Postnatal development of inner lamina II interneurons of the rat medullary dorsal horn

Abstract

Pain processing in young mammals is immature. Despite the central role of the medullary dorsal horn (MDH) in processing orofacial sensory information, the maturation of the neurons within the MDH has been largely overlooked. Combining in vitro electrophysiological recordings and 3D morphological analysis over the first postnatal month in rats, we investigated the agedependent development of the neurons within the inner lamina II (IIi) of the MDH. We show the lamina IIi neuronal population transition into a more hyperpolarized state, with modification of the action potential waveform, and a shift from single spiking, at early postnatal ages, to tonic firing and initial bursting at later stages. These physiological changes are associated with a strong structural remodelling of the neuronal morphology with most of the modifications occurring after the third postnatal week. Among the lamina IIi neuronal population, the subpopulation of interneurons expressing the g isoform of the protein kinase C (PKCg 1 ) are key elements for the circuits underlying facial mechanical allodynia. How do they develop from the rest of the lamina IIi constitute an important question that remained to be addressed. Here, we show that PKCg 1 interneurons display electrophysiological changes over time comparable with the PKCg 2 population. However, they show a distinctive increase of the soma volume and primary branches length, as opposed to the PKCg 2 population. Together, our data demonstrate a novel pattern of late postnatal maturation of lamina IIi interneurons, with a spotlight on PKCg 1 interneurons, that may be relevant for the development of orofacial sensitivity.

GABAA and Glycine Receptor-Mediated Inhibitory Synaptic Transmission onto Adult Rat Lamina IIi PKCγ-Interneurons: Pharmacological but Not Anatomical Specialization

“…Key elements for such circuits are interneurons within lamina II i that express the γ isoform of protein kinase C (PKCγ) [5,6,[9][10][11]. Direct evidence for the activation of lamina II i PKCγ + interneurons under mechanical allodynia comes from studies of PKCγ immunoreactivity [12,13] and anatomical markers of neuronal activation (Fos protein and pERK1/2) [5,6,[14][15][16][17]. Moreover, genetic [10,18] or pharmacological inactivation of PKCγ [5,6,14,16] prevents mechanical allodynia, whereas its activation is sufficient to induce it [16].…”