Two dyad-free Shaker-type K+ channel blockers from scorpion venom

Toxicon ◽  
2012 ◽  
Vol 59 (3) ◽  
pp. 402-407 ◽  
Author(s):  
Limei Zhu ◽  
Bin Gao ◽  
Lan Luo ◽  
Shunyi Zhu
Keyword(s):  
Scorpion Venom ◽  
K Channel ◽  
Channel Blockers ◽  
Type K

IA-type K+ channel blockers promote survival of cortical neurons in culture

Neuroreport ◽  
1997 ◽  
Vol 8 (8) ◽  
pp. 1803-1806 ◽  
Author(s):  
Marcos Emílio dos Santos Frizzo ◽  
Luis Barbeito
Keyword(s):  
Cortical Neurons ◽  
K Channel ◽  
Channel Blockers ◽  
Type K

scholarly journals The myth of scorpion suicide: are scorpions insensitive to their own venom?

1998 ◽  
Vol 201 (18) ◽  
pp. 2625-2636
Author(s):  
C Legros ◽  
MF Martin-Eauclaire ◽  
D Cattaert
Keyword(s):  
Action Potential ◽  
Procambarus Clarkii ◽  
Scorpion Venom ◽  
K Channel ◽  
Muscle Fibres ◽  
Channel Blockers ◽  
Na Channels ◽  
Nerve Fibres ◽  
K Channels ◽  
Voltage Gated

The resistance of the scorpion Androctonus australis to its own venom, as well as to the venom of other species, was investigated. A comparison of the electrical and pharmacological properties of muscle and nerve fibres from Androctonus australis with those from the crayfish Procambarus clarkii enabled us to understand the lack of effect of scorpion venom (110-180 microg ml-1) and purified toxins, which are active on voltage-gated Na+ and K+ channels, Ca2+-activated K+ channels, on scorpion tissues. Voltage-clamp experiments showed that peptide K+ channel blockers from scorpion and snake have no effect on currents in muscle and nerve fibres from either scorpions or crayfish. The scorpion toxin kaliotoxin (KTX), a specific blocker of Kv1.1 and Kv1.3 K+ channels, had no effect on muscle fibres of A. australis (2 micromol l-1) or P. clarkii (400 nmol l-1). Similarly, charybdotoxin (ChTX) had no effect on the muscle fibres of A. australis (10 micromol l-1) or P. clarkii (200 nmol l-1) and neither did the snake toxin dendrotoxin (DTX) at concentrations of 100 nmol l-1 in A. australis and 200 nmol l-1 in P. clarkii. These three toxins (KTX, ChTX and DTX) did not block K+ currents recorded from nerve fibres in P. clarkii. The pharmacology of the K+ channels in these two arthropods did not conform to that previously described for K+ channels in other species. Current-clamp experiments clearly indicated that the venom of A. australis (50 microg ml-1) had no effect on the shape of the action potential recorded from nerve cord axons from A. australis. At a concentration of 50 microg ml-1, A. australis venom greatly prolonged the action potential in the crayfish giant axon. The absence of any effect of the anti-mammal <IMG src="/images/symbols/&agr ;.gif" WIDTH="9" HEIGHT="12" ALIGN="BOTTOM" NATURALSIZEFLAG="3">-toxin AaH II (100 nmol l-1) and the anti-insect toxin AaH IT1 (100 nmol l-1) on scorpion nerve fibres revealed strong pharmacological differences between the voltage-gated Na+ channels of scorpion and crayfish. We conclude that the venom from A. australis is pharmacologically inactive on K+ channels and on voltage-sensitive Na+ channels from this scorpion.

Ionic channels in corneal endothelium

1996 ◽  
Vol 270 (4) ◽  
pp. C975-C989 ◽  
Author(s):  
J. L. Rae ◽  
M. A. Watsky
Keyword(s):  
Patch Clamp ◽  
Corneal Endothelium ◽  
Single Channel ◽  
Cell Voltage ◽  
Anion Channel ◽  
Ionic Channels ◽  
K Channel ◽  
Na Channel ◽  
Channel Blockers ◽  
K Currents

Single-channel patch-clamp techniques as well as standard and perforated-patch whole cell voltage-clamp techniques have been applied to the study of ionic channels in the corneal endothelium of several species. These studies have revealed two major K+ currents. One is due to an anion- and temperature-stimulated channel that is blocked by Cs+ but not by most other K+ channel blockers, and the other is similar to the family of A-currents found in excitable cells. The A-current is transient after a depolarizing voltage step and is blocked by both 4-aminopyridine and quinidine. These two currents are probably responsible for setting the -50 to -60 mV resting voltage reported for these cells. A Ca(2+)-activated ATP-inhibited nonselective cation channel and a tetrodotoxin-blocked Na+ channel are possible Na+ inflow pathways, but, given their gating properties, it is not certain that either channel works under physiological conditions. A large-conductance anion channel has also been identified by single-channel patch-clamp techniques. Single corneal endothelial cells have input resistances of 5-10 G omega and have steady-state K+ currents that are approximately 10 pA at the resting voltage. Pairs or monolayers of cells are electrically coupled and dye coupled through gap junctions.

