Muscarinic suppression of a novel voltage-sensitive K+ current in a vertebrate neurone

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Abstract

Cholinergic excitation of vertebrate neurones is frequently mediated through the action of acetylcholine on muscarinic (atropine-sensitve) receptors. This type of excitation differs substantially from the better known nicotinic excitation. One difference is that, instead of an increased membrane conductance, a decreased conductance (to K+ ions) frequently accompanies muscarinic depolarisation. This has been detected in sympathetic, cortical and hippocampal neurones. Using voltage-clamped frog sympathetic neurones we have now identified a distinctive voltage-sensitive K+-current, separate from the delayed rectifier current, as the prime target for muscarinic agonists. We have termed this current the M-current, IM.

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Voltage clamp studies of a transient outward membrane current in gastropod neural somata.

Guus G. C. F. Stevens, Stephen Connor (1971)

1. Outward directed membrane currents have been studied in voltage clamp experiments on isolated neural somata of the marine gastropod Anisodoris.2. Stepping the membrane potential from a hyperpolarized level to a value in the neighbourhood of resting potential (-35 to -50 mV at 5 degrees C) results in an outward current transient, I(A), which is apparently carried by potassium ions.3. The peak amplitude of I(A) is dependent upon both the holding voltage level and the test step voltage while the time courses of development and decay are independent of, or only slightly dependent on, these parameters.4. The developing and decaying phases of I(A) are approximated by exponentials, leading to time constants for development of 10-25 msec and for decay of 220-600 msec over the aggregate of cells studied (data at 5 degrees C). Q(10) for the processes is approximately 3.5. It is concluded that the transport mechanism for I(A) is at least operationally distinct from the mechanism underlying delayed outward current, I(K).

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The mechanism of excitation by acetylcholine in the cerebral cortex.

K Krnjević, L Renaud, R Pumain (1971)

1. The muscarinic depolarizing action of ACh on cortical neurones is associated with an increase in membrane resistance (mean DeltaV/DeltaR = 3.16 mV/MOmega).2. ACh also promotes repetitive firing by slowing repolarization after spikes.3. The depolarizing effect has a mean reversal level of -86.7 mV (with mean resting potential -56 mV).4. It is concluded that as a muscarinic excitatory agent, ACh probably acts by reducing the resting K(+) conductance of cortical neurones, and also the delayed K(+) current of the action potential.5. These results are discussed in relation to the possible role of ACh in cortical function.

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Three pharmacologically distinct potassium channels in molluscan neurones.

Hilary Thompson (1977)

1. Potassium currents were studied under voltage-clamp conditions in nerve cell bodies of the nudibranch Tritonia diomedia. 2. Potassium currents could be separated into three distinct components on the basis of their sensitivity to 4-aminopyridine (4-AP), tetraethyl-ammonium (TEA) and to Co2+ and Mn2+ ions. 3. A transient potassium current, similar to the fast outward current described by Connor & Stevens (1971b) and Neher (1971), was blocked by externally applied 4-AP but was much less sensitive to TEA or to Co2+ or Mn2+. A single 4-AP ion binds each receptor with an apparent dissociation constant of 1-5 X 10(-3) M. 4-AP decreases the rates of activation and inactivation and reduces the maximum conductance of transient current channels. 4. Delayed outward current was not effected by 4-AP at concentrations which blocked the transient current, but it could be divided into two components by external application of TEA and Co2+ or Mn2+. 5. A voltage-dependent component of delayed current, termed K-current, was blocked by TEA. Each K-current receptor binds a single TEA ion with an apparent dissociation constant of 8 X 10(-3) M. Co2+ and Mn2+ have little or no effect on K-current. 6. A second component of delayed outward current, termed C-current, depends on Ca2+ entry for its activation. It is similar to the Ca2+ dependent potassium current reported by Meech & Stranden (1975) in Helix cells. C-current is essentially blocked by 30 mM external Co2+ or Mn2+. It is little affected by TEA, however, being reduced by about 20% at a TEA concentration of 100 mM. 7. It is concluded that three sets of potassium selective channels contribute to the outward current and that these channels can be separated pharmacologically.

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Title: Nature

Abbreviated Title: Nature

Publisher: Springer Science and Business Media LLC

ISSN (Print): 0028-0836

ISSN (Electronic): 1476-4687

Publication date Created: February 1980

Publication date (Print): February 1980

Volume: 283

Issue: 5748

Pages: 673-676

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DOI: 10.1038/283673a0

PubMed ID: 6965523

SO-VID: 41f3a247-875a-47c7-9e25-ce5e9ea9c2ab

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Muscarinic suppression of a novel voltage-sensitive K+ current in a vertebrate neurone

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Most cited references 9

Voltage clamp studies of a transient outward membrane current in gastropod neural somata.

The mechanism of excitation by acetylcholine in the cerebral cortex.

Three pharmacologically distinct potassium channels in molluscan neurones.

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