{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,4]],"date-time":"2026-10-04T05:23:19Z","timestamp":1791091399013,"version":"4.1.0"},"reference-count":80,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal of Neurophysiology"],"published-print":{"date-parts":[[1998,3,1]]},"abstract":"<jats:p>Reeve, Alison J., Anthony H. Dickenson, and Nicola C. Kerr. Spinal effects of bicuculline: modulation of an allodynia-like state by an A<jats:sub>1<\/jats:sub>-receptor agonist, morphine, and an NMDA-receptor antagonist. J. Neurophysiol. 79: 1494\u20131507, 1998. Single-unit recordings were made in the intact anesthetized rat of the responses of dorsal horn neurons to C-, A\u03b4-, and A\u03b2-fiber stimulation. The postdischarge and windup responses of the same cells along with responses to innocuous stimuli, prod and brush, also were measured. The effects of (\u2212)-bicuculline-methobromide (0.5, 5, 50, and 250 \u03bcg) were observed on these neuronal responses. The C- and A\u03b4-fiber\u2013evoked responses were facilitated significantly in a dose-dependent manner. The input was facilitated, but as the final overall response was not increased by the same factor, windup appeared to be reduced. However, postdischarge, resulting from the increase in the excitability produced by windup, tended to be facilitated. After doses of \u22655 \u03bcg bicuculline, stimulation at suprathreshold A\u03b2-fiber\u2013evoked activity caused enhanced firing, mainly at later latencies corresponding to A\u03b4-fiber\u2013evoked activity in normal animals. Few cells responded consistently to brush and so no significant change was observed. Responses evoked by innocuous pressure (prod) always were observed in cells that concurrently responded to electrical stimulation with a C-fiber response. This tactile response was facilitated significantly by bicuculline. The effects of N<jats:sup>6<\/jats:sup>-cyclopentyladenosine (N<jats:sup>6<\/jats:sup>-CPA), an adenosine A<jats:sub>1<\/jats:sub>-receptor agonist, was observed after pretreatment with 50 \u03bcg bicuculline, as were the effects of morphine and 7-chlorokynurenate (7-CK). N<jats:sup>6<\/jats:sup>-CPA inhibited prod, C- and A\u03b4-fiber\u2013evoked responses as well as the initial and overall final response to the train of C-fiber strength stimuli. Inhibitions were reversed with 8(p-sulphophenyl) theophylline. Morphine, the mu-receptor agonist, also inhibited the postbicuculline responses to prod, C-, and A\u03b4-fiber responses and initial and final responses to a train of stimuli. Inhibitory effects of morphine were reversed partly by naloxone. 7-CK, an antagonist at the glycine site on the N-methyl-d-aspartate-receptor complex, inhibited the responses to C- and A\u03b4-fiber\u2013evoked activity as well as prod. The postdischarges were inhibited by this drug. Again both the initial and overall responses of the cell were inhibited. To conclude, bicuculline caused an increase in the responses of deep dorsal horn cells to prod, A\u03b4-fiber\u2013evoked activity, increased C-fiber input onto these cells along with the appearance of responses at latencies normally associated with A\u03b4 fibers, but evoked by suprathreshold A\u03b2-fiber stimulation. These alterations may be responsible for some aspects of the clinical phenomenon of allodynia and hyperalgesia. These altered and enhanced responses were modulated by the three separate classes of drugs, the order of effectiveness being 7-CK, N<jats:sup>6<\/jats:sup>-CPA, and then morphine.<\/jats:p>","DOI":"10.1152\/jn.1998.79.3.1494","type":"journal-article","created":{"date-parts":[[2017,12,25]],"date-time":"2017-12-25T07:08:18Z","timestamp":1514185698000},"page":"1494-1507","source":"Crossref","is-referenced-by-count":44,"title":["Spinal Effects of Bicuculline: Modulation of an Allodynia-Like State by an A<sub>1<\/sub>-Receptor Agonist, Morphine, and an NMDA-Receptor Antagonist"],"prefix":"10.1152","volume":"79","author":[{"given":"Alison J.","family":"Reeve","sequence":"first","affiliation":[{"name":"Department of Pharmacology, University College London, London WC1E 6BT, United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anthony H.","family":"Dickenson","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, University College London, London WC1E 6BT, United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nicola C.","family":"Kerr","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, University College London, London WC1E 6BT, United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.12-08-02901.1992"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1016\/0304-3959(88)90198-4"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.1994.sp020232"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1016\/0304-3959(94)90149-X"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1016\/0006-8993(78)90615-7"},{"key":"B6","first-page":"713","volume":"81","author":"Belfrage M.","year":"1995","journal-title":"Anesth. 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