Nucleus basalis neurons exhibit axonal branching with decreased impulse conduction velocity in rat cerebrocortex

Abstract

Single neurons in the basal forebrain (nucleus basalis area) were antidromically activated from the frontal or parietal cortex in anesthetized rats. Wide ranges of antidromic latencies were observed overall, with frontal and parietal stimulation yielding values ranging from 1.0 to 26.0 ms and 1.6-24.0 ms, respectively. Individual neurons often exhibited multiple antidromic latencies, such that deeper sites of stimulation or greater stimulation amplitudes generally yielded discretely different, shorter latencies than more superficial sites or lower amplitudes of stimulation. Single neurons were also often driven from neighboring sites (1-2 mm apart) within the frontal cortex, but no cell was coactivated from both frontal and parietal cortices. Finally, patterns and rates of spontaneous activity varied markedly among these cortically projecting neurons, with some cells being non-spontaneous and others exhibiting tonic rates of 30-40 Hz. Impulse waveforms also differed among driven cells, from relatively low-amplitude, negative spikes to large-amplitude, entirely positive spikes in unfiltered signals. These results indicate that cortically projecting, putatively cholinergic neurons in the basal fore-brain form a physiologically heterogeneous population in terms of impulse conduction velocity, spontaneous discharge, and spike waveforms. Our finding of multiple antidromic latencies and driving from neighboring sites indicate that these fibers may be highly branched in local terminal fields, but that individual cells may project exclusively to a single cortical area. Faster conduction velocities for deep compared to superficial cortical stimulation sites imply that these fibers may become non-myelinated upon entering cortical terminal fields, or that they may become markedly thinner as they travel within the cortex. This system of cholinergic cortical afferents differs in many physiologic aspects from the other non-thalamic cortical input systems of catecholamine or indoleamine neurons.