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TRANSLATIONAL PHYSIOLOGY

Longitudinal Depolarization Gradients Along the Somatodendritic Axis of CA1 Pyramidal Cells: A Novel Feature of Spreading Depression

¹Experimental and Computational Neurophysiology Laboratory, Department of Investigación-Histología, Hospital Ramón y Cajal, Madrid; ²Department of Matemática Aplicada, School of Biology, University Complutense of Madrid, Madrid; and ³School of Cieucias Experimentales y Salud, University of San Pablo, Madrid, Spain

Submitted 8 November 2004; accepted in final form 23 March 2005

We studied the subcellular correlates of spreading depression (SD) in the CA1 rat hippocampus by combining intrasomatic and intradendritic recordings of pyramidal cells with extracellular DC and evoked field and unitary activity. The results demonstrate that during SD only specific parts of the dendritic membranes are deeply depolarized and electrically shunted. Somatic impalements yielded near-zero membrane potential (V_m) and maximum decrease of input resistance (R_in) whether the accompanying extracellular negative potential (V_o) moved along the basal, the apical or both dendritic arbors. However, apical intradendritic recordings showed a different course of local V_m that is hardly detected from the soma. A decreasing depolarization gradient was observed from the edge of SD-affected fully depolarized subcellular regions toward distal dendrites. Within apical dendrites, the depolarizing front moved toward and stopped at proximal dendrites during the time course of SD so that distal dendrites had repolarized in part or in full by the end of the wave. The drop of local R_in was initially maximal at any somatodendritic loci and also recovered partially before the end of SD. This recovery was stronger and faster in far dendrites and is best explained by a wave-like somatopetal closure of membrane conductances. Cell subregions far from SD-affected membranes remain electrically excitable and show evoked unitary and field activity. We propose that neuronal depolarization during SD is caused by current flow through extended but discrete patches of shunted membranes driven by uneven longitudinal depolarization.

This article has been cited by other articles:

				O. Herreras, G. Somjen, and A. Strong Electrical prodromals of spreading depression void Grafstein's potassium hypothesis J Neurophysiol, November 1, 2005; 94(5): 3656 - 3657. [Full Text] [PDF]