| Substantia gelatinosa of Rolando | |
|---|---|
 Substantia gelatinosa of Rolando isRexed lamina II, labeled at upper left. | |
| Details | |
| Identifiers | |
| Latin | substantia gelatinosa cornu posterioris medullae spinalis |
| MeSH | D013376 |
| TA98 | A14.1.02.119 |
| TA2 | 6067 |
| FMA | 74019 |
| Anatomical terminology | |
Substantia gelatinosa of Rolando (SGR) (orgelatinous substance of the posterior horn), is a part of thespinal column. It forms the apex of theposterior grey column, one of threegrey columns in the spinal cord. It is a v-shaped, translucent mass ofneuroglia containing neuroglia cells and smallneurons. Its gelatinous appearance derives from abundantneuropil with fewmyelinated fibers.[1] It spans the entire spinal cord, extending into themedulla oblongata as thespinal trigeminal nucleus. Named afterLuigi Rolando, it corresponds toRexed lamina II.[2][3]
SGR, orlamina II, comprises outer and inner lamina II. In rodents, inner lamina II divides into dorsal and ventral sections, distinguished by their input and output projections.[4] SGR contains islet, central, stalked (large vertical), small vertical, and radial cells. Islet and small vertical cells primarily releaseGABA, inhibiting subsequent neurons, while large vertical and radial cells releaseglutamate, triggering depolarization. Central cells release either GABA or glutamate. These cells form synapses that receive inputs from each other and primaryafferent neurons, projecting to other lamina cells, creating complex excitatory and inhibitory circuits that transmit or suppress pain signals to the thalamus.[4]
SGR, alongside thenucleus proprius, serves as a synapse point for first-order neurons of thespinothalamic tract. It hosts numerousμ andκ-opioid receptors, bothpresynaptic andpostsynaptic that inhibit excitatory neurotransmitter release (e.g., substance P, glutamate) and hyperpolarize postsynaptic neurons to manage distal pain. Neuraxial opioid administration targets these receptors for analgesia.
C fibers, conveying slow, diffuse pain and temperature sensations, terminate in SGR. SomeA delta fibers, carrying fast, localized pain, also synapse there, passing through to thenucleus proprius, enabling cross-talk between pain pathways. C fibers in outer lamina II and dorsal inner lamina II release glutamate to excite neurons, with some releasingBDNF, which may excite or inhibit based on postsynaptic neuron traits. These fibers contribute to central sensitization in chronic pain. Fibers releasing peptides likeSST andGDNF may inhibit pain signaling.[4]
SGR projects excitatory signals to themarginal nucleus (lamina I) and laminae III–V.[4]
