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The Journal of Neuroscience, January 14, 2004, 24(2):350-355; doi:10.1523/JNEUROSCI.4933-03.2004

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BRIEF COMMUNICATION
Differential Calcium-Dependent Modulation of NMDA Currents in CA1 and CA3 Hippocampal Pyramidal Cells

Anton A. Grishin, Christine E. Gee, Urs Gerber, and Pascal Benquet

Brain Research Institute, University of Zurich, CH-8057 Zurich, Switzerland

Neuronal Ca²⁺ influx via NMDA receptors (NMDARs) is essential for the development and plasticity of synapses but also triggers excitotoxic cell death when critical intracellular levels are exceeded. Therefore, finely equilibrated mechanisms are necessary to ensure that NMDAR function is maintained within a homeostatic range. Here we describe a pronounced difference in the modulation of NMDA currents in two closely related hippocampal cell types, the CA1 and the CA3 pyramidal cells (PCs). Manipulations that increase intracellular Ca²⁺ levels strongly depressed NMDA currents in CA3 with only minor effects in CA1 PCs. Furthermore, activation of G_q-coupled metabotropic receptors potentiated NMDA currents in CA1 PCs but depressed them in CA3 PCs. Interestingly, the CA3 type modulation of NMDARs could be converted into CA1-like behavior, and vice versa, by increasing Ca²⁺ buffering in CA3 cells or decreasing Ca²⁺ buffering in CA1 cells, respectively. Our data suggest that a differential Ca²⁺ sensitivity of the regulatory cascades targeting NMDARs plays a key role in determining the direction and magnitude of NMDA responses in various types of neurons. These findings may have important implications for NMDA receptor-dependent synaptic plasticity and the differential sensitivity of CA1 and CA3 PCs to NMDAR-dependent ischemic cell death.

Key words: acetylcholine; ACh; depression; muscarinic; potentiation; glutamate; metabotropic glutamate receptor

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Received July 24, 2003; revised November 24, 2003; accepted November 24, 2003.

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