Prenatal specification and target induction underlie the enrichment of calcitonin gene-related peptide in the trigeminal ganglion neurons projecting to the cerebral vasculature.

The neurotransmitter calcitonin gene-related peptide (CGRP) is enriched in the adult rat trigeminal visceral projection to the cerebral arteries compared both to other neurotransmitters in this projection and to the percentage of CGRP-positive trigeminal cells projecting to cutaneous targets. In colchicine-treated ganglia approximately 30% of adult trigeminal ganglion cells projecting to the middle cerebral artery contain CGRP. Several possible developmental mechanisms underlying this enrichment were investigated. Some of this enrichment is accounted for by a prenatal selection of CGRP cells in the cerebrovascular projection. The remainder of the enrichment can be explained by a late (postnatal days 55-90) target-induced expression of CGRP in some trigeminal neurons innervating cerebral arteries. Most surprisingly, the massive postnatal regression in the trigeminal projection to the cerebral arteries (between postnatal days 5 and 55, cell death and axon retraction delete 3/4 of the neurons that innervate the middle cerebral artery neonatally) has no role in the CGRP enrichment in the cells remaining at maturity in this projection. These regressive events appear to affect equally the CGRP-positive and CGRP-negative populations. However, axon retraction is involved in the postnatal loss of CGRP enrichment seen in 1 small subpopulation of the trigeminal projection. Each trigeminal cell in this population sends axon collaterals to both the cerebral artery and the forehead skin neonatally, and then later most of these dually projecting neurons retract only their artery collaterals but do not die. A low percentage of CGRP-containing neurons does not appear to predate artery collateral retraction.(ABSTRACT TRUNCATED AT 250 WORDS)