Morphological Development of Thick-Tufted Layer V Pyramidal Cells in the Rat Somatosensory Cortex

Abstract

The thick-tufted layer V pyramidal (TTL5) neuron is a key neuron providing output from the neocortex. Although it has been extensively studied, principles governing its dendritic and axonal arborization during development are still not fully quantified. Using 3-D model neurons reconstructed from biocytin-labeled cells in the rat somatosensory cortex, this study provides a detailed morphological analysis of TTL5 cells at postnatal day (P) 7, 14, 21, 36, and 60. Three developmental periods were revealed, which were characterized by distinct growing rates and properties of alterations in different compartments. From P7 to P14, almost all compartments grew fast, and filopodia-like segments along apical dendrite disappeared; From P14 to P21, the growth was localized on specified segments of each compartment, and the densities of spines and boutons were significantly increased; From P21 to P60, the number of basal dendritic segments was significantly increased at specified branch orders, and some basal and oblique dendritic segments were lengthened or thickened. Development changes were therefore seen in two modes: the fast overall growth during the first period and the slow localized growth (thickening mainly on intermediates or lengthening mainly on terminals) at the subsequent stages. The lengthening may be accompanied by the retraction on different segments. These results reveal a differential regulation in the arborization of neuronal compartments during development, supporting the notion of functional compartmental development. This quantification provides new insight into the potential value of the TTL5 morphology for information processing, and for other purposes as well.

Preserving axosomatic spiking features despite diverse dendritic morphology

“…Table 3 summarizes key morphological properties of these cells. The statistics of this dataset matched the experimental statistics reported previously (Romand et al 2011), and thus indicated that the set of morphologies faithfully represents the TTC population in young Wistar rats. We note that the difference in surface area between morphologies was not only due to differences in total dendrite length, but also to differences in dendritic diameter.…”

“…Layer 5 thicktufted pyramidal cells (TTCs) are characterized by prototypical morphological features and can also be classified as an e-class, differing even from their neighboring L5 thintufted pyramidal cells in spike threshold, amplitude, halfwidth, and initial burst interspike interval (ISI) (Le ). Nevertheless, although TTCs have unique morphological characteristics, they vary widely in their dendritic length, surface area, and the complexity of their branching pattern (Le Be et al 2007;Romand et al 2011;Zhu 2000). A significant portion of the ionic current entering the axon via its membrane ion channels leaks axially into the soma and dendrites; similarly, currents entering the soma via its membrane ion channels leak primarily into the dendrites (Rall 1959).…”

Cell class-specific regulation of neocortical dendrite and spine growth by AMPA receptor splice and editing variants

“…We observed unedited GluA2(Q) transcripts in vivo and in OTC up until the first postnatal day, suggesting that some calciumpermeable GluA2 protein might well be present during the time when dendritic trees enlarge and synapses form by mechanisms not yet driven by sensory input (Romand et al, 2011). The immature brain employs unedited GluA2(Q) in addition to GluA2(R) to mediate the trophic actions of glutamate (Burnashev et al, 1992).…”

“…Development 138 (19) independent phase of growth (Romand et al, 2011). However, basal dendrites at this age are growth competent and respond, for instance, to TrkB ligands .…”

Insights into Rapid Modulation of Neuroplasticity by Brain Estrogens

“…This may suggest that cell type is important for determining both rapid estrogenic effects and the underlying molecular mechanisms and that there are compartment-specific (i.e., apical versus basal dendrites) 17b-estradiol signaling mechanisms. Such a scenario is not unprecedented because differential mechanisms have been described for the development and maintenance of apical and basal architecture (Romand et al, 2011;Srivastava et al, 2012c). If distinct regions of the dendritic tree contain specific molecular mechanisms that control dendritic arborization, it is plausible that a similar subcompartmental specialization may exist for the regulation of synapse structure.…”