Tolbert D L, Dunn R C, Vogler G A
J Comp Neurol. 1984 Oct 1;228(4):478-90. doi: 10.1002/cne.902280404.
The postnatal development of corticotrigeminal projections was studied in kittens following 3H-amino acid injections into the face area of the primary somatosensory cortex. Corticofugal axons grow into the brainstem and form the pyramidal tract prenatally. Corticotrigeminal projections begin to develop at the end of the first postnatal week. The earliest corticotrigeminal axons grow out of the pyramidal tract caudally and project into laminae III-V of the spinal trigeminal (Vs) nucleus caudalis. During the second postnatal week, corticotrigeminal axons grow out of the pyramidal tract in a caudal to rostral sequence and project up to the ventromedial borders of Vs-interpolaris, Vs-oralis, and to the principal trigeminal nucleus. Corticotrigeminal axons pause at the periphery of these nuclei for 1-2 days before penetrating the trigeminal neuropil and forming terminal arborizations in a centripetal direction. Coincident with the development of cortical projections to the principal trigeminal nucleus, some of the labeled axons which were in lamina III of Vs-caudalis project into lamina I and terminate. This sequence of development of corticotrigeminal projections closely parallels, albeit at a later time, the sequence of formation of the trigeminal nuclei, suggesting that the temporal sequence of cytogenesis of trigeminal neurons may be a factor which regulates their order of innervation by afferents. Corticotrigeminal projections develop bilaterally and, during the second postnatal week, are relatively equal in density in the ipsilateral and contralateral nuclei. Many of the ipsilateral corticotrigeminal projections are lost, however, after the second postnatal week, so that by the fourth postnatal week, corticotrigeminal projections are mainly contralateral and adultlike in their distribution. It remains to be determined whether the transience of ipsilateral corticotrigeminal projections is due to selective elimination of axon collaterals or to neuronal death.
