PubMed · 9274682
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P J Quinn, E P Larkin. Intent.. https://pubmed.ncbi.nlm.nih.gov/9274682/
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The nature of cerebral involvement in the acquisition of language was addressed in this longitudinal study of children with an early diagnosis of epilepsy with simple-partial seizures (SPE) and with epileptogenic foci localized in the left frontal (LF) lobe. Yearly evaluations of six SPE-LF children on tests of linguistic comprehension (pointing, understanding of narrative, and understanding of prepositions) and production (repetition, lexical diversity, and grammatical production) were carried out between the ages of 3 and 8 years and compared to those of large samples of control children on the same tasks and at each age level. Linguistic production of all children were transcribed, coded, and analyzed using the Child Language Data Exchange System (MacWhinney & Snow, 1991). Individual evolution trajectories revealed that SPE-LF children showed a clear dissociation in linguistic performance between comprehension and production. Linguistic comprehension gradually improved to reach normal performance levels by age 7 while linguistic production, even at later stages, remained quite poor. This dissociation in the development of linguistic performance in SPE-LF children suggests a complex interplay between brain maturation dynamics and dysfunction modulating the succession of stages in language development. The observed persistent deficits in specific aspects of linguistic performance argue for an early involvement of the anterior areas of the left cerebral hemisphere in the production of language.
The reelin gene encodes an extracellular protein that is crucial for neuronal migration in laminated brain regions. To gain insights into the functions of Reelin, we performed high-resolution in situ hybridization analyses to determine the pattern of reelin expression in the developing forebrain of the mouse. We also performed double-labeling studies with several markers, including calcium-binding proteins, GAD65/67, and neuropeptides, to characterize the neuronal subsets that express reelin transcripts. reelin expression was detected at embryonic day 10 and later in the forebrain, with a distribution that is consistent with the prosomeric model of forebrain regionalization. In the diencephalon, expression was restricted to transverse and longitudinal domains that delineated boundaries between neuromeres. During embryogenesis, reelin was detected in the cerebral cortex in Cajal-Retzius cells but not in the GABAergic neurons of layer I. At prenatal stages, reelin was also expressed in the olfactory bulb, and striatum and in restricted nuclei in the ventral telencephalon, hypothalamus, thalamus, and pretectum. At postnatal stages, reelin transcripts gradually disappeared from Cajal-Retzius cells, at the same time as they appeared in subsets of GABAergic neurons distributed throughout neocortical and hippocampal layers. In other telencephalic and diencephalic regions, reelin expression decreased steadily during the postnatal period. In the adult, there was prominent expression in the olfactory bulb and cerebral cortex, where it was restricted to subsets of GABAergic interneurons that co-expressed calbindin, calretinin, neuropeptide Y, and somatostatin. This complex pattern of cellular and regional expression is consistent with Reelin having multiple roles in brain development and adult brain function.
Tst-1/SCIP/Oct-6, a POU domain transcription factor, is transiently expressed by developing Schwann cells and is required for their normal development into a myelinating phenotype. In tst-1/scip/oct-6-null sciatic nerves, Schwann cells are transiently arrested at the "promyelinating" stage, when they have a one-to-one relationship with an axon but before they have elaborated a myelin sheath. To determine when Schwann cells express Tst-1/SCIP/Oct-6, we examined beta-galactosidase (beta-gal) expression in heterozygous tst-1/scip/oct-6 mice, in which one copy of the tst-1/scip/oct-6 gene has been replaced with the LacZ gene. beta-Gal expression from the LacZ gene seems to parallel Tst-1/SCIP/Oct-6 expression from the endogenous tst-1/scip/oct-6 gene in developing and regenerating sciatic nerves. Furthermore, electron microscopic examination of 5bromo-4-chloro-3-indolyl-beta-D-galactopyranoside- (X-gal) and halogenated indolyl-beta-D-galactoside- (Bluo-gal) stained nerves showed that promyelinating Schwann cells express the highest levels of beta-gal, both in developing and in regenerating nerves. Thus, the expression of beta-gal, a surrogate marker of Tst-1/SCIP/Oct-6, peaks at the same stage of Schwann cell development at which development is arrested in tst-1/scip/oct-6-null mice, indicating that Tst-1/SCIP/Oct-6 has a critical role in promyelinating Schwann cells.