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| 1 | Post-stroke pain hypersensitivity induced by experimental thalamic hemorrhage in rats is region-specific and demonstrates limited efficacy of gabapentin显示文摘Intractable central post-stroke pain(CPSP) is one of the most common sequelae of stroke, but has been inadequately studied to date. In this study, we first determined the relationship between the lesion site and changes in mechanical or thermal pain sensitivity in a rat CPSP model with experimental thalamic hemorrhage produced by unilateral intra-thalamic collagenase IV(ITC) injection. Then, we evaluated the efficacy of gabapentin(GBP), an anticonvulsant that binds the voltage-gated Ca2+ channel α2δ and a commonly used anti-neuropathic pain medication. Histological case-by-case analysis showed that only lesions confined to the medial lemniscus and the ventroposterior lateral/medial nuclei of the thalamus and/or the posterior thalamic nucleus resulted in bilateral mechanical pain hypersensitivity. All of the animals displaying CPSP also had impaired motor coordination, while control rats with intra-thalamic saline developed no central pain or motor deficits. GBP had a dose-related anti-allodynic effect after a single administration(1, 10, or 100 mg/kg) on day 7 post-ITC, with significant effects lasting at least 5 hfor the higher doses. However, repeated treatment, once a day for two weeks, resulted in complete loss of effectiveness(drug tolerance) at 10 mg/kg, while effectiveness remained at 100 mg/kg, although the time period of efficacious analgesia was reduced. In addition, GBP did not change the basal pain sensitivity and the motor impairment caused by the ITC lesion, suggesting selective action of GBP on the somatosensory system. | Fei Yang Han Fu Yun-Fei Lu Xiao-Liang Wang Yan Yang Fan Yang Yao-Qing Yu Wei Sun Jia-Shuang Wang Michael Costigan Jun Chen | 2014 | Neuroscience Bulletin2014，30，6： | 5 |
| 2 | Combining Human and Rodent Genetics to Identify New Analgesics显示文摘Most attempts at rational development of new analgesics have failed, in part because chronic pain involves multiple processes that remain poorly understood.To improve translational success, one strategy is to select novel targets for which there is proof of clinical relevance,either genetically through heritable traits, or pharmacologically. Such an approach by definition yields targets with high clinical validity. The biology of these targets can be elucidated in animal models before returning to the patients with a refined therapeutic. For optimal treatment, having biomarkers of drug action available is also a plus. Here we describe a case study in rational drug design: the use of controlled inhibition of peripheral tetrahydrobiopterin(BH4) synthesis to reduce abnormal chronic pain states without altering nociceptive-protective pain. Initially identified in a population of patients with low back pain, the association between BH4 production and chronic pain has been confirmed in more than 12 independent cohorts,through a common haplotype(present in 25% of Caucasians) of the rate-limiting enzyme for BH4 synthesis,GTP cyclohydrolase 1(GCH1). Genetic tools in mice have demonstrated that both injured sensory neurons and activated macrophages engage increased BH4 synthesis to cause chronic pain. GCH1 is an obligate enzyme for de novo BH4 production. Therefore, inhibiting GCH1 activity eliminates all BH4 production, affecting the synthesis of multiple neurotransmitters and signaling molecules and interfering with physiological function. In contrast, targeting the last enzyme of the BH4 synthesis pathway,sepiapterin reductase(SPR), allows reduction of pathological BH4 production without completely blocking physiological BH4 synthesis. Systemic SPR inhibition in mice has not revealed any safety concerns to date, and available genetic and pharmacologic data suggest