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Role for Calcium Signaling and Arachidonic Acid Metabolites in the Activity-Dependent Increase of AHP Amplitude in Leech T Sensory Neurons
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| Zeitschriftentitel: | Journal of Neurophysiology |
|---|---|
| Personen und Körperschaften: | , , |
| In: | Journal of Neurophysiology, 94, 2005, 2, S. 1066-1073 |
| Format: | E-Article |
| Sprache: | Englisch |
| veröffentlicht: |
American Physiological Society
|
| Schlagwörter: |
| author_facet |
Scuri, Rossana Mozzachiodi, Riccardo Brunelli, Marcello Scuri, Rossana Mozzachiodi, Riccardo Brunelli, Marcello |
|---|---|
| author |
Scuri, Rossana Mozzachiodi, Riccardo Brunelli, Marcello |
| spellingShingle |
Scuri, Rossana Mozzachiodi, Riccardo Brunelli, Marcello Journal of Neurophysiology Role for Calcium Signaling and Arachidonic Acid Metabolites in the Activity-Dependent Increase of AHP Amplitude in Leech T Sensory Neurons Physiology General Neuroscience |
| author_sort |
scuri, rossana |
| spelling |
Scuri, Rossana Mozzachiodi, Riccardo Brunelli, Marcello 0022-3077 1522-1598 American Physiological Society Physiology General Neuroscience http://dx.doi.org/10.1152/jn.00075.2005 <jats:p>Previous studies have revealed a new form of activity-dependent modulation of the afterhyperpolarization (AHP) in tactile (T) neurons of the leech Hirudo medicinalis. The firing of T cells is characterized by an AHP, which is mainly due to the activity of the Na<jats:sup>+</jats:sup>/K<jats:sup>+</jats:sup>ATPase. Low-frequency repetitive stimulation of T neurons leads to a robust increment of the AHP amplitude, which is correlated with a synaptic depression between T neuron and follower cells. In the present study, we explored the molecular cascades underlying the AHP increase. We tested the hypothesis that this activity-dependent phenomenon was triggered by calcium influx during neural activity by applying blockers of voltage-dependent Ca<jats:sup>2+</jats:sup>channels. We report that AHP increase requires calcium influx that, in turn, induces release of calcium from intracellular stores so sustaining the enhancement of AHP. An elevation of the intracellular calcium can activate the cytosolic isoforms of the phosholipase A2 (PLA2). Therefore we analyzed the role of PLA2 in the increase of the AHP, and we provide evidence that not only PLA2 but also the recruitment of arachidonic acid metabolites generated by the 5-lipoxygenase pathway are necessary for the induction of AHP increase. These data indicate that a sophisticated cascade of intracellular signals links the repetitive discharge of T neurons to the activation of molecular pathways, which finally may alter the activity of critical enzymes such as the Na<jats:sup>+</jats:sup>/K<jats:sup>+</jats:sup>ATPase, that sustains the generation of the AHP and its increase during repetitive stimulation. These results also suggest the potential importance of the poorly studied 5-lipoxygenase pathway in forms of neuronal plasticity.</jats:p> Role for Calcium Signaling and Arachidonic Acid Metabolites in the Activity-Dependent Increase of AHP Amplitude in Leech T Sensory Neurons Journal of Neurophysiology |
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| title |
Role for Calcium Signaling and Arachidonic Acid Metabolites in the Activity-Dependent Increase of AHP Amplitude in Leech T Sensory Neurons |
| title_unstemmed |
Role for Calcium Signaling and Arachidonic Acid Metabolites in the Activity-Dependent Increase of AHP Amplitude in Leech T Sensory Neurons |
| title_full |
Role for Calcium Signaling and Arachidonic Acid Metabolites in the Activity-Dependent Increase of AHP Amplitude in Leech T Sensory Neurons |
| title_fullStr |
Role for Calcium Signaling and Arachidonic Acid Metabolites in the Activity-Dependent Increase of AHP Amplitude in Leech T Sensory Neurons |
| title_full_unstemmed |
Role for Calcium Signaling and Arachidonic Acid Metabolites in the Activity-Dependent Increase of AHP Amplitude in Leech T Sensory Neurons |
