The time courses of intracellular free calcium and related electrical effects after injection of CaCl2 into neurons of the snail,Helix pomatia

Abstract

Controlled quantities of 100 mM aqueous CaCl2 solutions were pressure injected into voltage-clamped neurons with a resolution of 10(-11) 1. Ca2+-selective microelectrodes monitored the time course of changes in [Ca2+]i. At a membrane potential of -50 mV CaCl2 quantities in the range of 1% of the cell volume induced an inward current, associated with a conductance increase and having an equilibrium potential between -20 and +20 mV, which accompanied the rise in [Ca2+]i. An artifactual origin of the inward current by the injection procedure or by calcium screening of membrane sites could be excluded. The calcium-induced hyperpolarizing conductance, producing an outward current at -50 mV, followed the inward current and reached maximum during the late decline in [Ca2+]i. In most cases its development was separated from the inward current by an intermediate relative decrease of the membrane conductance. Neither of the two transient conductance increases showed a particular dependence on voltage. Renewed Ca2+ injection quickly decreased the calcium-induced hyperpolarizing conductance for several seconds. Ca2+ injections below 0.05% of the cell volume mostly produced pure outward currents or hyperpolarizing responses. Partial substitution of extracellular CaCl2 by NiCl2 decreased the hyperpolarizing response but not the initial inward current. The immediate effects of increased [Ca2+]i are activation of a depolarizing conductance and the partial block of the late hyperpolarizing conductance. The latter is probably produced through intermediate steps after increasing [Ca2+]i.

Intracellular calcium ions and calcium currents in perfused neurones of the snail, Lymnaea stagnalis.

“…The most common response that we observed in Lymnaea neurones was an increase in [Ca2+]j to values one to two orders of magnitude greater than the Ca2+ activity of the internal solution. The membrane channels through which extracellular Ca2+ enters the cell in this situation may be similar to the non-specific cation channel reported in cardiac muscle (Colquhoun, Neher, Reuter & Stevens, 1981) and neuroblastoma cells (Yellen, 1982), which is activated by internal Ca2+ at levels near 10-6 M. Although this channel does not pass Ca2+ in neuroblastoma cells, a Ca2+_ activated inward current has been reported in Helix neurones (Hofmeier & Lux, 1981) which is not carried by Na+ and may represent a channel similar to the one which we see in Lymnaea. The entry of Ca2+ becomes regenerative in Lymnaea neurones during perfusion with high-Ca2+ internal solutions, resulting in a form of Ca2+-induced Ca2+ release into the cytoplasm, which, however, can overwhelm the cell's intrinsic Ca2+ regulating systems only after a period of internal perfusion (with low-Ca2+ solutions) has somehow inactivated them.…”

Opposite Membrane Potential Changes Induced by Glucose Deprivation in Striatal Spiny Neurons and in Large Aspiny Interneurons

“…Low-Na ϩ -containing solutions significantly reduce the amplitude of the depolarization caused by glucose deprivation. A TTX-resistant Ca 2ϩ -activated nonspecific cationic current has been reported to act as a depolarizing driving force in neurons of invertebrates (Hofmeier and Lux, 1981) and in rat hippocampal neurons (Crepel et al, 1994). The finding that the aglycemia-induced depolarization is not altered by the intracellular injection of BAPTA, however, does not support the involvement of a Ca 2ϩ -activated conductance in the aglycemiainduced effects.…”

Repeated Negative DC Deflections in Rat Cortex following Middle Cerebral Artery Occlusion are Abolished by MK-801: Effect on Volume of Ischemic Injury

“…12, No.5, 1992 peated calcium flooding of the cytosol. Depolariza tion of neuronal membranes causes an opening of voltage-gated calcium channels and a rise of cyto plasmic Ca2+ activity (Hofmeier and Lux, 1981 ). One of the numerous biological effects of increased calcium activity is the suppression of protein syn thesis that in turn may be involved in the manifes tation of ischemic neuronal death (A varia and Kri vanek, 1973;Krivanek, 1978).…”