Block of squid axon K channels by internally and externally applied barium ions.

Armstrong, Clay M.; Swenson, Randolphe P.; Taylor, Stuart R.

doi:10.1085/jgp.80.5.663

Cited by 180 publications

(156 citation statements)

References 21 publications

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“…The second has been postulated for the mechanism of pharmaco-mechanical coupling in arteries Droogmans et al, 1977). In the present studies, contraction induced by Ba was preceded by membrane depolarization, probably because the ability of Ba to reduce G K (Hermsmeyer & Sperelakis, 1970;Armstrong et al, 1982). Moreover, as mentioned above, ACh and substance P did not effectively modify the membrane potential even when GK was decreased in the presence of Ba, suggesting that the first proposition is to be favoured.…”

Section: Discussionsupporting

confidence: 46%

Pharmaco‐mechanical coupling in the response to acetylcholine and substance P in the smooth muscle of the rat iris sphincter

Banno

Imaizumi

Watanabe

1985

British J Pharmacology

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1 In the rat iris sphincter muscle contractile responses to transmural stimulation consisted of two components, a fast cholinergic followed by a slow non-adrenergic, non-cholinergic (NANC) one. The magnitude of the latter varied widely and was on average 5% of that of the cholinergic component. 2 Exogenous substance P (I nM-l zM) produced a concentration-dependent contraction, the maximum amplitude of which was as large as that produced by acetylcholine (ACh).3 Capsaicin (IO IM) induced a transient contraction only once in each preparation. After the treatment with capsaicin the NANC component disappeared. 4 Neither nerve nor direct electrical stimulation with short pulses elicited any active change in the membrane potential under physiological conditions, but an action potential was triggered by direct stimulation when the extracellular Ca ion was totally replaced by Ba ion. Under the latter conditions spontaneous spike potentials occurred repetitively. 5 ACh and substance P produced a large contraction without modifying the membrane potential. This was also the case in the presence of 5 mm Ba. 6 These results suggest that substance P-ergic innervation may have a far lesser physiological significance than that which has been described in rabbits and that pure pharmaco-mechanical coupling is characteristic ofthe responses to acetylcholine, substance P, and nerve stimulation in the rat iris sphincter muscle.

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Section: Discussionsupporting

confidence: 46%

Pharmaco‐mechanical coupling in the response to acetylcholine and substance P in the smooth muscle of the rat iris sphincter

Banno

Imaizumi

Watanabe

1985

British J Pharmacology

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“…Rather unexpectedly, comparatively low concentrations of Ba2+ reduced IK by more than 50 %. Although Ba2+ can block IK of squid axons (Armstrong, Swenson & Taylor, 1982), such a phenomenon has not been reported before for mammalian brain neurones. It seems A. NISTRI AND E. CHERLTBINI plausible that inhibition of 'K by Ba21 may contribute to the generation of spike bursts produced by this divalent cation (Storm.…”

Section: Inactivation Of Ikmentioning

confidence: 76%

Inactivation characteristics of a sustained, Ca(2+)‐independent K+ current of rat hippocampal neurones in vitro.

