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Publication : Expression of cholecystokinin by neurons in mouse spinal dorsal horn.

First Author  Gutierrez-Mecinas M Year  2019
Journal  J Comp Neurol Volume  527
Issue  11 Pages  1857-1871
PubMed ID  30734936 Mgi Jnum  J:280700
Mgi Id  MGI:6355557 Doi  10.1002/cne.24657
Citation  Gutierrez-Mecinas M, et al. (2019) Expression of cholecystokinin by neurons in mouse spinal dorsal horn. J Comp Neurol 527(11):1857-1871
abstractText  Excitatory interneurons account for the majority of dorsal horn neurons, and are required for perception of normal and pathological pain. We have identified largely non-overlapping populations in laminae I-III, based on expression of substance P, gastrin-releasing peptide, neurokinin B, and neurotensin. Cholecystokinin (CCK) is expressed by many dorsal horn neurons, particularly in the deeper laminae. Here, we have used immunocytochemistry and in situ hybridization to characterize the CCK cells. We show that they account for ~7% of excitatory neurons in laminae I-II, but between a third and a quarter of those in lamina III. They are largely separate from the neurokinin B, neurotensin, and gastrin-releasing peptide populations, but show limited overlap with the substance P cells. Laminae II-III neurons with protein kinase Cgamma (PKCgamma) have been implicated in mechanical allodynia following nerve injury, and we found that around 50% of CCK cells were PKCgamma-immunoreactive. Neurotensin is also expressed by PKCgamma cells, and among neurons with moderate to high levels of PKCgamma, ~85% expressed CCK or neurotensin. A recent transcriptomic study identified mRNA for thyrotropin-releasing hormone in a specific subpopulation of CCK neurons, and we show that these account for half of the CCK/PKCgamma cells. These findings indicate that the CCK cells are distinct from other excitatory interneuron populations that we have defined. They also show that PKCgamma cells can be assigned to different classes based on neuropeptide expression, and it will be important to determine the differential contribution of these classes to neuropathic allodynia.
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