The presence of a calcium-activated nonspecific cationic (CAN) current in t
urtle motoneurons and its involvement in plateau potentials, bistability, a
nd windup was investigated by intracellular recordings in a spinal cord sli
ce preparation. In the presence of tetraethylammonium (TEA) and tetrodotoxi
n (TTX), calcium action potentials evoked by depolarizing current pulses we
re always followed by an afterdepolarization associated with a decrease in
input resistance. The presence of the afterdepolarization depended on the c
alcium spike and not on membrane potential. Replacement of extracellular so
dium by choline or N-methyl-D-glucamine (NMDG) reduced the afterdepolarizat
ion, confirming that it was mediated by a CAN current. Plateau potentials a
nd windup were evoked in response to intracellular current pulses in the pr
esence of agonist for different metabotropic receptors. Replacement of extr
acellular sodium by choline or NMDG did not abolish the generation of plate
au potentials, bistability, or windup, showing that Na+ was not the princip
al charge carrier. It is concluded that plateau potentials, bistability and
windup in turtle motoneurons do not depend on a CAN current even though it
s presence can be detected.