MEDIAL LEMNISCAL AND SPINAL PROJECTIONS TO THE MACAQUE THALAMUS - AN ELECTRON-MICROSCOPIC STUDY OF DIFFERING GABAERGIC CIRCUITRY SERVING THALAMIC SOMATOSENSORY MECHANISMS

The synaptic relationships formed by medial lemniscal (ML) or spinotha lamic tract (STT) axon terminals with neurons of the somatosensory ven troposterolateral thalamic nucleus of the macaque monkey have been exa mined quantitatively by electron microscopy. ML and STT axons were lab eled by the anterograde axon transport of WGA-HRP following injection of the tracer into the contralateral dorsal column nuclei, or the dors al horn of the spinal cord, respectively. Thalamic tissue was histoche mically reacted for the presence of HRP. Serial thin sections were sta ined with a gold-labeled antibody to GABA, to determine which neuronal elements exhibited GABA immunoreactivity (GABA-ir). Serially sectione d thalamic structures were recorded in electron micrographs and recons tructed in three dimensions by computer. Individual ML axon terminals form multiple synaptic contacts with segments of the proximal dendriti c trees of thalamocortical relay neurons and also synapse upon the den dritic appendages of GABA-ir interneurons (local circuit neurons). The se GABA-ir dendritic appendages contain synaptic vesicles and are pres ynaptic (presynaptic dendrites) to the same segments of relay neuron d endrites that receive ML contacts. When analyzed in serial sections an d reconstructed by computer, the ML terminals form triadic relationshi ps (ML, GABA appendage, and relay neuron dendrite) or more complex glo merular arrangements involving multiple appendages, all of which then contact the relay neuron dendritic segment. In contrast, multiple STT terminals make synaptic contacts along segments of projection neuron d endrites and are usually the only type of profile to contact that segm ent of dendrite. More than 85% of the spinal afferents form simple axo dendritic synapses with relay cells and do not contact GABA-ir appenda ges. The thalamic synaptic relationships of ML terminals are fundament ally different from those formed by the STT. Because STT neurons predo minately transmit information about noxious stimuli, the simple axoden dritic circuitry of the majority of these spinal afferents suggests th at the transmission of noxious information is probably not subject to GABAergic modulation by thalamic interneurons, in contrast to the GABA ergic processing of non-noxious information carried by the ML afferent s. The differences in the GABAergic circuits of the thalamus that medi ate ML and STT afferent information are believed to underlie different ial somatosensory processing in the forebrain. We suggest that changes in thalamic GABAergic dendritic appendages and GABA receptors followi ng CNS injury may play a role in the genesis of some central pain stat es.