CCK-ergic mechanisms in sensory systems

Scand J Clin Lab Invest Suppl. 2001:234:69-74.

Abstract

The histochemical analysis of cholecystokinin (CCK) systems in sensory systems has revealed involvement of CCK-ergic mechanisms both at the spinal level and in the viscero-sensory vagal pathway, with distinct differences between these two systems as well as between species. Thus, the CCK1 receptor is particularly abundant in rat nodose ganglion neurons which express the food intake-suppressing cocaine- and amphetamine-regulated transcript (CART) peptide(s), representing a likely link between gastrointestinal CCK and central feeding-regulatory centers. In contrast, rat dorsal root ganglions have lower numbers of CCK1 receptor mRNA-positive neurons, and CART is only expressed sparingly in this system. The CCK2 receptor is normally almost absent from both systems but is strongly upregulated after peripheral nerve injury, suggesting a role in regenerative and trophic phenomena as well as, at the spinal level, in nerve injury-induced pain. In man and monkey the CCK1 receptor seems important in the dorsal horn under normal conditions, indicating distinct species differences.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Cholecystokinin / physiology*
  • Ganglia, Spinal / physiology
  • Haplorhini
  • Humans
  • Nerve Tissue Proteins / genetics
  • Nerve Tissue Proteins / physiology
  • Neurons, Afferent / physiology*
  • Nodose Ganglion / physiology
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism
  • Rats
  • Receptor, Cholecystokinin A
  • Receptor, Cholecystokinin B
  • Receptors, Cholecystokinin / genetics
  • Receptors, Cholecystokinin / physiology

Substances

  • Nerve Tissue Proteins
  • RNA, Messenger
  • Receptor, Cholecystokinin A
  • Receptor, Cholecystokinin B
  • Receptors, Cholecystokinin
  • cocaine- and amphetamine-regulated transcript protein
  • Cholecystokinin