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Long-term adaptation of Ca2+-dependent behaviour in Paramecium tetraurelia
Journal article   Open access   Peer reviewed

Long-term adaptation of Ca2+-dependent behaviour in Paramecium tetraurelia

R R Preston and J A Hammond
Journal of experimental biology, v 201(Pt 11), pp 1835-1846
Jun 1998
DOI: https://doi.org/10.1242/jeb.201.11.1835
PMID: 9576893
url
https://doi.org/10.1242/jeb.201.11.1835View
Published, Version of Record (VoR)Maybe Open Access (Publisher Bronze),  Open

Abstract

Adaptation, Physiological Animals Barium - pharmacology Behavior, Animal - drug effects Calcium - pharmacology Calcium Channels - physiology Chemoreceptor Cells - physiology Kinetics Magnesium - pharmacology Membrane Potentials - drug effects Paramecium - physiology Potassium Chloride - administration & dosage Potassium Chloride - pharmacology Swimming
Prolonged exposure to KCl has long been recognized to modify swimming behaviour in Paramecium tetraurelia, a phenomenon known as 'adaptation'. In this study, we have investigated behavioural adaptation systematically. A 24 h exposure to 30 mmol l-1 KCl deprived cells of the ability to respond behaviourally to two established chemoeffectors. We also explored the effects of 30 mmol l-1 KCl on the duration of backward swimming induced by Ba2+ and Mg2+. A brief (60 min) exposure prevented cells from swimming backwards in response to either cation, but recovery was rapid (<60 min) following a return to control medium. Prolonged (48 h) exposure caused a more persistent loss of response to Ba2+, so that several hours was now required for recovery. Surprisingly, responses to Mg2+ reappeared during 6-8 h in KCl, with backward swimming durations increasing to more than 300 % of control values after 26 h. Thus, we can distinguish two phases to adaptation. The short-term phase is characterized by an inability to respond behaviourally to most stimuli and might be adequately explained in terms of Ca2+ channel inactivation and K+-induced shifts in membrane potential. The long-term phase is characterized by enhanced responses to Mg2+ (and also to Na+), suggesting that a more extensive reprogramming of membrane excitability may occur during chronic K+-induced depolarization.

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