A mutation that increases a novel calcium-activated potassium conductance ofParamecium tetraurelia

1986 ◽  
Vol 91 (2) ◽  
pp. 173-181 ◽  
Author(s):  
E. A. Richard ◽  
Y. Saimi ◽  
C. Kung
Keyword(s):  
Potassium Conductance ◽  
Calcium Activated Potassium Conductance

scholarly journals Presynaptic facilitation at the crayfish neuromuscular junction. Role of calcium-activated potassium conductance.

1991 ◽  
Vol 98 (6) ◽  
pp. 1181-1196 ◽  
Author(s):  
S Sivaramakrishnan ◽  
M S Brodwick ◽  
G D Bittner
Keyword(s):  
Neuromuscular Junction ◽  
Transmitter Release ◽  
Time Course ◽  
Potassium Conductance ◽  
Early Time ◽  
Release Mechanism ◽  
Free Calcium ◽  
Test Pulse ◽  
Current Pulses ◽  
Calcium Activated Potassium Conductance

Membrane potential was recorded intracellularly near presynaptic terminals of the excitor axon of the crayfish opener neuromuscular junction (NMJ), while transmitter release was recorded postsynaptically. This study focused on the effects of a presynaptic calcium-activated potassium conductance, gK(Ca), on the transmitter release evoked by single and paired depolarizing current pulses. Blocking gK(Ca) by adding tetraethylammonium ion (TEA; 5-20 mM) to a solution containing tetrodotoxin and aminopyridines caused the relation between presynaptic potential and transmitter release to steepen and shift to less depolarized potentials. When two depolarizing current pulses were applied at 20-ms intervals with gK(Ca) not blocked, the presynaptic voltage change to the second (test) pulse was inversely related to the amplitude of the first (conditioning) pulse. This effect of the conditioning prepulse on the response to the test pulse was eliminated by 20 mM TEA and by solutions containing 0 mM Ca2+/1 mM EGTA, suggesting that the reduction in the amplitude of the test pulse was due to activation of gK(Ca) by calcium remaining from the conditioning pulse. In the absence of TEA, facilitation of transmitter release evoked by a test pulse increased as the conditioning pulse grew from -40 to -20 mV, but then decreased with further increase in the conditioning depolarization. A similar nonmonotonic relationship between facilitation and the amplitude of the conditioning depolarization was reported in previous studies using extracellular recording, and interpreted as supporting an additional voltage-dependent step in the activation of transmitter release. We suggest that this result was due instead to activation of a gK(Ca) by the conditioning depolarization, since facilitation of transmitter release increased monotonically with the amplitude of the conditioning depolarization, and the early time course of the decay of facilitation was prolonged when gK(Ca) was blocked. The different time courses for decay of the presynaptic potential (20 ms) and facilitation (greater than 50 ms) suggest either that residual free calcium does not account for facilitation at the crayfish NMJ or that the transmitter release mechanism has a markedly higher affinity or stoichiometry for internal free calcium than does gK(Ca). Finally, our data suggest that the calcium channels responsible for transmitter release at the crayfish NMJ are not of the L, N, or T type.

Calcium-Activated Potassium Conductance

1987 ◽  
Vol 151 (4) ◽  
pp. 455-459 ◽  
Author(s):  
Timothy G. Dinan
Keyword(s):  
Sensory Processing ◽  
Potassium Conductance ◽  
Action Potential Generation ◽  
Potential Generation ◽  
Heterogenous Group ◽  
Antipsychotic Activity ◽  
Biochemical Studies ◽  
Dopamine Hypothesis ◽  
Calcium Activated Potassium Conductance ◽  
Physiological And Biochemical

Neuroleptics are structurally a heterogenous group of compounds which possess antipsychotic activity. They increase dopamine metabolites by blocking dopamine receptors and enhancing presynaptic turnover. This forms the cornerstone of the dopamine hypothesis of neuroleptic action, which is supported by wide-ranging behavioural, physiological and biochemical studies. It is, however, clear that neuroleptics are far less specific for the dopamine receptor than was previously considered. They influence a range of neuronal activities, including calcium-activated potassium conductance, which governs the rate of action potential generation by many neurones. Recent physiological studies indicate that all commonly used neuroleptics alter calcium-activated potassium conductance in central neurones, in concentrations similar to those achieved clinically. An adaptive increase in calcium-activated potassium conductance mechanisms in key sensory processing neurones would render the psychotic patient less susceptible to bombardment by environmental stimuli. This action may explain in part the therapeutic effect of neuroleptics.

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