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J Neurophysiol 94: 3884-3892, 2005. First published August 10, 2005; doi:10.1152/jn.01163.2004
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Potassium Currents in Isolated Statocyst Neurons and RPeD1 in the Pond Snail, Lymnaea stagnalis

Manabu Sakakibara1, Futoshi Okuda1, Kazutoku Nomura1, Kenji Watanabe1, Hongxu Meng2, Tetsuro Horikoshi1 and Ken Lukowiak3

1Laboratory of Neurobiological Engineering, Graduate School of High-Technology for Human Welfare, Tokai University, Numazu; 2Department of Physiological Science, School of Medicine, Tokai University, Isehara, Japan; and 3Department of Physiology and Biophysics, Faculty of Medicine, University of Calgary, Calgary, Alberta, Canada

Submitted 10 November 2004; accepted in final form 2 August 2005

To begin to determine the underlying neural mechanisms of memory formation, we studied two different cell types that play important roles in different forms of associative learning in Lymnaea. Statocyst neurons (hair cells) mediate classical conditioning, whereas RPeD1 is a site of memory formation induced by operant conditioning of aerial respiration. Because potassium (K+) channels play a critical role in neuronal excitability, we initiated studies on these channels in the aforementioned neurons. Three distinct K+ currents are expressed in the soma of both the hair cells and RPeD1. In hair cells and RPeD1, there is a fast activating and rapidly inactivating 4-aminopyridine (4-AP)-sensitive A current (IA), a tetraethyl ammonium (TEA)-sensitive delayed rectifying current, which exhibits slow inactivation kinetics (IKV), and a TEA- and 4-AP-insensitive Ca2+-dependent current (ICa-K). In hair cells, the activation voltage of IA; its half-maximal steady-state activation voltage and its half-maximal steady-state inactivation were at more depolarized levels than in RPeD1. The time constant of recovery from IA inactivation was slightly faster in hair cells. IA in hair cells is also smaller in amplitude than in RPeD1 and is activated at more depolarized potentials. In like manner, IKV is smaller in hair cells and is activated at more depolarized potentials than in RPeD1.


Address: M. Sakakibara, Laboratory of Neurobiological Engineering, Department of Biological Science and Technology, School of High-Technology for Human Welfare, Tokai University, 317 Nishino, Numazu 410-0321, Shizuoka, Japan (E-mail: manabu{at}tokai.ac.jp)







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