ALBERT

All Library Books, journals and Electronic Records Telegrafenberg

X
feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    facet.materialart.
    Unknown
    Corelease of two fast neurotransmitters at a central synapse (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-07-17
    Description: It is widely accepted that individual neurons in the central nervous system release only a single fast transmitter. The possibility of corelease of fast neurotransmitters was examined by making paired recordings from synaptically connected neurons in spinal cord slices. Unitary inhibitory postsynaptic currents generated at interneuron-motoneuron synapses consisted of a strychnine-sensitive, glycine receptor-mediated component and a bicuculline-sensitive, gamma-aminobutyric acid (GABA)A receptor-mediated component. These results indicate that spinal interneurons release both glycine and GABA to activate functionally distinct receptors in their postsynaptic target cells. A subset of miniature synaptic currents also showed both components, consistent with corelease from individual synaptic vesicles.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jonas, P -- Bischofberger, J -- Sandkuhler, J -- New York, N.Y. -- Science. 1998 Jul 17;281(5375):419-24.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Physiologisches Institut der Universitat Freiburg, D-79104 Freiburg, Germany. jonasp@ruf.uni-freiburg.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9665886" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Baclofen/pharmacology ; Bicuculline/pharmacology ; GABA Antagonists ; GABA-A Receptor Antagonists ; GABA-B Receptor Antagonists ; Glycine/*metabolism ; Glycine Agents/pharmacology ; In Vitro Techniques ; Interneurons/drug effects/*metabolism ; Motor Neurons/drug effects/*metabolism ; Patch-Clamp Techniques ; Presynaptic Terminals/*metabolism ; Rats ; Rats, Wistar ; Receptors, GABA-A/metabolism ; Receptors, GABA-B/metabolism ; Receptors, Glycine/antagonists & inhibitors/metabolism ; Spinal Cord/cytology ; Strychnine/pharmacology ; Synaptic Transmission/drug effects ; Synaptic Vesicles/metabolism ; gamma-Aminobutyric Acid/*metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 2
    facet.materialart.
    Unknown
    Erasure of a spinal memory trace of pain by a brief, high-dose opioid administration (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-01-17
    Description: Painful stimuli activate nociceptive C fibers and induce synaptic long-term potentiation (LTP) at their spinal terminals. LTP at C-fiber synapses represents a cellular model for pain amplification (hyperalgesia) and for a memory trace of pain. mu-Opioid receptor agonists exert a powerful but reversible depression at C-fiber synapses that renders the continuous application of low opioid doses the gold standard in pain therapy. We discovered that brief application of a high opioid dose reversed various forms of activity-dependent LTP at C-fiber synapses. Depotentiation involved Ca(2+)-dependent signaling and normalization of the phosphorylation state of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors. This also reversed hyperalgesia in behaving animals. Opioids thus not only temporarily dampen pain but may also erase a spinal memory trace of pain.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Drdla-Schutting, Ruth -- Benrath, Justus -- Wunderbaldinger, Gabriele -- Sandkuhler, Jurgen -- New York, N.Y. -- Science. 2012 Jan 13;335(6065):235-8. doi: 10.1126/science.1211726.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurophysiology, Center for Brain Research, Medical University of Vienna, A-1090 Vienna, Austria.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22246779" target="_blank"〉PubMed〈/a〉
    Keywords: Analgesics, Opioid/*administration & dosage ; Animals ; Calcium Signaling ; Evoked Potentials ; Hyperalgesia/chemically induced/drug therapy ; Long-Term Potentiation/*drug effects ; Male ; Naloxone/administration & dosage ; Nerve Fibers, Unmyelinated/*drug effects/physiology ; Nociceptive Pain/*drug therapy/physiopathology ; Phosphorylation ; Piperidines/*administration & dosage ; Protein Kinase C/antagonists & inhibitors/metabolism ; Protein Phosphatase 1/antagonists & inhibitors/metabolism ; Rats ; Rats, Sprague-Dawley ; Receptors, AMPA/metabolism ; Receptors, Opioid, mu/agonists/metabolism ; Sciatic Nerve/*drug effects/physiology ; Somatostatin/administration & dosage/analogs & derivatives ; Spinal Cord/physiology ; Synapses/*drug effects/physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 3
    facet.materialart.
