Restricted expression of LGR8 in intralaminar thalamic nuclei of rat brain suggests a role in sensorimotor systems

Ann N Y Acad Sci. 2005 May;1041:510-5. doi: 10.1196/annals.1282.076.

Abstract

LGR8 was recently identified as a cognate receptor for insulin-like peptide-3 (INSL3), and INSL3-LGR8 signaling is best known for its role in testis descent during development. LGR8 mRNA has been detected in various human tissues including brain, but the regional and cellular distribution of LGR8 expression in the mammalian central nervous system is unknown. Therefore, in this study we investigated the presence and localization of LGR8 mRNA in rat brain using reverse transcription-polymerase chain reaction and in situ hybridization histochemistry. Results revealed a distinct distribution of LGR8 in forebrain, with transcripts principally restricted to the posterior thalamus and highest densities detected in the parafascicular nucleus of both adult and developing rats. Unexpectedly, INSL3 mRNA was not detected in brain by similar methods, but preliminary electrophysiologic studies of parafascicular neurons revealed that INSL3 altered their activity. These findings suggest that LGR8 signaling may be involved in sensorimotor control in the rat and perhaps other species, particularly via actions on parafascicular neurons that project to basal ganglia and are depleted in Parkinson's disease.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aging / physiology
  • Animals
  • Brain / drug effects
  • Brain / metabolism*
  • Electrophysiology
  • Gene Expression / drug effects
  • Insulin / genetics
  • Insulin / metabolism
  • Insulin / pharmacology
  • Ligands
  • Male
  • Patch-Clamp Techniques
  • Proteins / genetics
  • Proteins / metabolism
  • Proteins / pharmacology
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism
  • Rats
  • Receptors, G-Protein-Coupled
  • Receptors, Peptide / genetics
  • Receptors, Peptide / metabolism*
  • Thalamic Nuclei / drug effects
  • Thalamic Nuclei / metabolism*

Substances

  • Insulin
  • Leydig insulin-like protein
  • Ligands
  • Proteins
  • RNA, Messenger
  • Receptors, G-Protein-Coupled
  • Receptors, Peptide
  • relaxin receptors