De novo expression of the neurokinin 1 receptor in spinal lamina I pyramidal neurons in polyarthritis

Abstract

Spinal lamina I (LI) neurons play a major role in the transmission and integration of pain-related information that is relayed to higher centers. Alterations in the excitability of these neurons influence chronic pain development, and expression of the neurokinin 1 receptor (NK-1r) is thought to play a major role in such changes. Novel expression of NK-1r may underlie hyperexcitability in new populations of LI neurons. LI projection neurons can be classified morphologically into fusiform, pyramidal, and multipolar cells, differing in their functional properties, with the pyramidal type being nonnociceptive. In agreement with this, we have shown that spinoparabrachial pyramidal neurons seldom express NK-1r, in contrast with the other two cell types. In this study we investigated in the rat the long-term changes in NK-1r expression by spinoparabrachial LI neurons following the unilateral injection in the hindpaw plantar surface of complete Freund's adjuvant (CFA). Cholera toxin subunit B (CTb) was injected unilaterally into the parabrachial nucleus. Our results revealed that, ipsilaterally, pyramidal neurons were seldom immunoreactive for NK-1r both in saline-injected and in CFA-injected rats, up to 10 days post-CFA. However, a considerable number of pyramidal cells were immunoreactive for NK-1r at 15, 21, and 30 days post-CFA. Our data raise the possibility -- which needs to be confirmed by electrophysiology -- that most LI projection neurons of the pyramidal type are likely nonnociceptive in naive animals but might become nociceptive following the development of arthritis.