| title_short |
Role for Calcium Signaling and Arachidonic Acid Metabolites in the Activity-Dependent Increase of AHP Amplitude in Leech T Sensory Neurons |
| title_sort |
role for calcium signaling and arachidonic acid metabolites in the activity-dependent increase of ahp amplitude in leech t sensory neurons |
| topic |
Physiology General Neuroscience |
| url |
http://dx.doi.org/10.1152/jn.00075.2005 |
| publishDate |
2005 |
| physical |
1066-1073 |
| description |
<jats:p>Previous studies have revealed a new form of activity-dependent modulation of the afterhyperpolarization (AHP) in tactile (T) neurons of the leech Hirudo medicinalis. The firing of T cells is characterized by an AHP, which is mainly due to the activity of the Na<jats:sup>+</jats:sup>/K<jats:sup>+</jats:sup>ATPase. Low-frequency repetitive stimulation of T neurons leads to a robust increment of the AHP amplitude, which is correlated with a synaptic depression between T neuron and follower cells. In the present study, we explored the molecular cascades underlying the AHP increase. We tested the hypothesis that this activity-dependent phenomenon was triggered by calcium influx during neural activity by applying blockers of voltage-dependent Ca<jats:sup>2+</jats:sup>channels. We report that AHP increase requires calcium influx that, in turn, induces release of calcium from intracellular stores so sustaining the enhancement of AHP. An elevation of the intracellular calcium can activate the cytosolic isoforms of the phosholipase A2 (PLA2). Therefore we analyzed the role of PLA2 in the increase of the AHP, and we provide evidence that not only PLA2 but also the recruitment of arachidonic acid metabolites generated by the 5-lipoxygenase pathway are necessary for the induction of AHP increase. These data indicate that a sophisticated cascade of intracellular signals links the repetitive discharge of T neurons to the activation of molecular pathways, which finally may alter the activity of critical enzymes such as the Na<jats:sup>+</jats:sup>/K<jats:sup>+</jats:sup>ATPase, that sustains the generation of the AHP and its increase during repetitive stimulation. These results also suggest the potential importance of the poorly studied 5-lipoxygenase pathway in forms of neuronal plasticity.</jats:p> |
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| author | Scuri, Rossana, Mozzachiodi, Riccardo, Brunelli, Marcello |
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| description | <jats:p>Previous studies have revealed a new form of activity-dependent modulation of the afterhyperpolarization (AHP) in tactile (T) neurons of the leech Hirudo medicinalis. The firing of T cells is characterized by an AHP, which is mainly due to the activity of the Na<jats:sup>+</jats:sup>/K<jats:sup>+</jats:sup>ATPase. Low-frequency repetitive stimulation of T neurons leads to a robust increment of the AHP amplitude, which is correlated with a synaptic depression between T neuron and follower cells. In the present study, we explored the molecular cascades underlying the AHP increase. We tested the hypothesis that this activity-dependent phenomenon was triggered by calcium influx during neural activity by applying blockers of voltage-dependent Ca<jats:sup>2+</jats:sup>channels. We report that AHP increase requires calcium influx that, in turn, induces release of calcium from intracellular stores so sustaining the enhancement of AHP. An elevation of the intracellular calcium can activate the cytosolic isoforms of the phosholipase A2 (PLA2). Therefore we analyzed the role of PLA2 in the increase of the AHP, and we provide evidence that not only PLA2 but also the recruitment of arachidonic acid metabolites generated by the 5-lipoxygenase pathway are necessary for the induction of AHP increase. These data indicate that a sophisticated cascade of intracellular signals links the repetitive discharge of T neurons to the activation of molecular pathways, which finally may alter the activity of critical enzymes such as the Na<jats:sup>+</jats:sup>/K<jats:sup>+</jats:sup>ATPase, that sustains the generation of the AHP and its increase during repetitive stimulation. These results also suggest the potential importance of the poorly studied 5-lipoxygenase pathway in forms of neuronal plasticity.</jats:p> |
