Blockade of Ca‐activated K conductance by apamin in rat sympathetic neurones

Kawai, Tadao; Watanabe, Minoru

doi:10.1111/j.1476-5381.1986.tb10175.x

Cited by 120 publications

(55 citation statements)

References 28 publications

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“…Non-axotomized rat sympathetic ganglion cells do not show ADPs (McAfee & Yarowsky, 1979;Kawai & Watanabe, 1986;Kawai & Watanabe, 1989;Sanchez-Vives & Gallego, 1993a), which is in accordance with the lack of inward tail currents in control cells bathed in 'ITX and TEA, even after increasing the current driving force by lowering the external Cl-concentration. Therefore, as discussed by Sanchez-Vives & Gallego (1993a), a new conductance appears at or near the cell body after axotomy.…”

Section: Discussionsupporting

confidence: 80%

“…Even in the presence of apamin (20 nm, n = 4), which blocks the slow AHP in these cells (Kawai & Watanabe, 1986), no ADPs were revealed by trains of spikes or depolarizing pulses (not shown). We tried to evoke the 'ADP in normal cells (n = 5) in the same conditions that we used to study the current in axotomized neurons: in the presence of TTX and TEA to block sodium and potassium currents.…”

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confidence: 92%

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

Sánchez-Vives

Gallego

1994

The Journal of Physiology

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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.

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Section: Discussionsupporting

confidence: 80%

mentioning

confidence: 92%

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

Sánchez-Vives

Gallego

1994

The Journal of Physiology

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“…This apparent absence of the apamin-sensitive, low conductance, CaZ+-activated K + channel accords with the ineffectiveness of apamin in the mammalian hippocampus [14,18], as distinct from the PNS of both amphibians and mammals [16,17].…”

Section: Introductionsupporting

confidence: 52%

“…Apamin inhibits the small conductance, Ca2+-dependent, voltage-insensitive K + channel [12] which appears to underlie the slow afterhyperpolarization that controls repetitive firing in the PNS [16,17]. By analogy, the slow after-hyperpolarization in the CNS may also be mediated by such low conductance channels although no apamin sensitivity has yet been reported therein ( [14,18]; but see [19]).…”

Section: Introductionmentioning

confidence: 99%

Dendrotoxin and charybdotoxin increase the cytosolic concentration of free Ca²⁺ in cerebrocortical synaptosomes: An effect not shared by apamin

1989

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Nanomolar concentrations of charybdotoxin or dendrotoxin increase the cytoplasmic free Ca 2+ concentration in isolated central nerve terminals. The effects of the two toxins, normally considered to be blockers of K ÷ channels controlled by voltage in a Ca2+-sensitive or -insensitive manner, respectively, show only marginal additivity. Apamin, an inhibitor of low conductance Ca 2÷-activated K ÷ channels, was without effect in either the absence or presence of dendrotoxin. The effect of charybdotoxin on polarized, isolated central nerve terminals seems to be mediated largely by a block of K ÷ channels sensitive to dendrotoxin. Apparently, these voltage-operated K ÷ channels make a more significant contribution to maintaining the polarized potential of synaptosomes than do those activated by Ca 2 ÷.

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“…The former is likely to be the Ic current (Dryer et al, 1991). Apamin is known to suppress the Ik(Ca) involved in the after-hyperpolarization of the action potential but not the Ih(Ca) involved in the repolarization of the action potential in autonomic neurones (Tanaka et al, 1986;Kawai & Watanabe, 1986;Dryer et al, 1991). Taken together with the present observations that show NO can depress both apamin and charybdotoxin-sensitive Ik(Ca) at times comparable to that of the repolarization phase of the action potential at about 5 ms (Dryer et al, 1991), it seems likely that both the Ic current involved in the repolarization of the action potential as well as the apamin-sensitive current involved in the after-hyperpolarization are depressed.…”

Section: Discussionmentioning

confidence: 99%

Nitric oxide modulation of calcium‐activated potassium channels in postganglionic neurones of avian cultured ciliary ganglia

