Sentence examples for sparse zones from inspiring English sources

These "afferent sparse zones" are located at a depth of ∼100 300 μm and ∼1000 1150 μm from the pia below the deeper POm axon band.

Dendritic segments located in these afferent sparse zones are likely to be activated mostly via intracortical connections that may explain the weak responsiveness of a subset of L5 neurons to single-whisker stimulation (de Kock et al. 2007).

Afferent sparse zones are apparent at a depth of ∼100 300 μm from the pia (corresponding to L2) and below ∼1000 μm depth (including the lower half of L5A and the upper half of L5B; Fig. 2 C, braces).

Using specific labeling of lemniscal and paralemniscal projections with fluorescent proteins in 2 different colors within the same tissue slice, we revealed an "overlap band" between 800 and 1000 μm depth and 2 afferent sparse zones, one in the supragranular layers (Keller et al. 1985; Lu and Lin 1993) and one in the infragranular layers, lacking intense axonal projections from either VPM or POm.

The infragranular afferent sparse zone was not noted in previous studies (Lu and Lin 1993; Kichula and Huntley 2008) and may warrant future in vivo studies to investigate if there are 3 rather than 2 functional sublayers of L5.

This layer is separated by a cell-sparse zone from a layer formed by lately born cells closer to the obliterated hippocampal fissure.

A major change in this group has come from the discovery that mutations of TUBA1A are responsible for 1 4% of classic (four-layered, with a cell-sparse zone) lissencephalies (Morris-Rosendahl et al., 2008; Kumar et al., 2010) and 30% of lissencephalies with cerebellar hypoplasia (Kumar et al., 2010).

Patients with TUBA1A-associated classic lissencephaly have either p.R402C mutations, resulting in frontal pachygyria and posterior agyria with a cell-sparse zone, or p.R402H mutations, resulting in nearly complete agyria; both of these phenotypes are essentially identical to those associated with LIS1 mutations (Kumar et al., 2010), suggesting involvement of the same molecular pathways.

Finally, hippocampus from age-matched control tissue processed for T417+ Elk-1 does not show advanced CA1 pathology or a sparse tangle zone in CA2 (Figure S2C).

The earliest generated postmitotic cells emigrate from the VZ to form initially the preplate (PP) (13, 14), which soon divides into the superficial cell sparse marginal zone (MZ) and a deeper subplate (SP) by the invasion of successive waves of neurons produced from the VZ.

In the CA2 region of hippocampus, note the sparse tangle population zone identified by both AT8 (Figure 4A, asterisk) and T417+ Elk-1 (Figure 4B, asterisk).