    Unknown
    Synaptic plasticity in spinal lamina I projection neurons that mediate hyperalgesia (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-02-22
    Description: Inflammation, trauma, or nerve injury may cause enduring hyperalgesia, an enhanced sensitivity to painful stimuli. Neurons in lamina I of the spinal dorsal horn that express the neurokinin 1 receptor for substance P mediate this abnormal pain sensitivity by an unknown cellular mechanism. We report that in these, but not in other nociceptive lamina I cells, neurokinin 1 receptor-activated signal transduction pathways and activation of low-threshold (T-type) voltage-gated calcium channels synergistically facilitate activity- and calcium-dependent long-term potentiation at synapses from nociceptive nerve fibers. Thereby, memory traces of painful events are retained.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ikeda, Hiroshi -- Heinke, Bernhard -- Ruscheweyh, Ruth -- Sandkuhler, Jurgen -- New York, N.Y. -- Science. 2003 Feb 21;299(5610):1237-40.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Physiology and Pathophysiology, Heidelberg University, D-69120 Heidelberg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12595694" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials/drug effects ; Animals ; Calcium/metabolism ; Calcium Channels, T-Type/*metabolism ; Excitatory Postsynaptic Potentials ; Hyperalgesia/*physiopathology ; Ion Channel Gating ; *Long-Term Potentiation ; Membrane Potentials ; Nerve Fibers, Unmyelinated/physiology ; Neurokinin-1 Receptor Antagonists ; Nickel/pharmacology ; Patch-Clamp Techniques ; Posterior Horn Cells/metabolism/*physiology ; Quinuclidines/pharmacology ; Rats ; Rats, Sprague-Dawley ; Receptors, N-Methyl-D-Aspartate/metabolism ; Receptors, Neurokinin-1/*metabolism ; Signal Transduction ; Substance P/pharmacology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 4
    facet.materialart.
    Unknown
    Synaptic amplifier of inflammatory pain in the spinal dorsal horn (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-06-17
    Description: Inflammation and trauma lead to enhanced pain sensitivity (hyperalgesia), which is in part due to altered sensory processing in the spinal cord. The synaptic hypothesis of hyperalgesia, which postulates that hyperalgesia is induced by the activity-dependent long-term potentiation (LTP) in the spinal cord, has been challenged, because in previous studies of pain pathways, LTP was experimentally induced by nerve stimulation at high frequencies ( approximately 100 hertz). This does not, however, resemble the real low-frequency afferent barrage that occurs during inflammation. We identified a synaptic amplifier at the origin of an ascending pain pathway that is switched-on by low-level activity in nociceptive nerve fibers. This model integrates known signal transduction pathways of hyperalgesia without contradiction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ikeda, Hiroshi -- Stark, Johanna -- Fischer, Harald -- Wagner, Matthias -- Drdla, Ruth -- Jager, Tino -- Sandkuhler, Jurgen -- P 18129/Austrian Science Fund FWF/Austria -- New York, N.Y. -- Science. 2006 Jun 16;312(5780):1659-62.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurophysiology, Center for Brain Research, Medical University of Vienna, Vienna, Austria.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16778058" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/metabolism ; Electric Stimulation ; Excitatory Postsynaptic Potentials ; Hyperalgesia/*physiopathology ; Inflammation/*physiopathology ; Long-Term Potentiation ; Nerve Fibers, Unmyelinated/*physiology ; Neuronal Plasticity ; Nitric Oxide/physiology ; Pain/*physiopathology ; Patch-Clamp Techniques ; Periaqueductal Gray/physiology ; Posterior Horn Cells/*physiopathology ; Rats ; Rats, Sprague-Dawley ; Signal Transduction ; Spinal Cord/physiopathology ; Synapses/physiology ; *Synaptic Transmission
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 5
    facet.materialart.
    Unknown
    Induction of synaptic long-term potentiation after opioid withdrawal (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-07-11
    Description: mu-Opioid receptor (MOR) agonists represent the gold standard for the treatment of severe pain but may paradoxically also enhance pain sensitivity, that is, lead to opioid-induced hyperalgesia (OIH). We show that abrupt withdrawal from MOR agonists induces long-term potentiation (LTP) at the first synapse in pain pathways. Induction of opioid withdrawal LTP requires postsynaptic activation of heterotrimeric guanine nucleotide-binding proteins and N-methyl-d-aspartate receptors and a rise of postsynaptic calcium concentrations. In contrast, the acute depression by opioids is induced presynaptically at these synapses. Withdrawal LTP can be prevented by tapered withdrawal and shares pharmacology and signal transduction pathways with OIH. These findings provide a previously unrecognized target to selectively combat pro-nociceptive effects of opioids without compromising opioid analgesia.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Drdla, Ruth -- Gassner, Matthias -- Gingl, Ewald -- Sandkuhler, Jurgen -- P 18129/Austrian Science Fund FWF/Austria -- New York, N.Y. -- Science. 2009 Jul 10;325(5937):207-10. doi: 10.1126/science.1171759.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurophysiology, Center for Brain Research, Medical University of Vienna, Spitalgasse 4, 1090 Vienna, Austria.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19590003" target="_blank"〉PubMed〈/a〉
    Keywords: Analgesics, Opioid/administration & dosage/*adverse effects/pharmacology ; Animals ; Calcium/metabolism ; Enkephalin, Ala(2)-MePhe(4)-Gly(5)-/administration & dosage/adverse ; effects/pharmacology ; Evoked Potentials ; GTP-Binding Proteins/metabolism ; Hyperalgesia/chemically induced ; *Long-Term Potentiation/drug effects ; Male ; Nerve Fibers, Unmyelinated/physiology ; Patch-Clamp Techniques ; Piperidines/administration & dosage/adverse effects/pharmacology ; Posterior Horn Cells/drug effects/physiology ; Rats ; Rats, Sprague-Dawley ; Receptors, N-Methyl-D-Aspartate/metabolism ; Receptors, Opioid, mu/*agonists ; Signal Transduction ; Substance Withdrawal Syndrome/*physiopathology ; Synapses/drug effects/*physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...