The Journal of Neurophysiology Vol. 87 No. 2 February 2002, pp. 1169-1174
Copyright ©2002 by the American Physiological Society

RAPID COMMUNICATION

Distance-Dependent Ni²⁺-Sensitivity of Synaptic Plasticity in Apical Dendrites of Hippocampal CA1 Pyramidal Cells

 ¹Department of System Neuroscience, Tokyo Metropolitan Institute for Neuroscience, Tokyo 183-8526;  ²Core Research for Evolutional Science and Technology, Japan Science and Technology Corporation, Saitama 332-0012; and  ³Department of Biological Sciences, Tokyo Metropolitan University, Tokyo 192-0397, Japan

Isomura, Yoshikazu, Yoko Fujiwara-Tsukamoto, Michiko Imanishi, Atsushi Nambu, and Masahiko Takada. Distance-Dependent Ni²⁺-Sensitivity of Synaptic Plasticity in Apical Dendrites of Hippocampal CA1 Pyramidal Cells. J. Neurophysiol. 87: 1169-1174, 2002. Low concentration of Ni²⁺, a T- and R-type voltage-dependent calcium channel (VDCC) blocker, is known to inhibit the induction of long-term potentiation (LTP) in the hippocampal CA1 pyramidal cells. These VDCCs are distributed more abundantly at the distal area of the apical dendrite than at the proximal dendritic area or soma. Therefore we investigated the relationship between the Ni²⁺-sensitivity of LTP induction and the synaptic location along the apical dendrite. Field potential recordings revealed that 25 µM Ni²⁺ hardly influenced LTP at the proximal dendritic area (50 µm distant from the somata). In contrast, the same concentration of Ni²⁺ inhibited the LTP induction mildly at the middle dendritic area (150 µm) and strongly at the distal dendritic area (250 µm). Ni²⁺ did not significantly affect either the synaptic transmission at the distal dendrite or the burst-firing ability at the soma. However, synaptically evoked population spikes recorded near the somata were slightly reduced by Ni²⁺ application, probably owing to occlusion of dendritic excitatory postsynaptic potential (EPSP) amplification. Even when the stimulating intensity was strengthened sufficiently to overcome such a reduction in spike generation during LTP induction, the magnitude of distal LTP was not significantly recovered from the Ni²⁺-dependent inhibition. These results suggest that Ni²⁺ may inhibit the induction of distal LTP directly by blocking calcium influx through T- and/or R-type VDCCs. The differentially distributed calcium channels may play a critical role in the induction of LTP at dendritic synapses of the hippocampal pyramidal cells.