Improved technique for stereotactic placement of nerve grafts between two locations inside the rat brain

Gómez‐Pinedo, Ulises; Félez, M. Carmen; Sancho-Bielsa, Francisco J.; Vidueira, Sandra; Cabanes, Carmen; Soriano, María Vicenta García; García‐Verdugo, José Manuel; Barcia, Juan A.

doi:10.1016/j.jneumeth.2008.07.008

Cited by 6 publications

(6 citation statements)

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“…Using both in vitro and in vivo models through a series of elegant studies Guerri's laboratory has clearly established that chronic ethanol treatment induces astroglial activation and astrogliosis in brain as indicated by marked upregulation of GFAP immunoreactivity within hypertrophic astrocytes, (Wilhelmsson et al 2006; Chvatal et al 2007; Gomez-Pinedo et al 2008). TLR are pattern recognition receptors that activate NF-κB transcription.…”

Section: Astrocytes and Microglia Are Activated In Addictionmentioning

confidence: 99%

Induction of innate immune genes in brain create the neurobiology of addiction

Crews

Zou

Qin

2011

Brain, Behavior, and Immunity

280

244

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Addiction occurs through repeated abuse of drugs that progressively reduce behavioral control and cognitive flexibility while increasing limbic negative emotion. Recent discoveries indicate neuroimmune signaling underlies addiction and co-morbid depression. Low threshold microglia undergo progressive stages of innate immune activation involving astrocytes and neurons with repeated drug abuse, stress, and/or cell damage signals. Increased brain NF-κB transcription of proinflammatory chemokines, cytokines, oxidases, proteases, TLR and other genes create loops amplifying NF-κB transcription and innate immune target gene expression. Human post-mortem alcoholic brain has increased NF-κB and NF-κB target gene message, increased microglial markers and chemokine-MCP1. Polymorphisms of human NF-κB1 and other innate immune genes contribute to genetic risk for alcoholism. Animal transgenic and genetic studies link NF-κB innate immune gene expression to alcohol drinking. Human drug addicts show deficits in behavioral flexibility modeled pre-clinically using reversal learning. Binge alcohol, chronic cocaine, and lesions link addiction neurobiology to frontal cortex, neuroimmune signaling and loss of behavioral flexibility. Addiction also involves increasing limbic negative emotion and depression-like behavior that is reflected in hippocampal neurogenesis. Innate immune activation parallels loss of neurogenesis and increased depression-like behavior. Protection against loss of neurogenesis and negative affect by anti-oxidant, anti-inflammatory, anti-depressant, opiate antagonist and abstinence from ethanol dependence link limbic affect to changes in innate immune signaling. The hypothesis that innate immune gene induction underlies addiction and affective disorders creates new targets for therapy.

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Section: Astrocytes and Microglia Are Activated In Addictionmentioning

confidence: 99%

Induction of innate immune genes in brain create the neurobiology of addiction

Crews

Zou

Qin

2011

Brain, Behavior, and Immunity

280

244

View full text Add to dashboard Cite

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“…OEGs permit the entry of axons from the olfactory nerves into the olfactory bulb and have been extensively used a permissive cells for axonal reentry in spinal cord and spinal root repair . In our study, OEGs have favored the entry of dopaminergic axons into the graft and they have also permitted the reentry of axons back into the brain.…”

Section: Discussionmentioning

confidence: 71%

“…The grafting procedure is original (previously reported in Gómez‐Pinedo et al) and was designed to implant peripheral nerve grafts. It was designed to overcome the difficulty of placing a flaccid material joining two desired nuclei within the CNS.…”

Section: Discussionmentioning

confidence: 99%

“…After two centrifugations (1000 rpm, 10 min), the pellet was suspended in Dulbecco's Modified Eagle's Medium (DMEM)/F12 (Gibco) with 10% fetal bovine serum (Gibco), 1% glutamine (Hyclone), 2% penicillin–streptomycin (Hyclone), and 1% gentamicin (Hyclone) and seeded into a 60‐mm cell culture dish (Corning) with 5 × 10 6 cells and incubated for 24 h (37°C and 5% CO 2 ). Cells in passage 4 were prepared to be implanted following the method proposed by the laboratory of Gómez‐Pinedo et al…”

Section: Methodsmentioning

confidence: 99%

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Bridges of biomaterials promote nigrostriatal pathway regeneration

et al. 2018

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Repair of central nervous system (CNS) lesions is difficulted by the lack of ability of central axons to regrow, and the blocking by the brain astrocytes to axonal entry. We hypothesized that by using bridges made of porous biomaterial and permissive olfactory ensheathing glia (OEG), we could provide a scaffold to permit restoration of white matter tracts. We implanted porous polycaprolactone (PCL) bridges between the substantia nigra and the striatum in rats, both with and without OEG. We compared the number of tyrosine-hydroxylase positive (TH+) fibers crossing the striatal-graft interface, and the astrocytic and microglial reaction around the grafts, between animals grafted with and without OEG. Although TH+ fibers were found inside the grafts made of PCL alone, there was a greater fiber density inside the graft and at the striatal-graft interface when OEG was cografted. Also, there was less astrocytic and microglial reaction in those animals. These results show that these PCL grafts are able to promote axonal growth along the nigrostriatal pathway, and that cografting of OEG markedly enhances axonal entry inside the grafts, growth within them, and re-entry of axons into the CNS. These results may have implications in the treatment of diseases such as Parkinson's and others associated with lesions of central white matter tracts. © 2018 Wiley Periodicals, Inc. J Biomed Mater Res Part B: Appl Biomater, 2018.

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“…18 The specific GAP-43 antibody used is a commercially available rabbit polyclonal antibody specific to growth cone-expressed protein (Abcam ab16053). 32 Tissue sections mounted on slides were washed with PBS and then treated with 0.5% Triton ϫ-100 in PBS for 10 minutes. The sections were treated with blocking buffer (10% horse serum in PBS and 0.1% Triton ϫ-100) and then incubated 30 minutes at 4°C with primary antibodies (diluted in blocking buffer).…”

Section: Immunocytochemistry and Digital Imaging Analysismentioning

confidence: 99%