Differential Expression of Calcitonin Gene-Related Peptide, a-CGRP mRNA, Choline Acetyltransferase, and Low Affinity Nerve Growth Factor Receptor in Cranial Motoneurons After Hypoglossal Nerve Injury During Postnatal Development.

摘要

This study examined the temporal expression of calcitonin gene- related peptide (CGRP), choline acetyltransferase (ChAT), and low-affinity nerve growth factor receptor (LNGFR) in hypoglossal motoneurons during postnatal development and after hypoglossal nerve injury. CORP is a putative neurotrophic factor that coexists with acetyicholine, the neurotransmitter present in hypoglossal motoneurons. ChAT is a key enzyme involved in the synthesis of acetyicholine and is a specific marker for cholinergic neurons. Hypoglossal motoneurons transiently express LNGFR. These molecules were assessed using immunocytochemistry. Ribonuclease protection assay was performed to determine if peptide changes were preceded by changes in a- CORP mRNA expression. Postnatally, CORP and ChAT are expressed at low levels during the first postnatal week and increase to maximal levels during the second postnatal week. While ChAT expression is maintained at these levels in adult motoneurons, CGRP is decreased and maintained at low levels in the adult. LNGFR is expressed at maximal levels during the first postnatal week and disappears by the third postnatal week. The onset of the CGRP, ChAT, and LNGFR changes was the same after axonal damage to motoneurons of increasing postnatal ages. The progression of changes in CGRP after onset was age-related and likely to depend upon the developmental stage of motoneuron interaction with its target and/or its environment. a-CORP mRNA was upregulated soon after each nerve injury in the 10 and 21 day postnatal (dpn) rats, but subsequent elevations in gene expression were limited to the 21 dpn experimental rats. After onset, the progression of changes in ChAT and LNGFR in postnatal motoneurons was not age- related but injury-specific as reported for adult motoneurons (Armstrong et al., 1991, Borke Ct al., 1992). The magnitude of the initial reduction of ChAT was injury-specific for the 21 dpn rats but not for the 10 and 14 dpn rats.