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Substantia gelatinosa neurons in the medullary dorsal horn: An intracellular labeling study in the rat

Morphologic features and electrical membrane properties of neurons in the substantia gelatinosa (SG) of the caudal spinal trigeminal nucleus (the medullary dorsal horn; MDH) were examined in the rat. Intracellular recording and biocytin‐injection combined with histochemical staining were performed in horizontal slices. Twenty‐four SG (lamina II) neurons were recorded stably and stained successfully. Both projection neurons (PNs; n = 9) that sent axons to regions outside the MDH and intrinsic neurons (INs; n = 15) that sent axons only to the MDH were observed. The INs were divided into those with dense axonal arborization (INDAs; n = 7) and those with sparse axonal arborization (INSAs; n = 8). In the PNs, the dendrites with spines spread to all MDH layers (laminae I–III). The main axons sent collaterals within the SG and rostrally, caudally, or medially to laminae I and III of the MDH, interpolar spinal trigeminal nucleus, spinal tract of the trigeminal nerve, or upper cervical cord segments. In the INDAs, the dendrites arising from the rostral and caudal pole of the cell bodies mainly extended rostrally and caudally parallel to the rostrocaudal axis of the SG: the dendritic trees were elongated and oval in shape and were confined within the SG. The axonal field of each INDA, a dense mesh of axonal processes, was elongated and oval in shape and almost was confined within the SG. In the INSAs, a small, round cell body was located in the center of each dendritic field, which usually was limited within the SG. Axonal processes ran radially to spread to all layers of the MDH, constituting round or oval axonal fields. The three groups of SG neurons showed more or less different intracellular responses to current injections. In particular, adaptation of spike frequency, hyperpolarizing sag, and rebound excitation were observed in the PNs and INSAs but not in the INDAs. Slow ramp depolarization and slow afterdepolarization were recorded only in INDAs. J. Comp. Neurol. 411:399–412, 1999. © 1999 Wiley‐Liss, Inc.