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.

Distribution of corticospinal motor neurons in the postnatal rat: Quantitative evidence for massive collateral elimination and modest cell death

“…The occurrence of cell death in cortical layer V has been a subject for dispute. Through extrapolation of quantitative results from subpopulations in the cortex, several investigators proposed that neuronal cell death in layer V is small to negligible or even absent (Stanfield et al, 1982;Finlay and Slattery, 1983;Heumann and Leuba, 1983;Crandell et al, 1985;Luskin and Schatz, 1985;Chun and Schatz, 1989;Ferrer et al, 1992). The present study provides detailed quantitative evidence that modest cell death (approximately 10%) does occur in the rat cortex.…”

“…In rats, minute cell death has been suggested to occur in cortical layer V during the first postnatal wkek (Ferrer et al, 19921, but no quantification has been performed. Other studies that have reported on naturally occurring cell death of CSMN subscribe to a general view that death among these neurons is small to negligible (Das and Hine, 1972;Kalil and Schneider, 1975;Heumann et al, 1978;Stanfield et al, 1982;Finlay and Slattery, 1983;Heumann and Leuba, 1983;Crandell et al, 1985;Luskin and Schatz, 1985;Ramirez and Kalil, 1985;Chun and Schatz, 1989;Merline and Kalil, 1990). The apparent "cell loss" in the developing cortex, as established with retrograde labeling at different postnatal ages, is considered to be the result of elimination of transient collateral branches to the spinal cord (Stanfield et al, 1982;Stanfield, 1984;Crandell et al, 1985;O'Leary and Stanfield, 1985).…”

“…Most knowledge has been derived from studies of the transient projection from the rat occipital (visual) cortex to the spinal cord (Stanfield et al, 1982). In specific subpopulations of the CSMN, the presence of collateral elimination has been demonstrated (Crandell et al, 1985). However, a detailed and conclusive quantitative analysis of the whole cortical layer V has never been performed, which leaves open questions about developmental cell death and axonal elimination of CSMN.…”

Independent Controls for Neocortical Neuron Production and Histogenetic Cell Death

“…The radial dimension of these fields approximately doubles between P0 and P14 (data not shown). It has been estimated elsewhere that the three cortical fields increase in their tangential dimensions 2.0-to 2.5-fold Rice and van Loos, 1977;Heumann et al, 1978;Crandall et al, 1985]. Thus, the total volumetric increase in these fields may be as much as 4-to 5-fold between P0 and P14.…”

“…In mouse, the cortical plate at P0 differentiates into layers II/III and IV with discernible evidence for this transformation apparent at P4 [Rice and van der Loos, 1977]. Similarly, the subplate at P0 corresponds to layers V and VI [Crandall and Caviness, 1984;Crandall et al, 1985]. Even though the essential architectonic features of these layers already allow a partition of the subplate at P0, by convention the laminar terminology is applied only from about P4 after neuronal migration across the subplate is completed [Gadisseux et al, 1990;Gadisseux, 1995].…”