Specific neuronal subpopulations in the rat basolateral amygdala express high levels of nonphosphorylated neurofilaments

Cortical pyramidal neurons (PNs) containing nonphosphorylated neurofilaments (NNFs) localized with the SMI‐32 monoclonal antibody have been shown to be especially vulnerable to degeneration in Alzheimer's disease (AD). The present investigation is the first to study the expression of SMI‐32+ NNFs in neurons of the basolateral nuclear complex of the amygdala (BNC), which contains cortex‐like PNs and nonpyramidal neurons (NPNs). We observed that PNs in the rat basolateral nucleus (BL), but not in the lateral (LAT) or basomedial (BM) nuclei, have significant levels of SMI‐32‐ir in their somata with antibody diluents that did not contain Triton X‐100, but staining in these cells was greatly attenuated when the antibody diluent contained 0.3% Triton. Using Triton‐containing diluents, we found that all SMI‐32+ neurons in all three of the BNC nuclei were NPNs. Using a dual‐labeling immunoperoxidase technique, we demonstrated that most of these SMI‐32+ NPNs were parvalbumin‐positive (PV+) or somatostatin‐positive NPNs but not vasoactive intestinal peptide‐positive or neuropeptide Y‐positive NPNs. Using a technique that combines retrograde tracing with SMI‐32 immunohistochemistry using intermediate levels of Triton in the diluent, we found that all BNC neurons projecting to the mediodorsal thalamic nucleus (MD) were large NPNs, and most were SMI‐32+. In contrast, BNC neurons projecting to the ventral striatum or cerebral cortex were PNs that expressed low levels of SMI‐32 immunoreactivity (SMI‐32‐ir) in the BL, and no SMI‐32‐ir in the LAT or BM. These data suggest that the main neuronal subpopulations in the BNC that degenerate in AD may be PV+ and MD‐projecting NPNs.