IN-VITRO KAINATE INJURY TO LARGE, SMI-32(+) SPINAL NEURONS IS CA2+ DEPENDENT

THE non-phosphorylated neurofilament marker, SMI-32, identifies ventra l horn motor neurons in spinal cord slice. We show here that SMI-32 ma rks a subset of spinal cord neurons in culture. Many of these neurons ('large SMI-32(+) neurons') have morphological characteristics of iden tified motor neurons in vitro: large cell body size (> 20 mu m), exten sive neuritic arborization and, generally, one particularly long proce ss. These neurons are preferentially injured by brief (40 min) kainate exposures, but not by NMDA exposures. This rapidly triggered damage t o large SMI-32(+) neurons is Ca2+ dependent. In addition, most of the SMI-32(+) neurons exhibit kainate-stimulated Co2+ uptake, a histochemi cal technique which marks neurons possessing Ca2+-permeable AMPA/kaina te receptor-gated channels. The unusual vulnerability of large SMI-32( +) spinal neurons to kainate toxicity may result from rapid Ca2+ entry through Ca2+-permeable AMPA/kainate channels.