Research article summary (published 20 Apr 2009):

Regulation of cation channel voltage and Ca2+ dependence by multiple modulators.

Full Abstract

Ion channel regulation is key to controlling neuronal excitability. However, the extent that modulators and gating factors interact to regulate channels is less clear. For Aplysia, a nonselective cation channel plays an essential role in reproduction by driving an afterdischarge in the bag cell neurons to elicit egg-laying hormone secretion. We examined the regulation of cation channel voltage and Ca2+ dependence by protein kinase C (PKC) and inositol trisphosphate (IP3)-two prominent afterdischarge signals. In excised, inside-out patches, the channel remained open longer and reopened more often with depolarization from -90 to +30 mV. As previously reported, PKC could closely associate with the channel and increase activity at -60 mV. We now show that, following the effects of PKC, voltage dependence was shifted to the left (essentially enhanced), particularly at more negative voltages. Conversely, the voltage dependence of channels lacking PKC was shifted to the right (essentially suppressed). Predictably, activity was increased at all Ca2+ concentrations following the effects of PKC; nevertheless, Ca2+ dependence was actually shifted to the right. Moreover, whereas IP3 did not alter activity at -60 mV, it drastically shifted Ca2+ dependence to the right-an outcome largely reversed by PKC. With respect to the afterdischarge, these data suggest PKC initially upregulates the channel by direct gating and shifting voltage dependence to the left. Subsequently, PKC and IP3 attenuate the channel by suppressing Ca2+ dependence. This ensures hormone delivery by allowing afterdischarge initiation and maintenance but also prevents interminable bursting. Similar regulatory interactions may be used by other neurons to achieve diverse outputs.

Author information

Author/s: Gardam, Kate E (KE); Magoski, Neil S (NS);

Affiliation: Queen's University, Department of Physiology, 4th Floor, Botterell Hall, 18 Stuart St., Kingston, ON K7L 3N6, Canada.

Journal and publication information

Publication Type: Journal Article; Research Support, Non-U.S. Gov't

Journal: Journal of neurophysiology (J Neurophysiol), published in United States. (Language: eng)

Reference: 2009-Jul; vol 102 (issue 1) : pp 259-71

Dates: Created 2009/06/30; Completed 2009/09/10;

PMID: 19386758, status: MEDLINE (last retrieved date: 9/10/2009)

Sourced from the National Library of Medicine. Abstract text and other information may be subject to copyright.

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MeSH headings (categories)

This article was linked to the MeSH Headings (categories) shown below.

Adenosine Triphosphate - pharmacology Adenylyl Imidodiphosphate - pharmacology Analysis of Variance Animals Aplysia Biophysical Processes - drug effects; physiology Calcium - pharmacology Cations - metabolism; pharmacology Cells, Cultured Dose-Response Relationship, Drug Drug Interactions

Drug Interactions Electric Conductivity Electric Stimulation Inositol 1,4,5-Trisphosphate - pharmacology Ion Channel Gating - drug effects; physiology Ion Channels - physiology Membrane Potentials - drug effects; physiology Models, Biological Neurons - drug effects; physiology Patch-Clamp Techniques - methods Protein Kinase C - pharmacology

Note: Bold headings indicate primary MeSH headings or qualifiers.

Associated Chemicals: Cations (0) ; Ion Channels (0) ; Adenylyl Imidodiphosphate (25612-73-1) ; Adenosine Triphosphate (56-65-5) ; Calcium (7440-70-2) ; Inositol 1,4,5-Trisphosphate (85166-31-0) ; Protein Kinase C (EC 2.7.11.13)

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