Serotonergic modulation of afterhyperpolarization in a neuron that contributes to learning in the leech
Journal of Neurophysiology, ISSN: 0022-3077, Vol: 99, Issue: 2, Page: 605-616
2008
- 13Citations
- 31Captures
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Metrics Details
- Citations13
- Citation Indexes13
- 13
- CrossRef9
- Captures31
- Readers31
- 31
Article Description
Modulation of afterhyperpolarization (AHP) represents an important mechanism by which excitability of a neuron can be regulated. In the leech brain, sensitization enhances excitability of the S-cell, an interneuron thought to play an important role in this form of nonassociative learning. This increase in excitability is serotonin (5-HT) dependent, but it is not known whether changes in AHP contribute to 5-HT-mediated enhancement of excitability. Therefore electrophysiological recordings and computational modeling were used to determine whether 5-HT enhances excitability via modulation of AHP. 5-HT reduced S-cell AHP and this decrease in the AHP corresponded with an increase in excitability. Little or no AHP is observed in the presence of Ca -free saline, suggesting the involvement of Ca- dependent K channels. Furthermore, AHP amplitude decreased following treatment with drugs (tubocurare and charybdotoxin) that block Ca -dependent K channel activity. The S-cell also exhibits an afterdepolarization (ADP), which is usually masked by the AHP, and was inhibited by the Na channel blocker saxitoxin. A model of the S-cell AHP was constructed using two Ca-dependent K currents and a Na-driven ADP current. Reduction of the model conductances underlying the AHP to mimic the effects of 5-HT was sufficient to enhance excitability. These findings were confirmed in occlusion experiments in which pretreatment with tubocurare was able to block 5-HT-mediated decreases in mAHP levels and increases in excitability. These data show that modulation of S-cell AHP can contribute to 5-HT-mediated increases in excitability and that the S-cell afterpotential is due to the combined effects of AHP- and ADP-producing currents. Copyright © 2008 The American Physiological Society.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=39149124098&origin=inward; http://dx.doi.org/10.1152/jn.00989.2007; http://www.ncbi.nlm.nih.gov/pubmed/18046001; https://www.physiology.org/doi/10.1152/jn.00989.2007; http://www.physiology.org/doi/10.1152/jn.00989.2007; https://www.physiology.org/action/captchaChallenge?redirectUrl=https%3A%2F%2Fwww.physiology.org%2Fdoi%2Ffull%2F10.1152%2Fjn.00989.2007
American Physiological Society
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