similar responses in humans. Finally, because it is present in vivo only when SPR is inhibited, sepiapterin serves as a reliable biomarker of target engagement, allowing potential quantification of drug efficacy. The emerging development of therapeutics that target BH4 synthesis to treat chronic pain illustrates the power of combining human and mouse genetics: human genetic studies for clinical selection of relevant targets,coupled with causality studies in mice, allowing the rational engineering of new analgesics. | Alban Latremoliere Michael Costigan | 2018 | Neuroscience Bulletin2018，34，1： | 3 |
| 3 | Longitudinal variability in hydraulic geometry and substrate characteristics of a Great Plains sand-bed river显示文摘 | Katie H. Costigan Melinda D. Daniels Joshuah S. Perkin Keith B. Gido | 2013 | Geomorphology2013，，： | 2 |
| 4 | Successful treatment of neuropathies,in patients with diabetes mellitus显示文摘 | Krendel D A Costigan DA Hopkins LC | 1995 | Arch Neurol1995，52，5： | 1 |
| 5 | Slug flow regime identification from dy-namic void fraction measurement in vertical air-water flows显示文摘 | Costigan G Whalley P B | 1997 | International Journal of Multiphase Flow1997，23，2： | 1 |
| 6 | Fetal neurobehavioural development显示文摘 | DIPIETRO JA HODGSON DM COSTIGAN KA | 1996 | Child Dev1996，67，： | 1 |
| 7 | The natural history of the systemic inflammatory response syndrome (SIRS) A prospective study显示文摘 | RANGEL FRAUSTO S PITTTET D COSTIGAN M | | 0，，02： | 1 |
| 8 | Complement induction in spinal cord microglia results in anaphylatoxin C5a-mediated pain hypersensitivity显示文摘 | Griffin R S Costigan M Brenner G J | 2007 | J Neurosci2007，27，32： | 1 |
| 9 | Transcriptional and posttranslational plasticity and the generation of inflammatory pain显示文摘 | Woolf C J Costigan M | 1999 | Proc Natl Acad Sci U S A1999，96，14： | 1 |
| 10 | Knee and hip kinetics during normal stair climbing显示文摘 | Costigan P Deluzio K Wyss U | 2002 | Gait Posture2002，16，1： | 1 |
| 11 | Neurotro- phins: peripherally and centrally acting modulators of tactile stimulus-induced inflammatory pain hypersensitivity显示文摘 | Mannion R J Costigan M Decosterd I | 1999 | Proe Natl Aead Sei U S A1999，96，16： | 1 |
| 12 | A Multi-Dimensional Study of Trust in Organizations 显示文摘 | COSTIGAN R D LLTER S S BERMAN J J | 1998 | Journal of Managerial Issues1998，10，3： | 1 |
| 13 | Slug flow regime identification from dynamic void fraction measurements in vertical air-water flows 显示文摘 | COSTIGAN G WHALLEY P B | 1997 | International Journal of Multi-phase Flow1997，23，2： | 1 |
| 14 | Structure and transcription of a human gene for H1 RNA,the RNA component of human RNase P显示文摘 | Baer M Nilsen TW Costigan C | 1990 | Nucleic Acids Res1990，18，1： | 1 |
| 15 | The natural history of the systemic inflammatory response syndrome (SIRS),a prospective study 显示文摘 | Rangel-Frauslo MS Pitel D Costigan M | 1995 | JAMA1995，237，： | 1 |
| 16 | Neuropathic pain: a maladaptive response of the nervous system to damage 显示文摘 | Costigan M J Scholz CJ Woolf | 2009 | Annu Rev Neurosci2009，，32： | 1 |
| 17 | Knee and hip kinetics during normal stair climbing 显示文摘 | COSTIGAN P A DATRICK A DELUZIO K WYSS U P | 2002 | Gait and Posture2002，16，1： | 1 |
| 18 | The natural history of the systemic inflammatory response syndrome (SIRS),A prospective study显示文摘 | Rangel-Frausto MS Pitier D Costigan M | 1995 | JAMA1995，273，2： | 1 |
| 19 | Implementing Crypto - graphic Pairings on Smartcards显示文摘 | Scott M Costigan N Abdulwahab W | 2006 | Lecture Notes in Computer Science Cryptographic Hardware and Embedded Systems-CHES Volume2006，4249，： | 1 |
| 20 | The2010Canadian-Cardiol vascular Society guidelines for the diagnosis and man-agement of heart failure update:heart failure and pregnency,mangemengt,and quality improvement assurance programs显示文摘 | Howle JG McKelvie RS Costigan J | 2010 | Can J Cardiol2010，15，26： | 1 |
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