Voltage dependent switch in the activity mode of the K+ channel in presynaptic nerve terminals

Butkevich, Alexander; Ohana, Ora; Meir, Amit; Rahamimoff, Rami

doi:10.1097/00001756-199707280-00024

Cited by 4 publications

(3 citation statements)

References 20 publications

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“…For example, the proportion of time that BK channels spent in mode 2 was increased by incubation with PKA or by increasing the concentration of intracellular Ca¥. However, unlike the A_type K¤ channel in Torpedo synaptosomes (Butkevich et al 1997), mode switching of BK channel activity in the present study is independent of membrane voltage such that the frequency of either mode is the same at all voltages examined. The addition of alkaline phosphatase and consequent likely removal of a crucial phosphate group from the BK channel irreversibly switches its gating into mode 2.…”

Section: Modal Switchingcontrasting

confidence: 48%

“…It has been reported that BKCa channel activity from rat brain synaptosomes incorporated into lipid bilayers display long periods (seconds) of channel closures (Farley & Rudy, 1988) which may be reminiscent of mode switching. In addition, K¤ channel activity recorded from fused Torpedo synaptosomes, which exhibited the kinetic properties of an A_type K¤ channel, also displayed mode switching in a voltagedependent manner (Butkevich et al 1997). The reasons why these channels undergo sudden transitions in their kinetic behaviour is not well understood, but there may be physiological mechanisms that contribute to or control this activity.…”

Section: Modal Switchingmentioning

confidence: 99%

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Mode switching characterizes the activity of large conductance potassium channels recorded from rat cortical fused nerve terminals

Smith

Ashford

1998

The Journal of Physiology

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Inside‐out recordings from rat cortical fused nerve terminals indicate that the most common channel observed was a large conductance K+ (BK) channel with characteristics dissimilar to conventional cell body calcium‐activated BK (BKCa) channels. BK channels exhibit mode switching between low (mode 1) and high (mode 2) activity, an effect not influenced by membrane voltage. Increasing internal Ca2+ concentration increased time spent in mode 2 as did application of protein kinase A, an effect not mimicked by protein kinase C or protein kinase G. Mode 1 activity was voltage independent although depolarization increased mode 2 channel activity. Global average channel activity was voltage and Ca2+ dependent. Alkaline phosphatase treatment induced channel activity to reside permanently in mode 2, where activity was voltage and Ca2+ dependent but unaffected by protein kinases A, G or C. Internal application of tetraethylammonium blocked BK channel activity in a manner identical to that reported for BKCa channels. These results indicate that nerve terminal membranes have large conductance K+ channels with significant differences in gating kinetics and regulation of activity compared with BKCa channels of other neuronal preparations. The BK channel subtype may play a unique physiological role specific to the nerve terminal.

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Section: Modal Switchingcontrasting

confidence: 48%

Section: Modal Switchingmentioning

confidence: 99%

Mode switching characterizes the activity of large conductance potassium channels recorded from rat cortical fused nerve terminals

Smith

Ashford

1998

The Journal of Physiology

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“…Under appropriate experimental conditions, oscillations in the activity of the channel with a period of approximately 20 s can be observed (Rahamimo¡ et al 1995) (¢gure 2b). Experimental evidence shows that these properties are likely to result from the entry of the channel into the voltage-dependent inactivated state (Butkevich et al 1997). We speculate that these properties may be of importance in frequency modulation phenomena.…”

Section: (I) the Bursting Potassium Channelmentioning

confidence: 74%

Multitude of ion channels in regulation of transmitter release

Rahamimoff

Butkevich

Duridanova

et al. 1999

Phil. Trans. R. Soc. Lond. B

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The presynaptic nerve terminal is of key importance in communication in the nervous system. Its primary role is to release transmitter quanta on the arrival of an appropriate stimulus. The structural basis of these transmitter quanta are the synaptic vesicles that fuse with the surface membrane of the nerve terminal, to release their content of neurotransmitter molecules and other vesicular components. We subdivide the control of quantal release into two major classes: the processes that take place before the fusion of the synaptic vesicle with the surface membrane (the pre-fusion control) and the processes that occur after the fusion of the vesicle (the post-fusion control). The pre-fusion control is the main determinant of transmitter release. It is achieved by a wide variety of cellular components, among them the ion channels. There are reports of several hundred different ion channel molecules at the surface membrane of the nerve terminal, that for convenience can be grouped into eight major categories. They are the voltage-dependent calcium channels, the potassium channels, the calcium-gated potassium channels, the sodium channels, the chloride channels, the non-selective channels, the ligand gated channels and the stretch-activated channels. There are several categories of intracellular channels in the mitochondria, endoplasmic reticulum and the synaptic vesicles. We speculate that the vesicle channels may be of an importance in the post-fusion control of transmitter release.

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