The influence of chemical agents on the level of ionized [Ca2+] in squid axons.

Abstract

Squid giant axons injected with either aequorin or arsenazo III and bathed in 3 mM Ca (Na) seawater were transferred to 3 mM Ca (K) seawater and the response of the aequorin light or the change in the absorbance of arsenazo III was followed . These experimental conditions were chosen because they measure the change in the rate of Na/Ca exchange in introducing Ca into the axon upon depolarization ; [Cal. is too low to effect a channel-based system of Ca entry. This procedure was applied to axons treated with a variety of compounds that have been implicated as inhibitors of Na/Ca exchange. The result obtained was that the substances tested could be placed in three groups . (a) Substances that were without effect on Ca entry effected by Na/Ca exchange were : D600 at 10-100 FM, nitrendipine at 1-5 uM, Ba2+ and Mg" at concentrations of 10-50 mM, lidocaine at 0.1-10 mM, cyanide at 2 mM, adriamycin at a concentration of 3,M, chloradenosine at 35 ,AM, 2,4-diaminopyridine at 1 mM, Cs' at 45-90 mM, and tetrodotoxin at 10'. (b) Substances that had a significant inhibitory effect on Na/Ca exchange were : Mn2+ , Cd2+ , and Las" at 1-50 mM, and quinidine at 50 pM . (c) There were also blocking agents and biochemical inhibitors whose action appeared to be the inhibition of nonmitochondrial Ca buffering in axoplasm rather than an inhibition of Na/Ca exchange . These were the general anesthetic 1-octanol at 0.1 mM and 1 mM orthovanadate plus apyrase.

Effects of the anesthetics heptanol, halothane and isoflurane on gap junction conductance in crayfish septate axons: A calcium- and hydrogen-independent phenomenon potentiated by caffeine and theophylline, and inhibited by 4-aminopyridine

“…In a double whole-cell clamp study octanol decreased junctional conductance to 4% of control values with patch-pipette solutions weakly buffered for Ca 2+ (0. I mM EGTA), and to 30% with strongly buffered solutions (5 mM EGTA) (Veenstra & De Haan, 1988), A moderate increase in [Ca2+] i was monitored with the Ca 2+ indicator arsenazo lIl in squid axons exposed to alkanols (Requena et al, 1985;Vassort et al, 1986). In contrast, Meda et al (1986) reported no significant changes in [Ca2+] i measured with quin-2, in exocrine pancreas treated with heptanol.…”

“…However, Veenstra and DeHaan (1988) observed only a partial reduction of junctional conductance with octanol in embryonal cardiac cells dialyzed by patch pipettes strongly buffered for Ca :+ , while complete uncoupling was seen only with weak Ca > buffers. Furthermore, Requena et al (1985) and Vassort, Whittembury and Mullins (1986) monitored a small increase in [Ca2+]i with arsenazo II!in squid axons treated with octanol.…”

Pre‐ and postsynaptic volatile anaesthetic actions on glycinergic transmission to spinal cord motor neurons

“…This result suggests that en¯urane increases in mIPSC frequency are due to increases in intraterminal calcium, and that both exchange and release are involved. Several studies suggest that volatile anaesthetics can increase intracellular calcium by increasing leakage from intracellular stores (Blanck et al, 1992;Hossain & Evers, 1994;Requena et al, 1985;Vassort et al, 1986).…”

Control of the Na-Ca exchanger in isolated heart cells. I. Induction of Na-Na exchange in sodium-loaded cells by intracellular calcium.

“…[6][7][8][9][10] Although the participation of the exchanger in excitation-contraction coupling in heart has long been postulated, its role has remained controversial. There is mounting evidence that the exchanger does have a major role in calcium efflux11-14 and perhaps also in calcium influx during excitation.1516 To elucidate this role it is important that the properties of the exchanger in heart be well understood.…”