Sodium-activated potassium conductance participates in the depolarizing afterpotential following a single action potential in rat hippocampal CA1 pyramidal cells.
The depolarizing afterpotential (DAP) following an action potential increases the excitability of a neuron. Mechanisms related to the DAP following an antidromic or current-induced spike were studied in CA1 pyramidal cells by whole-cell recordings in hippocampal slices in vitro. In DAP-holding voltage curves, the DAP at 10 ms after the spike peak (DAP10) was extrapolated to reverse at about -50 mV. Increase of extracellular K(+) concentration increased DAP and neuronal bursting. DAP10 reversal potential shifted positively with an increase in [K(+)](o) and with the blockade of K(+) conductance using pipettes filled with Cs(+). Similarly, extracellular tetraethylammonium (TEA; 10 mM), 4-aminopyridine (3-10 mM) increased DAP and shifted the DAP10 reversal potential to a depolarizing direction. Decrease of [Ca(2+)](o) did not alter DAP significantly, suggesting a nonessential role of Ca(2+) in the DAP. Perfusion of tetrodotoxin (TTX; 0.1-1 microM) and replacement of extracellular Na(+) by choline(+) suppressed both spike height and DAP simultaneously. Replacement of extracellular Na(+) by Li(+) increased DAP and spike bursts, and caused a positive shift of the DAP10 reversal potential. It is suggested that Li(+) increased DAP by blocking an Na(+)-activated K(+) current. In summary, multiple K(+) conductances are normally active during the DAP following a single action potential.
Liu
Xinhuai
X
Department of Physiology, University of Western Ontario, London, ON, Canada.
Stan Leung
L
L
D015761:4-Aminopyridine / Q000494:pharmacology; D000200:Action Potentials / Q000187:drug effects / Q000502:physiology*; D000818:Animals; D002118:Calcium / Q000378:metabolism; D002614:Chelating Agents / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D004347:Drug Interactions; D004533:Egtazic Acid / Q000031:analogs & derivatives* / Q000494:pharmacology; D004558:Electric Stimulation / Q000379:methods; D005071:Evoked Potentials / Q000187:drug effects / Q000502:physiology; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D005110:Extracellular Space / Q000187:drug effects / Q000378:metabolism; D005260:Female; D018756:GABA Antagonists / Q000494:pharmacology; D006624:Hippocampus / Q000166:cytology*; D066298:In Vitro Techniques; D007736:Kynurenic Acid / Q000494:pharmacology; D008094:Lithium / Q000378:metabolism; D008297:Male; D009431:Neural Conduction / Q000187:drug effects / Q000502:physiology*; D018408:Patch-Clamp Techniques / Q000379:methods; D010852:Picrotoxin / Q000494:pharmacology; D026902:Potassium Channel Blockers / Q000494:pharmacology; D015221:Potassium Channels / Q000502:physiology*; D017966:Pyramidal Cells / Q000187:drug effects / Q000502:physiology*; D011810:Quinoxalines / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D012964:Sodium / Q000378:metabolism*; D026941:Sodium Channel Blockers / Q000494:pharmacology; D019789:Tetraethylammonium / Q000494:pharmacology; D013779:Tetrodotoxin / Q000494:pharmacology
D015761:4-Aminopyridine; D002118:Calcium; D002614:Chelating Agents; D004533:Egtazic Acid; D018691:Excitatory Amino Acid Antagonists; D018756:GABA Antagonists; D007736:Kynurenic Acid; D008094:Lithium; D010852:Picrotoxin; D026902:Potassium Channel Blockers; D015221:Potassium Channels; D011810:Quinoxalines; D012964:Sodium; D026941:Sodium Channel Blockers; D019789:Tetraethylammonium; D013779:Tetrodotoxin; C056723:FG 9041; C025603:1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid