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The Journal of Neuroscience, May 11, 2005, 25(19):4793-4800; doi:10.1523/JNEUROSCI.5256-04.2005

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Behavioral/Systems/Cognitive
Inhibition of Conditioned Stimulus Pathway Phosphoprotein 24 Expression Blocks the Reduction in A-Type Transient K⁺ Current Produced by One-Trial In Vitro Conditioning of Hermissenda

Ebenezer N. Yamoah,¹ Snezana Levic,¹ John B. Redell,² and Terry Crow³

¹Center for Neuroscience, Department of Otolaryngology, University of California, Davis, California 95616, and ²Vivian L. Smith Center for Neurologic Research and ³Department of Neurobiology and Anatomy, University of Texas Medical School, Houston, Texas 77225

Long-term intrinsic enhanced excitability is a characteristic of cellular plasticity and learning-dependent modifications in the activity of neural networks. The regulation of voltage-dependent K⁺ channels by phosphorylation/dephosphorylation and their localization is proposed to be important in the control of cellular plasticity. One-trial conditioning in Hermissenda results in enhanced excitability in sensory neurons, type B photoreceptors, of the conditioned stimulus pathway. Conditioning also regulates the phosphorylation of conditioned stimulus pathway phosphoprotein 24 (Csp24), a cytoskeletal-related protein containing multiple -thymosin-like domains. Recently, it was shown that the downregulation of Csp24 expression mediated by an antisense oligonucleotide blocked the development of enhanced excitability in identified type B photoreceptors after one-trial conditioning without affecting short-term excitability. Here, we show using whole-cell patch recordings that one-trial in vitro conditioning applied to isolated photoreceptors produces a significant reduction in the amplitude of the A-type transient K⁺ current (I_A) detected 1.5-16 h after conditioning. One-trial conditioning produced a depolarized shift in the steady-state activation curve of I_A without altering the inactivation curve. The conditioning-dependent reduction in I_A was blocked by preincubation of the photoreceptors with Csp antisense oligonucleotide. These results provide an important link between Csp24, a cytoskeletal protein, and regulation of voltage-gated ion channels associated with intrinsic enhanced excitability underlying pavlovian conditioning.

Key words: Hermissenda; Csp24; one-trial pavlovian conditioning; -thymosin repeat protein; intrinsic enhanced excitability; A-type K⁺ current

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Received Dec 23, 2004; revised April 5, 2005; accepted April 7, 2005.

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