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The Journal of Neuroscience, August 31, 2005, 25(35):8037-8047; doi:10.1523/JNEUROSCI.1903-05.2005

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Cellular/Molecular
Association/Dissociation of a Channel–Kinase Complex Underlies State-Dependent Modulation

Neil S. Magoski¹ and Leonard K. Kaczmarek²

¹Department of Physiology, Queen's University, Kingston, Ontario, Canada K7L 3N6, and ²Department of Pharmacology, Yale University, New Haven, Connecticut 06520

Although ion channels are regulated by protein kinases, it has yet to be established whether the behavioral state of an animal may dictate whether or not modulation by a kinase can occur. Here, we describe behaviorally relevant changes in the ability of a nonselective cation channel from Aplysia bag cell neurons to be regulated by protein kinase C (PKC). This channel drives a prolonged afterdischarge that triggers the release of egg-laying hormone and a series of reproductive behaviors. The afterdischarge is followed by a lengthy refractory period, during which additional bursting cannot be elicited. Previously, we reported that, in excised inside-out patches, the cation channel is closely associated with PKC, which increases channel activity. We now show that this channel–kinase association is plastic, because channels excised from certain neurons lack PKC-dependent modulation. Although direct application of PKC-activating phorbol ester to these patches had no effect, exposing the neurons themselves to phorbol ester reinstated modulation, suggesting that an absence of modulation was attributable to a lack of associated kinase. Furthermore, modulation was restored by pretreating neurons with either PP1 [4-amino-5-(4-methylphenyl)-7-(t-butyl)pyrazolo[3,4-d]pyrimidine] or SU6656, inhibitors of Src tyrosine kinase, an enzyme whose Src homology 3 domain is required for channel–PKC association. Neurons that were stimulated to afterdischarge and had entered the prolonged refractory period were found to have more phosphotyrosine staining and less channel–PKC association than unstimulated neurons. These findings suggest that Src-dependent regulation of the association between the cation channel and PKC controls both the long-term excitability of these neurons and their ability to induce reproduction.

Key words: Aplysia; bag cell neurons; nonselective cation channel; protein kinase C; metaregulation; excitability

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Received May 12, 2005; revised July 22, 2005; accepted July 26, 2005.

This article has been cited by other articles:

				K. E. Gardam and N. S. Magoski Regulation of Cation Channel Voltage and Ca2+ Dependence by Multiple Modulators J Neurophysiol, July 1, 2009; 102(1): 259 - 271. [Abstract] [Full Text] [PDF]

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