regions of Rats with Neuropathic Pain

et al. 2009

View full text Add to dashboard Cite

show abstract

“…In a rat model of neuropathic pain, the Ca-binding proteins calmodulin and calretinin as well as protein-tyrosin phosphatase A, Ras-related protein RAB-15, and stress-activated protein kinase JNK3 showed lower levels. Higher levels were found for DRP2, interleukin-1, Rab-3A and 1B, somatropin, myosin regulatory light chain, and neuronalkinesin heavy chain [69,70]. In an ischemia model, increased expression for the signaling molecules platelet activation factor receptor and retinal guanyl cyclase 2 were observed [68].…”

Section: Signal Transduction Proteinsmentioning

confidence: 92%

“…Neuropathic pain, in contrast to nociceptive pain, is described as "burning", "electric", "tingling", and "shooting" in nature [69,70]. Limited proteomic analysis of neuropathic pain exists so far.…”

Section: Neuropathic Painmentioning

confidence: 99%

“…Increased levels for fructosebiphosphate aldolase were also observed in bipolar disorder [55]. In an animal model of neuropathic pain, several proteins involved in metabolic pathways were found to have altered levels, alpha enolase, cell division protein kinase 4, delayed recitifier K 1 channel (all increased), nitric oxide synthase 3, phosphorylase B kinase catalytic chain, porphobilinogen deaminase, and ubiquinone biosynthesis protein (decreased) [69,70]. In a rat model of hypoxia, the levels of NADH dehydrogenase Fe-S protein decreased [127] and in a model of stroke, propionyl CoA carboxylase and vasolin-containing protein showed altered phosphorylation patterns [128].…”

Section: Energy Metabolism Proteinsmentioning

confidence: 99%

“…There are several proteins known to be involved in electroacupuncture; however, it is not known how these proteins interact with each other and which their physiological roles are. Rat brainstem tissues following ligation of lumbar 5 and 6 (L5, L6) spinal nerves, which generate a model of peripheral neuropathic pain, were used in connection to proteomics analysis by Alzate et al [70]. Gineste et al [178] carried out a comparative study of the profile of protein expression in CSF from rats exposed to either injection of complete Freund's adjuvant (CFA), which is a model of inflammatory pain, or chronic constriction injury (CCI), which is a model of neuropathic pain.…”

Section: Animal Modelsmentioning

confidence: 99%

See 2 more Smart Citations

Proteomics‐driven progress in neurodegeneration research

Fountoulakis

Κοσσίδα

2006

Electrophoresis

View full text Add to dashboard Cite

Proteomics-driven progress in neurodegeneration researchProteomics technologies have been widely used in the investigation of neurodegenerative and psychiatric disorders, and in particular in the detection of differences between healthy individuals and patients suffering from such diseases. Thus, brain and cerebrospinal fluid (CSF) samples from patients with Alzheimer's disease, Down syndrome, Pick's disease, Parkinson's disease, schizophrenia, and other disorders as well as brain and CSF from animals serving as models of neurological disorders have been analyzed by proteomics. 2-DE followed by MALDI-TOF-MS has been mainly applied as this proteomics approach provides the possibility of convenient quantification of protein levels and detection of post-translational modifications. About 330 unique proteins with deranged levels and modifications have been detected by proteomics approaches to be related to neurodegeneration and psychiatric disorders. They are mainly involved in metabolism pathways, cytoskeleton formation, signal transduction, guidance, detoxification, transport, and conformational changes. In this article, we provide a summary of the major contributions of proteomics technologies in the study of neurodegenerative and psychiatric diseases, in particular, in the detection of changes in protein levels and modifications related to these disorders. IntroductionNeurodegeneration is a major hallmark of a series of genetic and acquired disorders of the central nervous system (CNS), like Alzheimer's disease (AD), Down syndrome (DS), Pick's disease, Creutzfeldt-Jakob disease (CJD), and Parkinson's disease, which result in severe cognitive and motor deficits. A common characteristic of these diseases is that they are multifactorial.Their molecular basis is unknown and individual biomarkers are not reliable. Genomics and proteomics approaches have been applied to obtain a better understanding of neurodegeneration and psychiatric disorders. Genomics has been used to map and identify genes that are mutated in a wide variety of such disorders, like presenilins in AD. Next to genomics, which only provides a partial view of the biological problem, proteomics is widely used in clinical diagnosis as well and many changes in protein levels associated with specific diseases have been identified [1,2].Proteomics is a technology-driven science that studies the proteins of the various biological systems, their structures, interactions, post-translational modifications, and in particular the changes in their levels and modifications, which are the result of specific diseases or are induced by external factors.

show abstract

Current awareness on comparative and functional genomics

2005

Comp Funct Genom

View full text Add to dashboard Cite

In order to keep subscribers up‐to‐date with the latest developments in their field, this current awareness service is provided by John Wiley & Sons and contains newly‐published material on comparative and functional genomics. Each bibliography is divided into 16 sections. 1 Reviews & symposia; 2 General; 3 Large‐scale sequencing and mapping; 4 Genome evolution; 5 Comparative genomics; 6 Gene families and regulons; 7 Pharmacogenomics; 8 Large‐scale mutagenesis programmes; 9 Functional complementation; 10 Transcriptomics; 11 Proteomics; 12 Protein structural genomics; 13 Metabolomics; 14 Genomic approaches to development; 15 Technological advances; 16 Bioinformatics. Within each section, articles are listed in alphabetical order with respect to author. If, in the preceding period, no publications are located relevant to any one of these headings, that section will be omitted

show abstract

Proteomic identification of brainstem cytosolic proteins in a neuropathic pain model

Cited by 34 publications

References 30 publications

Effect of Memantine on the Levels of Neuropeptides and Microglial Cells in the Brain Regions of Rats with Neuropathic Pain

Effect of Memantine on the Levels of Neuropeptides and Microglial Cells in the Brain Regions of Rats with Neuropathic Pain

Proteomics‐driven progress in neurodegeneration research

Current awareness on comparative and functional genomics

Contact Info

Product

Resources

About