Çetiner

Bennett

1993

British J Pharmacology

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1 A study has been made of the modulation of calcium-activated potassium channels in cultured neurones of avian ciliary ganglia by sodium nitroprusside and L-arginine.2 Sodium nitroprusside (100 gM) reduced the net outward current by 22± 1% at 4.8 ms (mean ± s.e.mean) and 25 ± 1% at 350 ms during a test depolarization to + 40 mV from a holding potential of -40 mV. The outward current remained reduced for the duration of the recording following a single application of sodium nitroprusside. These effects did not occur if the influx of calcium ions was first blocked with Cd2+ (500 ytM). Application of ferrocyanide (100 j.M) reduced the net outward current by only 6 ± 3% at 350 ms during a test depolarization to + 40 mV.3 L-Arginine (270 IM) reduced the net outward current on average by 19 ± 2% at 4.8 ms and 22 ± 2% at 350 ms during a test depolarization to + 40 mV. The current remained in this reduced state for the duration of the recording following a single application of L-arginine. These effects were reduced to 11 ± 1% at 4.8 ms and 11 ± 2% at 350 ms in the presence of Nw-nitro-L-arginine methyl ester (L-NAME, 100 gM). 4 In order to alleviate the dependence of calcium-activated potassium channels (Ik(Ca)) on the inward flux of calcium ions, the patch-clamp pipettes were filled with a solution containing 100 gM CaC12, and the Ca2+ in the bathing solution was replaced with EGTA. Under these conditions sodium nitroprusside reduced the total outward current during a depolarizing pulse of + 40 mV by 9 ± 1% at 4.8 ms and by 36 ± 3% at 350 ms. L-Arginine (270 gM) reduced this current under the same conditions by 9 ± 1% at 4.8ms and by 35 ± 2% at 350ms. 5 Calcium-activated potassium currents were sensitive to apamin (50 nM), as this reduced the outward current by 23 ± 3% at 350 ms when a high calcium-containing pipette was used during a depolarizing command to +40 mV. L-Arginine still decreased the outward current in the presence of apamin (50 nM), by 5 ± 1% at 4.8 ms and by 19 ± 2% at 350 ms, indicating that L-arginine could reduce an apamin-insensitive Ik(Ca) 6 Calcium-activated potassium currents were also sensitive to charybdotoxin (10 nM), as this reduced the outward current by 34 ± 4% at 350 ms when a high calcium-containing pipette was used during a depolarizing command to + 40 mV. L-Arginine still decreased the outward current in the presence of charybdotoxin, by 6 ± 1% at 4.8 ms and 12 ± 4% at 350 ms, showing that L-arginine could reduce a charybdotoxin-insensitive Ik(Ca). 7 The present results indicate that NO-synthase in ciliary ganglia can modulate Ik(Ca) by a method which is independent of the action of NO on the calcium channels. The Ik(ca) is decreased significantly at 4.8 ms into a depolarizing pulse, at a time that would decrease the rate of repolarization of the action potential. Ik(Ca) is also reduced at longer times (350 ms), indicating an affect on the inactivating process.

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Blockade of Ca‐activated K conductance by apamin in rat sympathetic neurones

Cited by 120 publications

References 28 publications

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

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

Dendrotoxin and charybdotoxin increase the cytosolic concentration of free Ca²⁺ in cerebrocortical synaptosomes: An effect not shared by apamin

Nitric oxide modulation of calcium‐activated potassium channels in postganglionic neurones of avian cultured ciliary ganglia

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Blockade of Ca‐activated K conductance by apamin in rat sympathetic neurones

Cited by 120 publications

References 28 publications

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

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

Dendrotoxin and charybdotoxin increase the cytosolic concentration of free Ca2+ in cerebrocortical synaptosomes: An effect not shared by apamin

Nitric oxide modulation of calcium‐activated potassium channels in postganglionic neurones of avian cultured ciliary ganglia

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Dendrotoxin and charybdotoxin increase the cytosolic concentration of free Ca²⁺ in cerebrocortical synaptosomes: An effect not shared by apamin