Tm. Hennessey et al., LYSOZYME ACTS AS A CHEMOREPELLENT AND SECRETAGOGUE IN PARAMECIUM BY ACTIVATING A NOVEL RECEPTOR-OPERATED CA++ CONDUCTANCE, The Journal of membrane biology, 148(1), 1995, pp. 13-25
Using combined intracellular recordings and behavioral bioassays, it w
as found that lysozyme has two different effects in Paramecium, depend
ing upon the concentrations used. At low concentrations (0.5 nM to 1.0
mu M) it acts as an effective chemorepellent that causes reliable ele
ctrophysiological changes. Lysozyme-induced somatic depolarizations, i
solated by blocking K+ channels with Cs-TEA, showed concentration depe
ndencies that were well correlated with chemorepulsion. Ion dependency
experiments showed that these were Ca++ based depolarizations. Additi
on of either Na+ or Mg++ improves chemorepulsion by providing addition
al depolarizations, Both the depolarizations and chemorepulsion were b
locked by 10 mu M neomycin, suggesting that the depolarization is nece
ssary for this chemosensory transduction event. At higher concentratio
ns (100 mu M), lysozyme is a secretagogue. A transient inward current,
recorded in Ca++ alone solutions with Cs-TEA present, was seen in res
ponse to high lysozyme concentrations. The amplitude of this inward cu
rrent was well correlated with exocytosis. Addition of neomycin (1.0 m
M) eliminated both the inward current and exocytosis, suggesting a cau
sal relationship, Neither amiloride or W-7, compounds previously sugge
sted to affect the electrophysiological responses to secretagogues, ha
d any significant effects, The mucopolysaccharide hydrolysis activity
of lysozyme was not required for any of these responses. We propose th
at Paramecium have a high affinity receptor on the body plasma membran
e that responds to either lysozyme or a related compound to cause an i
ncrease in a novel body Ca++ conductance. This receptor-operated Gate
conductance causes membrane depolarization and chemorepulsion at low c
oncentrations and triggers a sufficient Ca++ in-flux at high concentra
tions to cause exocytosis.