Effect of metabolic inhibition on K+ channels in pyramidal cells of the hippocampal CA1 region in rat brain slices.

Abstract

1. The effect of metabolic inhibition on membrane potential and ionic conductances of K+ channels was studied with the patch-clamp technique in pyramidal cells in the CAl region of the hippocampus. Individual cells were visualized in brain slices from rats aged between 9 and 19 days using infrared video microscopy. Excitability was inhibited by tetrodotoxin. 2. Dinitrophenol (DNP), carbonyl cyanide p-trifluoromethoxyphenylhydrazone (FCCP) and cyanide hyperpolarized the majority of the cells. The resting potential (V) was -55-3 + 0-23 mV (n = 147). In response to DNP the change in V was -3-9 + 0-76 mV (n = 59), with a normal distribution ranging between +9 0 and -16 mV.3. Metabolic inhibition increased the resting conductance (grest) and the conductance related to the delayed outward current measured at V = -20 mV (9)(10)(11)(12)(13)(14)(15)(16)(17)(18)(19)(20), and decreased the conductance of the early outward A-current (gA).

Effect of Valproate, Lamotrigine and Levetiracetam on Excitability and Firing Properties of CA1 Neurons in Rat Brain Slices

“…Control cells as well as drug treated ones showed a continuous mean hyperpolarization which may be due to the gradual exchange of solution content, causing a drift in the junction potential at the interface between pipette solution and cytoplasm. Before drug treatment, V 0 was similar to the value found in earlier patch-clamp studies on CA1 cells (Hyllienmark and Brismar 1996;Englund et al 2004).…”

FCCP depolarizes plasma membrane potential by activating proton and Na+ currents in bovine aortic endothelial cells

“…creased K + conductance [21], but the proposed nature of the K + conductance mediating this response differs between studies [16,19,24]. In contrast, FCCP evoked a rapid depolarization in rat carotid body type I cells, which was found to be due to the inhibition of a background K + conductance and the generation of an unidentified small inward current [3].…”

“…In rat dissociated hippocampal neurons, FCCP hyperpolarized the majority of the cells [16], mimicking the responses to hypoxia in those cells [10]. This hyperpolarization was clearly driven by an in-…”

Mice transgenically overexpressing sulfonylurea receptor 1 in forebrain resist seizure induction and excitotoxic neuron death

“…Although K ATP channels may help regulate seizure thresholds (19,20) and sensitivity to metabolic stress of neurons in the hippocampus and other brain regions (21)(22)(23), this concept remains controversial (13,16). While some investigations suggest that the neuroprotective actions of SUR openers in the hippocampus in vitro may not be mediated by K ATP channels (24,25), single-cell reverse transcriptase-PCR studies indicate that the heterogeneous K ATP channel subunit composition in hippocampal neuron subpopulations may explain their differential sensitivity to hypoxia and excitotoxicity Abbreviations: CMK, calcium-calmodulin kinase II␣; Hsp, heat-shock protein; KA, kainic acid; KATP, ATP-sensitive potassium; Kir, inwardly rectifying potassium; SUR, sulfonylurea receptor; Tg, transgenic; WT, wild type. § To whom reprint requests should be addressed.…”