Galanin-R1 and -R2 Receptor MRNA Expression During the Development of Rat Brain Suggests Differential Subtype Involvement in Synaptic Transmission and Plasticity

The present study employed 35S-labelled oligonucleotides and in situ hybridization to examine the distribution in the developing rat brain of mRNA encoding two galanin receptor subtypes, i.e. Gal-R1 and Gal-R2. Gal-R1 and/or Gal-R2 mRNA was detected at embryonic day (E) 20 and from postnatal day (P) 0-70. Gal-R1 mRNA was highly expressed in olfactory regions, ventral hippocampal CA fields, dorsomedial thalamic areas and many hypothalamic nuclei at all ages studied. In adult brain, Gal-R2 mRNA was most abundant in the dentate gyrus, anterior and posterior hypothalamus, raphe and spinal trigeminal nuclei, and in the dorsal motor nucleus of the vagus. At P0-P7, Gal-R2 mRNA was more widely distributed and abundant than at other ages, with highest levels of expression detected throughout the neocortex and thalamus. Thus, Gal-R2 transcripts had a more restricted distribution than Gal-R1 and were differentially abundant at different ages, while the distribution and relative abundance of Gal-R1 mRNA did not alter substantially during postnatal development. In general, Gal-R1 and -R2 mRNAs were localized in regions previously shown to contain [125I]-galanin binding sites and galanin-positive terminals in adult brain. Galanin-immunostaining was assessed in postnatal brain to determine whether peptide innervation correlated with observed transient receptor expression, but was not particularly enriched in Gal-R2 mRNA-positive areas of P4 or P7 brain. These results, together with earlier findings [e.g. Burazin, T. C. D. & Gundlach, A. L. (1998) J. Neurochem., 71, 879-882], suggest that Gal-R1 receptors have a broad role in normal synaptic transmission, while Gal-R2 receptors, in addition to a similar role in particular pathways, may be involved in processes prominent during the establishment and maturation of synaptic connections in developing brain and during neural damage and repair in the mature nervous system.