Synaptically activated increases in Ca2+ concentration in hippocampal CA1 pyramidal cells are primarily due to voltage-gated Ca2+ channels
H Miyakawa, WN Ross, D Jaffe, JC Callaway… - Neuron, 1992 - cell.com
Neuron, 1992•cell.com
Changes in intracellular Caz+ concentration ([Ca*+] J in the soma and dendrites of
hippocampal CA1 pyramidal neurons were measured using intracellularly injected fura-2. A
large component of the [Ca*+] i elevation caused by high frequency stimulation of the
Schaffer collaterals was correlated with the Na+ spikes triggered by the excitatory
postsynaptic potentials (EPSPs). These spikes were generated in the soma and proximal
dendrites and stimulated Ca*+ entry through voltage-gated Ca*+ channels. Suppressing …
hippocampal CA1 pyramidal neurons were measured using intracellularly injected fura-2. A
large component of the [Ca*+] i elevation caused by high frequency stimulation of the
Schaffer collaterals was correlated with the Na+ spikes triggered by the excitatory
postsynaptic potentials (EPSPs). These spikes were generated in the soma and proximal
dendrites and stimulated Ca*+ entry through voltage-gated Ca*+ channels. Suppressing …
Summary
Changes in intracellular Caz+ concentration ([Ca*+] J in the soma and dendrites of hippocampal CA1 pyramidal neurons were measured using intracellularly injected fura-2. A large component of the [Ca*+] i elevation caused by high frequency stimulation of the Schaffer collaterals was correlated with the Na+ spikes triggered by the excitatory postsynaptic potentials (EPSPs). These spikes were generated in the soma and proximal dendrites and stimulated Ca*+ entry through voltage-gated Ca*+ channels. Suppressing spikes by hyperpolarizing the soma or by injecting QX-314 revealed a smaller nonspike compo nent of Ca*+ entry. A substantial fraction of this component was mediated by the action of the EPSPs on voltagc-gated Ca*+ channels, because it persisted in 2-amino-5-phosphonovaleric acid and because it was usually reduced when Ca*+ channel activity was sup pressed by hyperpolarization. Ca*+ entry through the N-methyl-o-aspartate receptor channel could not be detected with certainty, perhaps because it was highly localized.
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