Control of the repetitive discharge of rat CA 1 pyramidal neurones in vitro.

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Abstract
Experiments using intracellular recording techniques were performed on rat hippocampal neurons in vitro, to study the discharge properties of these cells. When CA 1 pyramidal cells were excited by injecting long depolarizing current pulses (.apprx. 600-800 ms), they responded with an initial rapid action potential discharge which slowed, or accommodated, and then stopped after 200-300 ms. The train of action potentials was followed by a hyperpolarization which was due primarily to Ca-activated K conductance (GK(Ca)). The amplitude of this hyperpolarization increased with an increasing number of action potentials in the initial discharge. Blocking the Ca-activated K conductance, by injecting EGTA [ethylene glycol-bis(.beta.-aminoethyl ether)N,N,N,N''-tetraacetic acid] into the cell, by bathing the cell in Cd, a Ca channel blocker, or by bathing the cell in Ca-free medium, reduced the after-hyperpolarization (a.h.p.) and accommodation such that the frequency of action potential discharge increased and the duration of this discharge was prolonged. Blocking the Ca-activated K conductance had a greater effect on discharge frequency later in the action potential train, as late interspike intervals were shortened more than early ones by the application of Cd or of Ca-free medium. This was presumably because the Ca-activated K conductance was more developed later in the train. Accommodation was not completely abolished in the absence of Ca and presence of Cd, suggesting that other factors, in addition to Ca-activated K conductance, contributed to this process. This remaining accommodation was reduced by low doses of carbachol, suggesting that the M-current also plays a role in accommodation. Accommodation of the action potential discharge of hippocampal pyramidal cells may be regulated by at least 2 K currents: the Ca-activated K current and the M-current. Both of these currents are turned on during excitation of the neuron and act in an inhibitory manner on that neuron to limit further action potential discharge.