Development of the spinal‐medullary projection from the mouse barrel field

Abstract
Neurons in layer V of the murine posteromedial barrel subfield (PMBSF) project to structures at or caudal to the spinal-medullary junction. During postnatal development a reduction occurs in the density of the neurons which form this projection. In principle, three processes might be expected to contribute to this reduction: cell death, tissue growth, and axon pruning. Three different paradigms in which cells of origin of the projection are labeled retrogradely with True Blue, injected into the spinal-medullary junction, taken together with an estimate of the relative growth of layer V, provide separate estimates of the magnitude and rate of reduction consequent to these different processes during the first 3 postnatal weeks. The density of neurons in an index sector of layer V of the PMBSF which contribute to the projection at varied ages is estimated by injections made at a range of ages from postnatal day 1 (P1) to P16, with a survival of 4 days in each instance. Overall reduction in density is 80%. The component due primarily to axon pruning is estimated to be 50% by injections delivered at graded ages from P1 to P16 with survival to P20 in each instance. The component of the reduction attributable to increase in volume is estimated at 30% by a series of injections delivered at P1 with graded survival times from P5 through P20. A reduction due to cell death is not identified. The reduction in density due to tissue growth is essentially linear through the interval P5–P11. At all ages, neuronal somata of origin of the spinal-medullary projection are located within layer V. Subsequent to P15 they are confined to sublayer Vb; at earlier ages somata in Va and Vc also contribute axons to the projection. Although volume increase due to growth of the neuropil reduces the density of the population contributing to the projection equally in all three sublayers, final elimination of all contributions from Va and Vc depends upon axon pruning.