Chronic hypoxia selectively augments endothelium-dependent pulmonary arterial vasodilation

1996 ◽  
Vol 270 (3) ◽  
pp. H888-H896 ◽  
Author(s):  
T. C. Resta ◽  
B. R. Walker
Keyword(s):  
Chronic Hypoxia ◽  
K Channel ◽  
Channel Blockers ◽  
No Donors ◽  
Question Mark ◽  
Pulmonary Vasodilator ◽  
Pulmonary Arterial ◽  
Arterial Dilation ◽  
Spermine Nonoate ◽  
Increased Activity

We have previously demonstrated that chronic hypoxia (CH) augments pulmonary arterial dilation to the endothelium-derived nitric oxide (EDNO)-dependent pulmonary vasodilator arginine vasopressin (AVP). The present study examined 1) whether this enhanced vasoreactivity is observed with other agents that act by stimulating constitutive NO synthase (cNOS), 2) whether CH increases arterial vascular smooth muscle sensitivity to NO, and 3) whether endogenous endothelin (ET) or an endothelium-derived hyperpolarizing factor (EDHF) contributes to this altered arterial reactivity following CH. We examined responses to the receptor-mediated EDNO-dependent dilators histamine and ET-1, the nonreceptor-mediated EDNO-dependent dilator ionomycin, and the NO donors 1, 3-propanediamine, N- inverted question mark4-[1-(3-aminopropyl)-2-hydroxy-2-nitrosohydrazino] butyl inverted question mark (spermine NONOate) and S-nitroso-N-acetylpenicillamine (SNAP) in U-46619-constricted, isolated perfused lungs from control and CH rats. Additional experiments examined responses to AVP in the presence of the ET-receptor antagonist PD-145065 or the K+ channel blockers glibenclamide or tetraethylammonium (TEA) in lungs from each group. Microvascular pressure was assessed by double occlusion, allowing calculation of segmental resistances. Total and arterial vasodilatory responses to histamine, ET-1, and ionomycin were augmented in lungs from CH vs. control animals. However, CH did not alter the vasodilation to spermine NONOate or SNAP. PD-145065, glibenclamide, and TEA had no effect on responses to AVP in either group. We conclude that increased activity of arterial cNOS may be responsible for the augmented pulmonary arterial dilation to EDNO-dependent vasodilators following CH.

scholarly journals PSD95 scaffolding of the Shaker ‐type K + channel enables PKA‐dependent phosphorylation and vasodilation of cerebral arteries (1057.7)

2014 ◽  
Vol 28 (S1) ◽  
Author(s):  
Christopher Moore ◽  
Piper Nelson ◽  
Nikhil Parelkar ◽  
Hillary Hanvey ◽  
Nancy Rusch ◽  
...  
Keyword(s):  
Cerebral Arteries ◽  
K Channel ◽  
Type K

Long-lasting reduction of excitability by a sodium-dependent potassium current in cat neocortical neurons

1989 ◽  
Vol 61 (2) ◽  
pp. 233-244 ◽  
Author(s):  
P. C. Schwindt ◽  
W. J. Spain ◽  
W. E. Crill
Keyword(s):  
Voltage Clamp ◽  
Time Course ◽  
Outward Current ◽  
Repetitive Firing ◽  
K Channel ◽  
Channel Blockers ◽  
Dantrolene Sodium ◽  
Current Time ◽  
Tail Current ◽  
Neocortical Neurons

1. The function and ionic mechanism of a slow outward current were studied in large layer V neurons of cat sensorimotor cortex using an in vitro slice preparation and single microelectrode voltage clamp. 2. With Ca2+ influx blocked, a slow relaxation ("tail") of outward current followed either (1) repetitive firing evoked for 1 s or (2) a small 1-s depolarizing voltage clamp step that activated the persistent Na+ current of neocortical neurons, INaP. When a depolarization that activated INaP was maintained, an outward current gradually developed and increased in amplitude over a period of tens of seconds to several minutes. An outward tail current of similar duration followed repolarization. The slow outward current was abolished by TTX, indicating it depended on Na+ influx. 3. With Ca2+ influx blocked, the onset of the slow Na+-dependent outward current caused spike frequency adaptation during current-evoked repetitive firing. Following the firing, the decay of the Na+-dependent current caused a slow afterhyperpolarization (sAHP) and a long-lasting reduction of excitability. It also was responsible for habituation of the response to repeated identical current pulses. 4. The Na+-dependent tail current had properties expected of a K+ current. Membrane chord conductance increased during the tail, and tail amplitude was reduced or reversed by membrane potential hyperpolarization and raised extracellular K+ concentration [( K+]0). 5. The current tail was reduced reversibly by the K+ channel blockers TEA (5-10 mM), muscarine (5-20 microM), and norepinephrine (100 microM). These agents also resulted in a larger, more sustained inward current during the preceding step depolarization. Comparison of current time course before and after the application of blocking agents suggested that, in spite of its capability for slow buildup and decay, the onset of the Na+-dependent outward current occurs within 100 ms of an adequate step depolarization. 6. With Ca2+ influx blocked, extracellular application of dantrolene sodium (30 microM) had no clear effect on the current tail or the corresponding sAHP.(ABSTRACT TRUNCATED AT 400 WORDS)

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