Do subplate neurons comprise a transient population of cells in developing neocortex of rats?

Studies were undertaken to determine whether neurons of the subplate layer represent a transient or stable population of cells in developing neocortex of rat. The first set of studies sought to determine the fraction of subplate neurons that is lost during early postnatal development. The optical dissector method was used to analyze fluorescently stained material in animals the age of postnatal day 0 (P0) to P40. These results demonstrate a reduction of slightly less than half of the total number of subplate neurons from P0 to P40. Counts of labeled cells in littermates at varied ages after [(3)H]thymidine or BRDU treatment on gestational day 14 (G14 - birthdate of occipital subplate neurons) or G18 (birthdate of layers III-IV neurons) demonstrate loss of approximately 50% of neurons in the subplate layer between P0 and P40, somewhat greater than the loss of neurons from cortical layers III-IV. The second set of studies investigated whether subplate neurons display cellular atrophy during postnatal development. Analysis of subplate neurons injected intracellularly with Lucifer yellow in fixed slice preparations indicates no reduction in soma size, number of dendrites, or extent of dendritic fields of subplate neurons taken from animals age P0 to P60. The third set of studies investigated whether functional markers of subplate neurons are reduced during postnatal development. Analysis of tissue stained histochemically for cytochrome oxidase or acetylcholinesterase, or stained immunocytochemically for GABA, somatostatin, or neuropeptide Y, demonstrate a remarkable loss of expression of staining patterns from late gestational ages to P20. These data demonstrate that, although subplate neurons seem not to be a transient population of cells in the usual sense of being eliminated by cell death or structural atrophy, the loss of histochemical and immunocytochemical markers indicates that they may be a functionally transient population of cells.

Reduction of transiently expressed acetylcholinesterase activity in developing thalamocortical projections does not affect the mature pattern of basal forebrain projections to visual cortex.

Experiments tested the hypothesis that acetylcholinesterase (AChE) activity, expressed transiently in developing thalamocortical projections, serves to limit the growth of basal forebrain cholinergic projections into thalamocortical recipient zones. Newborn rats were subjected to enucleation, a procedure that eliminates transient AChE activity in developing visual cortex. After 3-8 weeks survival, AChE histochemical techniques revealed no alteration in the pattern of AChE positive basal forebrain axons in visual cortex. These data indicate that transient AChE activity in developing sensory cortex does not limit ingrowth of basal forebrain cholinergic axons.

Postnatal migration of neurons and formation of laminae in rat cerebral cortex.

Migration of neurons and formation of laminae in the developing neocortex were studied by means of thymidine autoradiography. Timed pregnant rats received a single pulse injection of [3H]thymidine in the morning of embryonic day (E)13, 14, 15, 16, 17, 18 or 19. Pups were killed on postnatal day (P)0, 1, 2, 3, 4, 6, 10, 30, or 60 and brains were processed for autoradiography. Neurons in posterior (visual) cortical areas labeled by [3H]thymidine administration on E13 or E14 were found predominantly in the cortical subplate; cells labeled on E15 in layer VI; cells labeled on E16 in layers VI and V, cells labeled on E17 in layers V and IV; E18 in layers IV and III; and E19 in layers III and II. By the day of birth (P0), neurons labeled from E13-16 injections were already in their mature laminae in cortex. Many of the cells labeled on E17 were still situated within the cell-dense cortical plate (CP) at P0, and within layer V by P1. Cells labeled on E18 were found in the most superficial part of the CP on P0, in the deep part of the CP on P1, and formed layer IV on P2 and P3. At P0, many E19 labeled cells appeared to be in migration to the cortex and were found in the CP on P1, in layer III by P4, and in layer II by P6. Cells in the auditory cortex labeled by [3H]thymidine injections on a particular day were situated more superficially than comparable labeled cells in the visual cortex, indicating a lateral to medial gradient in which the auditory cortex is formed earlier than the visual cortex. Distributions of labeled cells in the somatosensory cortex were similar to those in the visual cortex. These data provide a detailed and comprehensive description of the position of varied populations of cortical neurons during the early postnatal period, as well as a description of the formation of cortical laminae at times when major systems of afferents are growing into the cortex and making synaptic connections with their target cells.

[Neurologic disorders and cerebral lesion in children with TGA (transposition of the great arteries) (author's transl)]. / Neurologische Veränderungen und cerebrale Läsionen bei Kindern mit Transposition der grossen Arterien (TGA).

118 consecutive patients with TGA were examined for neurologic disorders (ND) and cerebral lesions (CL) between 1967--1979 of whom 43 are alive. 66 had simple TGA, 52 had VSD, PS and/or coarctation as additional lesion.--43 were corrected surgically of whom 32 are alive.--Neurologic examination was performed in all, EEG, CT, arteriography, scintigraphy and autopsy when necessary or possible. Patholog. findings (CL, ND) were detected in 66; 47 had definite ND or CL, while 19 showed gross motor development delay. 52 of 118 children with TGA were without neurolog. or cerebral pathology. --Several factors were investigated for their etiologic influence: 1. Additional cardiac lesions played no significant role. 2. The lower O2 saturation in the ascending aorta of the fetal circulation in TGA may be of importance. 3. Red blood count, hemoglobin, hematocrit were higher in the group with ND or CL. 4. Early appearance of cerebral lesion should suggest earlier corrective surgery.