Some aspects of the electroanatomy of dendrites.

An understanding of the neuronal function requires the knowledge of the electroanatomy of dendrites, which comprise the major area and receive the main input in most neurons. Some simplifying assumptions are necessary to describe the electrical characteristics of the dendritic tree. The applicability of the simplified model of a combined equivalent dendritic cylinder proposed by Rall, was tested and verified by a combined analysis of anatomic and electrical data from the same spinal motoneurons. Assuming a uniform somadendritic membrane, estimates of the specific membrane resistance (RM: 2,700 +/- 920 omegacm2) were made by relating the neuronal input resistance with the combined dendritic trunk parameter (sigmaD3/2: 320 +/- 150-10(-6) CM3/2). From these combined anatomic and electrical data the dendritic electrotonic lengths (Lgeom: 1.5 +/- 0.3 times the length constant) were derived. Comparable L values (Ltrans: 1.5 +/- 0.3) resulted independently from analysis of membrane voltage transients during current steps. The linear dendritic cable model has proved its applicability for the analysis of small voltage deflections during current step applications at the soma as well as for the analysis of the majority of minimal postsynaptic potentials (PSP's). During the transmission along the dendritic cable the PSP undergoes changes in shape. These changes often permit a determination of the distance of the dendritic input from the soma. Unfortunately, the attenuation of the dendritic signal cannot be directly assessed. Dendritic synaptic transmission can be observed in isolation in chromatolytic motoneurons because the somal synapses are peeled off from the soma by proliferating glial cells in the course of retrograde reaction. These observations support the prediction that the PSP's with relatively short rise-times and duration originate from synapses near the soma. It may be questioned as to whether the linear dendritic cable approximation also applies to the larger voltage displacements during excitatory synaptic action. Particularly interesting is an increase of the apparent membrane resistance during depolarization known as anomalous rectification. The anomalous rectification could be reversibly eliminated and turned into a normal rectification by the application of cobalt ions or other calcium antagonists. Therefore, it appears likely that this phenomenon is caused by a voltage-(and time-) dependent reaction of the membrane, consisting of a smoothly increased calcium conductance during depolarizations that are even subthreshold for eliciting action potentials. Such a process would result in a shortening of the dendritic electrotonic length and in facilitating the postsynaptic excitatory transmission.