723 research outputs found
Anticonvulsant A(1) receptor-mediated adenosine action on neuronal networks in the brainstem-spinal cord of newborn rats
No full textMembrane potential of ventral respiratory group neurons as well as inspiratory-related cranial (hypoglossal) and spinal (C-1-Th-4) nerve activities were analysed in brainstem-spinal cord preparations from neonatal rats. Block of Cl--mediated inhibition with bicuculline (plus strychnine) affected neither rhythmic depolarizations nor spike discharge in 23 of 30 ventral respiratory group cells. In the other seven neurons, block of inhibitory postsynaptic potentials evoked pronounced depolarizations and spike discharge that was synchronous with seizure-like spinal nerve activity. Respiratory hypoglossal nerve activity persisted after transection at the spinomedullary junction, whereas spinal rhythm was blocked. After transection, the moderate bicuculline-evoked seizure-like perturbation of hypoglossal nerve activity was abolished and rhythmic ventral respiratory group neuron activity was not disturbed, whereas epileptiform discharge persisted in spinal nerves. The seizure-like nerve activity and depolarization of the minor subpopulation of perturbed ventral respiratory group neurons were reversed by either adenosine or the A(1) adenosine receptor agonist 2-chloro-N-6-cyclopentyladenosine. The A(2) receptor agonist CGS 21860 had no effect, In control preparations, inspiratory nerve activity and membrane potential fluctuations (29 of 35 cells) were nor changed by adenosine, 2-chloro-N-6-cyclopentyladenosine or CGS 21860. In the other six cells, adenosine evoked a hyperpolarization (<10 mV) with no major change in input resistance. The anticonvulsant effects of adenosine and 2-chloro-N-6-cyclopentyladenosine were antagonized by the A(1) adenosine receptor blocker 8-cyclopentyl-1,3-dipropylxanthine. After pre-incubation with 8-cyclopentyl-1,3-dipropylxanthine, bicuculline also evoked seizure-like discharge in the hypoglossal nerve. The results indicate that seizure-like spinal motor output of the respiratory network upon block of Cl--mediated inhibition is caused by disinhibition of spinal neuronal networks with afferent connections to the ventral respiratory group. Presynaptic Al adenosine receptors exert an anticonvulsant action on the disinhibited spinal motor network, but have no depressing effect per se on the isolated medullary respiratory network. (C) 2000 IBRO. Published by Elsevier Science Ltd
Hencke - Juxta
No full textHENCKE - JUXTA
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J. Rosenthal: Allgemeine Physiologie der Muskeln und Nerven. 2. umgearb. Aufl. Internat. wiss. Bibl. 27. Leipzig, Brockhaus, 1899. 324 S.
No full textJ. ROSENTHAL: ALLGEMEINE PHYSIOLOGIE DER MUSKELN UND NERVEN. 2. UMGEARB. AUFL. INTERNAT. WISS. BIBL. 27. LEIPZIG, BROCKHAUS, 1899. 324 S.
Zeitschrift für Psychologie und Physiologie der Sinnesorgane (-)
Zeitschrift für Psychologie und Physiologie der Sinnesorgane (21) (a0006)
J. Rosenthal: Allgemeine Physiologie der Muskeln und Nerven. 2. umgearb. Aufl. Internat. wiss. Bibl. 27. Leipzig, Brockhaus, 1899. 324 S. (21) (p0390
How Do You Say: I Love You?
No full textSwihart JJ. Wie sage ich: "Ich liebe dich"? Hilfen für d. Gespräch mit d. Partner. R.-Brockhaus-Taschenbuch. Vol 289. Schütze SB, tran. Wuppertal: Brockhaus; 1979
Kommentar zum Titus-Brief
No full textGuthrie D, Motyer JA. Kommentar zum Titus-Brief. Schütze SB, tran.; In: Guthrie D, Motyer JA, eds. Brockhaus-Kommentar zur Bibel, Teil 4: Matthäus – Offenbarung. Wuppertal: Brockhaus; 1985
Englisches naturwissenschaftlich-technisches Lesebuch für Höhere Technische Lehranstalten und zum Selbststudium für Studirende, Lehrer, Techniker, Industrielle
No full text3.Teil Bau-Ingenieurwesenmit sprachlichen und sachlichen Erläuterungen von F. J. WershovenGeschenkexlibris-Etikette: "Geschenk aus dem Nachlasse von August Waldner." 002230365_0001 Exemplar der ETH-BIBExlibrisstempel: "Schweizerische Bauzeitung Redaction, A. Waldner, Ing. Zürich" 002194263_0001 Exemplar der ETH-BIBIndirektes handschriftliches Exlibris: "1907, 136", das ist August Waldner 002194263_0003 Exemplar der ETH-BI
Johann van Eyck und seine Nachfolger.
No full textVorlageform des Erscheinungsvermerks: Leipzig: F. A. Brockhaus. Frankfurt a. M.: J. D. Sauerländer. 1830.Europeana-GoogleBook
Putešestvie na vostok E. J. Vys. Gosudarja Naslědnika Cesarevika <dt.>
No full textOrientreise Seiner Majestät des Kaisers von Russland, Nikolaus II. als Grossfürst-Thronfolger 1890-189
ATP-independent anoxic activation of ATP-sensitive K+ channels in dorsal vagal neurons of juvenile mice in situ
No full textThe role of ATP in anoxic activation of ATP-sensitive K+ (K-ATP) channels was studied in dorsal vagal neurons of mouse brainstem slices. In the whole-cell configuration, cyanide-induced chemical anoxia evoked within 10 s a 300-pA outward current that gave rise to a hyperpolarization of 24 mV. These responses were mimicked by nitrogen-aerated saline, rotenone or diazoxide and abolished by tolbutamide. The cyanide-induced hyperpolarization was due to activation of 70 pS K-ATP channels that were half-maximally blocked by 5 muM internal ATP, Dialyzing the cells with either 1, 20 or 0 mM ATP did not, however, affect the time to onset, the kinetics or the magnitude of the cyanide-induced hyperpolarization. Impairment of ATP consumption by ouabain, vanadate or reduced temperature had no effect either. Thus, anoxia-induced activation of these K-ATP channels cannot be explained by a fall of cellular ATP or a concomitant rise of ADP. Anoxia-related changes of the actin cytoskeleton or the composition of the plasma membrane are also not likely to be involved, as cytochalasin D did not affect the cyanide-evoked hyperpolarization and phosphatidylinositol 4,5-bisphosphate failed to decrease the ATP sensitivity of single K-ATP channels. Finally, because of a lack of effects of reduced/oxidized glutathione and the oxidase blocker diphenyliodonium on the cyanide-induced hyperpolarization, cellular redox state does not appear to be involved. Our results indicate that despite a high sensitivity to ATP in excised patches, anoxic activation of K-ATP channels is independent of cellular ATP. Rather the ATP block seems to be removed as a consequence of impaired mitochondrial function. (C) 2002 IBRO. Published by Elsevier Science Ltd. All rights reserved
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