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The types of neuron which contain protein kinase C gamma in rat spinal cord
Protein kinase C (PKC) is thought to have a role in sensitization of dorsal horn neurons in certain pain states, and a recent study has reported that mice which lack the γ isoform (PKCγ) show reduced neuropathic pain after peripheral nerve injury. Although PKCγ is present at high levels in the ventr...
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Published in: | Brain research 1999-06, Vol.833 (1), p.71-80 |
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Main Authors: | , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | Protein kinase C (PKC) is thought to have a role in sensitization of dorsal horn neurons in certain pain states, and a recent study has reported that mice which lack the γ isoform (PKCγ) show reduced neuropathic pain after peripheral nerve injury. Although PKCγ is present at high levels in the ventral part of lamina II we have limited information concerning the types of neuron in which it is located. In this study we have used immunocytochemistry to characterise the neurons which contain PKCγ. Immunoreactive neurons were concentrated in ventral lamina II, but were also present in lamina III. Some weakly-immunoreactive neurons were located in the dorsal part of lamina II and in lamina I. The great majority (92%) of cells with PKCγ were not GABA-immunoreactive, and these cells are likely to be excitatory interneurons. Dual-immunofluorescence labelling showed that PKCγ was not randomly distributed amongst non-GABAergic neurons, since it was present in 76% of cells with neurotensin and 45% of those with somatostatin, but only 5% of those with the μ-opioid receptor (MOR-1). Cells with the neurokinin 1 receptor are found in lamina I and lamina III, and PKCγ was present in 22% and 37% of these populations, respectively. These results suggest that excitatory interneurons in laminae II and III which lack the μ-opioid receptor may have a significant role in generating neuropathic pain. |
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ISSN: | 0006-8993 1872-6240 |
DOI: | 10.1016/S0006-8993(99)01500-0 |