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

Abstract

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.

Electric stimulation fMRI of the perforant pathway to the rat hippocampus

“…Standard surgical and stereotaxic procedures were applied for the placement of recording and stimulating electrodes, as previously described [7,8]. The local anesthetic xylocaine was used additionally for the surgery area.…”

Metabolic Challenge to Glia Activates an Adenosine-Mediated Safety Mechanism that Promotes Neuronal Survival by Delaying the Onset of Spreading Depression Waves

“…Also well known is the tight metabolic coupling between neurons and glial cells (reviewed in Araque et al, 2001), which, in the context of energy shortage, is indicated by the disruption of tissue homeostasis in parallel with the gradual decline of the electrical activity and irreversible injury to neurons on selective blockage of the glial Krebs cycle (Largo et al, 1996). In this process, a rapid loss of excitatory synaptic transmission is followed by the spontaneous development of periinfarct-like waves of spreading depression (SD) (Hossman, 1996;Canals et al, 2005b). Although SD has little impact in normal tissue (Herreras and Somjen, 1993), it kills neurons in brain regions deprived of glial activity according to a spatiotemporal pattern, which closely reproduces the sequence of events in the penumbra of an ischemic focus (Fabricius et al, 2006).…”

Role of HCN Channels in Neuronal Hyperexcitability after Subarachnoid Hemorrhage in Rats

“…In these brain areas, HCN1 subunits are densely distributed and expressed on the dendritic spines of pyramidal neurons (Magee, 1998;Lörincz et al, 2002;Notomi and Shigemoto, 2004;Nusser, 2009), and are involved in the integration of excitatory synaptic input and thereby influences the excitability of neural network (Magee, 1999;Williams and Stuart, 2003;Oviedo and Reyes, 2005;Tsay et al, 2007). Interestingly, cortical spreading depolarization is more readily provoked in hippocampus CA1 sector and neocortex (Somjen, 2001), and its generation as well as propagation is also greatly dependent on the apical dendrites of pyramidal neurons (Canals et al, 2005;Henning et al, 2005;Takano et al, 2007). Therefore, we speculate that HCN1 channels are potential regulative targets which contribute to the formation of neuronal hyperexcitability after SAH.…”