Calcium‐dependent chloride current induced by axotomy in rat sympathetic neurons.

Abstract

1. Seven to ten days after sectioning their axons, rat sympathetic neurons were studied using intracellular recording techniques in an in vitro preparation of the superior cervical ganglion. 2. In 75 % of axotomized cells, an after-depolarization (ADP) was observed following spike firing or depolarization with intracellular current pulses. Discontinuous single-electrode voltage-clamp techniques were employed to study the ADP. When the membrane potential was clamped at the resting level just after an action potential, a slow inward current wa.s recorded in cells that showed an ADP. 3. In the presence of ITX and TEA, inward peaks and outward currents were recorded during depolarizing voltage jumps, followed by slowly decaying inward tail currents accompanied by large increases in membrane conductance. The inward peak and tail currents activated between -10 and -20 mV and reached maximum amplitudes around 0 mV. With depolarizing jumps to between +40 and +50 mV, net outward currents were recorded during the depolarizing jumps but inward tail currents were still activated. 4. In the presence of the Ca2+ channel blocker cadmium, or when Ca2+ was substituted by Mg2+, the ADP disappeared. In voltage-clamped cells, cadmium blocked the inward tail currents. The reversal potential for the inward tail current was approximately -15 mV.

Mouse sperm membrane potential: changes induced by Ca2+

“…This result suggests the participation of a Ca2+-modulated CI channel, which would open as Ca 2÷ enters the cell [21]. However, > 50% of the Ca-ith remains in low [C1-]e, arguing, that other ion permeabilities are involved in this response.…”

“…Niflumic acid, a C1-channel blocker [21], required a 6-min incubation to fully cause its effect (~40% inhibition of the Ca- Table 1 ith), at concentrations commonly used in other cells (<200 pM) Effect of ouabain or niflumic acid on Er and the Ca-ith [22]. Higher concentrations (> 350/tM) inhibited up to 73% Ouabain (tiM) n E, (mV) Ca-ith (mV) inhibition % (Fig.…”

Ca2+-activated Cl− channels at a glance

“…The CaCC current is upregulated in DRG neurons following axotomy (Sánchez-Vives and Gallego, 1994;André et al, 2003), suggesting that CaCCs have a role in neuropathic pain or nerve regeneration. In addition, in injured DRG neurons, the activity of Cl -channels generally results in further excitation (Sung et al, 2000), which might enhance CaCC effects, leading to increased neuropathic pain.…”

Spinal Cord Injury Induces Changes in Electrophysiological Properties and Ion Channel Expression of Reticulospinal Neurons in Larval Lamprey

“…For axotomized mouse DRG neurons (Andre et al, 2003a) and injured rat sympathetic neurons (Sanchez-Vives and Gallego, 1994), there is an increase in calcium-activated chloride currents.…”