Long-term potentiation at C-fibre synapses by low-level presynaptic activity <it>in vivo</it>
<p>Abstract</p> <p>Inflammation, trauma or nerve injury trigger low-level activity in C-fibres and may cause long-lasting hyperalgesia. Long-term potentiation (LTP) at synapses of primary afferent C-fibres is considered to underlie some forms of hyperalgesia. In previous studies, h...
| Main Authors: | , |
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| Format: | Article |
| Language: | English |
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SAGE Publishing
2008-05-01
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| Series: | Molecular Pain |
| Online Access: | http://www.molecularpain.com/content/4/1/18 |
| _version_ | 1818039826643943424 |
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| author | Sandkühler Jürgen Drdla Ruth |
| author_facet | Sandkühler Jürgen Drdla Ruth |
| author_sort | Sandkühler Jürgen |
| collection | DOAJ |
| description | <p>Abstract</p> <p>Inflammation, trauma or nerve injury trigger low-level activity in C-fibres and may cause long-lasting hyperalgesia. Long-term potentiation (LTP) at synapses of primary afferent C-fibres is considered to underlie some forms of hyperalgesia. In previous studies, high- but not low-frequency conditioning stimulation of C-fibres has, however, been used to induce LTP in pain pathways. Recently we could show that also conditioning low-frequency stimulation (LFS) at C-fibre intensity induces LTP <it>in vitro </it>as well as in the intact animal, i.e. with tonic descending inhibition fully active. In the slice preparation, this form of LTP requires a rise in postsynaptic Ca<sup>2+</sup>-concentration and activation of Ca<sup>2+</sup>-dependent signalling pathways. Here, we investigated the signalling mechanisms underlying this novel form of LTP <it>in vivo</it>. We found that the signal transduction pathways causing LFS-induced LTP <it>in vivo </it>include activation of neurokinin 1 and N-methyl-D-aspartate receptors, rise of [Ca<sup>2+</sup>]<sub>i </sub>from intracellular stores and via T-type voltage-dependent Ca<sup>2+ </sup>channels, activation of phospholipase C, protein kinase C and Ca<sup>2+</sup>-calmodulin dependent kinase II. These pathways match those leading to hyperalgesia in behaving animals and humans. We thus propose that LTP induced by low-level activity in C-fibres may underlie some forms of hyperalgesia.</p> |
| first_indexed | 2024-12-10T08:04:48Z |
| format | Article |
| id | doaj.art-dab6ee88392d43ce94d1deee007bcf24 |
| institution | Directory Open Access Journal |
| issn | 1744-8069 |
| language | English |
| last_indexed | 2024-12-10T08:04:48Z |
| publishDate | 2008-05-01 |
| publisher | SAGE Publishing |
| record_format | Article |
| series | Molecular Pain |
| spelling | doaj.art-dab6ee88392d43ce94d1deee007bcf242022-12-22T01:56:42ZengSAGE PublishingMolecular Pain1744-80692008-05-01411810.1186/1744-8069-4-18Long-term potentiation at C-fibre synapses by low-level presynaptic activity <it>in vivo</it>Sandkühler JürgenDrdla Ruth<p>Abstract</p> <p>Inflammation, trauma or nerve injury trigger low-level activity in C-fibres and may cause long-lasting hyperalgesia. Long-term potentiation (LTP) at synapses of primary afferent C-fibres is considered to underlie some forms of hyperalgesia. In previous studies, high- but not low-frequency conditioning stimulation of C-fibres has, however, been used to induce LTP in pain pathways. Recently we could show that also conditioning low-frequency stimulation (LFS) at C-fibre intensity induces LTP <it>in vitro </it>as well as in the intact animal, i.e. with tonic descending inhibition fully active. In the slice preparation, this form of LTP requires a rise in postsynaptic Ca<sup>2+</sup>-concentration and activation of Ca<sup>2+</sup>-dependent signalling pathways. Here, we investigated the signalling mechanisms underlying this novel form of LTP <it>in vivo</it>. We found that the signal transduction pathways causing LFS-induced LTP <it>in vivo </it>include activation of neurokinin 1 and N-methyl-D-aspartate receptors, rise of [Ca<sup>2+</sup>]<sub>i </sub>from intracellular stores and via T-type voltage-dependent Ca<sup>2+ </sup>channels, activation of phospholipase C, protein kinase C and Ca<sup>2+</sup>-calmodulin dependent kinase II. These pathways match those leading to hyperalgesia in behaving animals and humans. We thus propose that LTP induced by low-level activity in C-fibres may underlie some forms of hyperalgesia.</p>http://www.molecularpain.com/content/4/1/18 |
| spellingShingle | Sandkühler Jürgen Drdla Ruth Long-term potentiation at C-fibre synapses by low-level presynaptic activity <it>in vivo</it> Molecular Pain |
| title | Long-term potentiation at C-fibre synapses by low-level presynaptic activity <it>in vivo</it> |
| title_full | Long-term potentiation at C-fibre synapses by low-level presynaptic activity <it>in vivo</it> |
| title_fullStr | Long-term potentiation at C-fibre synapses by low-level presynaptic activity <it>in vivo</it> |
| title_full_unstemmed | Long-term potentiation at C-fibre synapses by low-level presynaptic activity <it>in vivo</it> |
| title_short | Long-term potentiation at C-fibre synapses by low-level presynaptic activity <it>in vivo</it> |
| title_sort | long term potentiation at c fibre synapses by low level presynaptic activity it in vivo it |
| url | http://www.molecularpain.com/content/4/1/18 |
| work_keys_str_mv | AT sandkuhlerjurgen longtermpotentiationatcfibresynapsesbylowlevelpresynapticactivityitinvivoit AT drdlaruth longtermpotentiationatcfibresynapsesbylowlevelpresynapticactivityitinvivoit |