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1 Laboratory of Neurobiological Engineering, Tokai University, Numazu, Shizuoka, Japan; Department of Physiology, Tokai University, Isehara, Kanagawa, Japan
* To whom correspondence should be addressed. E-mail: manabu{at}tokai.ac.jp.
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 whilst RPeD1 is a site of memory formation induced by operant conditioning of aerial respiration. Since 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.
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