title: Differential expression of neuronal voltage-gated sodium channel mRNAs during the development of the rat trigeminal ganglion.
abstract: The developmental pattern of sodium channel expression in neurons of primary sensory ganglia is likely reflected in the electrical behavior of these cells. Little information is available on how voltage-gated sodium channels in sensory neurons are expressed during development in the trigeminal-innervated craniofacial region, where sensitivity is fundamental during early stages of life. Using in situ hybridization, we here demonstrate a differential both regional and transcript-dependent distribution of sodium channel alpha- and beta-subunits between Embryonic day (E)15 and Postnatal day (P)5/6 in the rat trigeminal ganglion. Na(v)1.3 mRNA was strongly expressed at E15, but declined to low levels at P5/P6. Na(v)1.8 was expressed at E15, increased to reach maximum levels at P1 and then decreased. Na(v)1.9 mRNA was detected at E19, reached a maximum at P1, and was then reduced. beta1 mRNA showed a steady rise in expression from E17, while beta2 mRNA was widely expressed from P1. beta 3 mRNA was detected at E15, reached a maximum at E19 followed by a decrease in expression. In the ophthalmic TG portion, there was a higher expression level of Na(v)1.8 and Na(v)1.9 between E19 and P5/P6 as compared to the maxillary/mandibular part, indicating an unexpected positional difference in channel distribution. mRNA levels of p11, which facilitates the expression of Na(v)1.8, were high at all stages. These findings show that trigeminal ganglion sodium channel transcripts mature in steps that are specific for each transcript. They also raise the possibility that different facial regions could differ in the ability to transmit sensory signals during early life.
authors.affiliation: Center for Oral Biology, Novum, Karolinska Institutet, POB 4064, SE-141 04 Huddinge, Sweden.
authors.forename: Jonas
authors.initials: J
authors.lastname: Thun
authors.forename: Anna-Karin
authors.initials: AK
authors.lastname: Persson
authors.forename: Kaj
authors.initials: K
authors.lastname: Fried
mesh_terms: D000818:Animals; D017306:Annexin A2 / Q000235:genetics; D005260:Female; D018507:Gene Expression Regulation, Developmental; D017403:In Situ Hybridization; D062552:NAV1.3 Voltage-Gated Sodium Channel; D062559:NAV1.8 Voltage-Gated Sodium Channel; D062558:NAV1.9 Voltage-Gated Sodium Channel; D009419:Nerve Tissue Proteins / Q000235:genetics*; D009437:Neuralgia / Q000235:genetics / Q000503:physiopathology; D009479:Neuropeptides / Q000235:genetics*; D011247:Pregnancy; D021122:Protein Subunits / Q000235:genetics; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D011984:Sensory Receptor Cells / Q000502:physiology; D015222:Sodium Channels / Q000235:genetics*; D012668:Trigeminal Ganglion / Q000166:cytology / Q000196:embryology* / Q000502:physiology*
chemical_list: D017306:Annexin A2; D062552:NAV1.3 Voltage-Gated Sodium Channel; D062559:NAV1.8 Voltage-Gated Sodium Channel; D062558:NAV1.9 Voltage-Gated Sodium Channel; D009419:Nerve Tissue Proteins; D009479:Neuropeptides; D021122:Protein Subunits; D012333:RNA, Messenger; C568319:Scn10a protein, rat; C113705:Scn11a protein, rat; C478638:Scn3a protein, rat; D015222:Sodium Channels