Filipov V. К+-activated Na+-gated potassium conductance in isolated pyramidal neurons of rat

Українська версія

Thesis for the degree of Candidate of Sciences (CSc)

State registration number

0499U001788

Applicant for

Specialization

  • 03.00.02 - Біофізика

22-06-1999

Specialized Academic Board

Д 26.198.01

Bogomoletz Institute of Physiology National of science of Ukraine

Essay

The dissertation is devoted to investigation of the responses of acutely isolated pyramidal neurons to rapidly altered external [K+] using the whole-cell patch clamp and concentration clamp techniques. The excitation of densely packed mammalian central neurons is followed by a substantial transitory elevation of external K+ concentration. This phenomenon may have a different functional significance depending on how the resting membrane conductance mechanisms react to the changes in the gradient of these ions. We have found that in the hippocampal and cortex neurons of rat a large fraction of the membrane conductance in the vicinity of the resting potential is provided by the K+ permeability mechanism which is gated by external K+ and Na+. Elevation of [K+]out induced a biphasic inward current at membrane potentials more negative than the reversal potential for K+ ions. This current consisted of an "instantaneously" increased leakage component and a slowly activated current (t = 40 - 50 ms at 21OC) desi gnated below as IDK. The latter demonstrated a first order activation kinetics with a remarkably high Q10 = 7.31 (n = 8). Potential at which IDK disappeared was found to be virtually indistinguishable from EK (n = 19). Qualitatively this voltage was shifted in accordance with the changes in EK like in the case of a typical inward rectifier. IDK was absent in the peripheral sensory neurons as well as in the Purkinje neurons. IDK may well be involved in the shaping of the response of the pyramidal neurons to the waves of external potassium elicited by the activity of neighbouring neurons. Its role could be in delaying the K+ - induced drop of the input resistance so that the late post - synaptic inhibition would not be excessively shunted.

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