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| spelling | Scuri, Rossana Mozzachiodi, Riccardo Brunelli, Marcello 0022-3077 1522-1598 American Physiological Society Physiology General Neuroscience http://dx.doi.org/10.1152/jn.00075.2005 <jats:p>Previous studies have revealed a new form of activity-dependent modulation of the afterhyperpolarization (AHP) in tactile (T) neurons of the leech Hirudo medicinalis. The firing of T cells is characterized by an AHP, which is mainly due to the activity of the Na<jats:sup>+</jats:sup>/K<jats:sup>+</jats:sup>ATPase. Low-frequency repetitive stimulation of T neurons leads to a robust increment of the AHP amplitude, which is correlated with a synaptic depression between T neuron and follower cells. In the present study, we explored the molecular cascades underlying the AHP increase. We tested the hypothesis that this activity-dependent phenomenon was triggered by calcium influx during neural activity by applying blockers of voltage-dependent Ca<jats:sup>2+</jats:sup>channels. We report that AHP increase requires calcium influx that, in turn, induces release of calcium from intracellular stores so sustaining the enhancement of AHP. An elevation of the intracellular calcium can activate the cytosolic isoforms of the phosholipase A2 (PLA2). Therefore we analyzed the role of PLA2 in the increase of the AHP, and we provide evidence that not only PLA2 but also the recruitment of arachidonic acid metabolites generated by the 5-lipoxygenase pathway are necessary for the induction of AHP increase. These data indicate that a sophisticated cascade of intracellular signals links the repetitive discharge of T neurons to the activation of molecular pathways, which finally may alter the activity of critical enzymes such as the Na<jats:sup>+</jats:sup>/K<jats:sup>+</jats:sup>ATPase, that sustains the generation of the AHP and its increase during repetitive stimulation. These results also suggest the potential importance of the poorly studied 5-lipoxygenase pathway in forms of neuronal plasticity.</jats:p> Role for Calcium Signaling and Arachidonic Acid Metabolites in the Activity-Dependent Increase of AHP Amplitude in Leech T Sensory Neurons Journal of Neurophysiology |
| spellingShingle | Scuri, Rossana, Mozzachiodi, Riccardo, Brunelli, Marcello, Journal of Neurophysiology, Role for Calcium Signaling and Arachidonic Acid Metabolites in the Activity-Dependent Increase of AHP Amplitude in Leech T Sensory Neurons, Physiology, General Neuroscience |
| title | Role for Calcium Signaling and Arachidonic Acid Metabolites in the Activity-Dependent Increase of AHP Amplitude in Leech T Sensory Neurons |
| title_full | Role for Calcium Signaling and Arachidonic Acid Metabolites in the Activity-Dependent Increase of AHP Amplitude in Leech T Sensory Neurons |
| title_fullStr | Role for Calcium Signaling and Arachidonic Acid Metabolites in the Activity-Dependent Increase of AHP Amplitude in Leech T Sensory Neurons |
| title_full_unstemmed | Role for Calcium Signaling and Arachidonic Acid Metabolites in the Activity-Dependent Increase of AHP Amplitude in Leech T Sensory Neurons |
| title_short | Role for Calcium Signaling and Arachidonic Acid Metabolites in the Activity-Dependent Increase of AHP Amplitude in Leech T Sensory Neurons |
| title_sort | role for calcium signaling and arachidonic acid metabolites in the activity-dependent increase of ahp amplitude in leech t sensory neurons |
| title_unstemmed | Role for Calcium Signaling and Arachidonic Acid Metabolites in the Activity-Dependent Increase of AHP Amplitude in Leech T Sensory Neurons |
| topic | Physiology, General Neuroscience |
| url | http://dx.doi.org/10.1152/jn.00075.2005 |