Nistri

Cherubini

1992

The Journal of Physiology

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SUMMARY1. Current or voltage clamp recordings from CA3 neurones of the adult rat hippocampal slice were performed to study the inactivation properties of a slow outward K+ current identified as the delayed rectifier (IK).2. In current clamp experiments, burst firing evoked from resting membrane potential by intracellular current injection was reduced or blocked by conditioning hyperpolarizing pre-pulses of 20-40 mV amplitude. This effect was inhibited by tetraethylammonium (TEA; 20 mM) but was unaffected by Cs' (3 mM), 4-aminopyridine (4-AP; 2 mm), carbachol (30-50 ,rm), mast cell degranulating peptide (MCDP; 300 nM), thyrotrophin releasing hormone (TRH; 1 /LM) or by a Ca2"-free solution containing Mn2+ or Co2+ (2 mM).3. Single-electrode voltage clamp experiments were carried out on neurones superfused with Ca2+-free solution, containing tetrodotoxin (TTX; 1 gM), Mn2+ or Co2+ (2 mM), 4-AP (2 mM), Cs' (3 mM) and carbachol (30 ,M).Step depolarizations from a holding potential of -55 mV activated an outward current which reached a plateau after 200 ms, followed by an outward tail current. Such an outward current had the characteristics of IK.4. The outward currents were significantly potentiated by conditioning hyperpolarizing pre-pulses suggesting the IK was reduced by a voltage-dependent inactivation process. Removal of inactivation was a function of the amplitude of the conditioning hyperpolarizing pre-pulse. At a holding potential of -55 mV removal of inactivation was time dependent with a time constant of 211 ms. High K+ (12'5 or 21-5 mM) solutions did not affect the inactivation characteristics of IK.5. Tetraethylammonium (20 mM) or low concentrations of Ba21 (0'1 mM) readily depressed the outward current without significantly affecting the inactivation process. Dendrotoxin (200 nM) also depressed such a slow current but, in addition, increased the inactivation process of IK.6. It is suggested that removal of inactivation of IK by hyperpolarization can modulate cell excitability by fully restoring the ability ofIK to inhibit burst firing of CA3 hippocampal neurones.MS 9583

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“…7 (Miller, 1987). Available electrophysiological (Armstrong, Swenson & Taylor, 1982) and molecular (Isacoff, Lopez, Jan & Jan, 1993) evidence strongly suggests that the binding site for Ba2+ in K+ channels is in the deep pore (H5) region. This is not the case for 4-AP where, although the amino acid residues within the pore region influence binding, the critical residues appear to lie outside this area on the cytoplasmic side of the channel (Howe & Ritchie, 1991; (Choquet & Korn, 1992) where open channel block has also been reported.…”

Section: Discussionmentioning

confidence: 99%

Block by 4‐aminopyridine of a Kv1.2 delayed rectifier K+ current expressed in Xenopus oocytes.

Russell

Publicover

Hart

et al. 1994

The Journal of Physiology

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1. The blocking action of 4-aminopyridine (4-AP) on a delayed rectifier K,12 K+ channel expressed in oocytes was investigated at room temperature (22°C) and physiological temperature (34°C) using the double-electrode voltage clamp and patch clamp techniques. 2. At room temperature, 4-AP (100 uM) inhibition occurred only after activation of current. The rate of onset of block was dependent upon the length of time current was activated by a depolarizing step. Similarly, removal of block required current activation. The degree of steady-state block by 4-AP was not reduced by increasingly more depolarized step potentials. The degree of steady-state block also did not change over the duration of a I s step.3. When channels were nearly fully inactivated, 4-AP produced no additional block of a subsequent depolarizing step, suggesting that 4-AP did not bind when channels were in the inactivated state. In single channel experiments, 4-AP decreased the mean open time in a dose-dependent manner but did not alter the single-channel current amplitude. 4. At 34°C the I-V relationship and inactivation curve shifted to more negative potentials. Increasing the temperature to 34°C did not alter the degree of block by 4-AP, although the rate of onset of block was greatly enhanced.

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Block of squid axon K channels by internally and externally applied barium ions.

Abstract: We have studied the interactions of Ba ion with K channels. Ba t+ blocks these channels when applied either internally or externally in millimolar concentrations . Periodic depolarizations enhance block with internal Bat+ , but

Cited by 180 publications

References 21 publications

Pharmaco‐mechanical coupling in the response to acetylcholine and substance P in the smooth muscle of the rat iris sphincter

Pharmaco‐mechanical coupling in the response to acetylcholine and substance P in the smooth muscle of the rat iris sphincter

Inactivation characteristics of a sustained, Ca(2+)‐independent K+ current of rat hippocampal neurones in vitro.

Block by 4‐aminopyridine of a Kv1.2 delayed rectifier K+ current expressed in Xenopus oocytes.

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