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PubMed1984

[Spatial organization and interrelation of structural elements of the 1st layer of the neocortex].

Investigating topography and structure of elements in the layer I of the fields 4, 3, 1 of the human neocortex (4 cases) and M1, Ep zones in the cat neocortex (5 cases) by means of modified methods of Golgi, Peters and Kluver-Barerr, it became possible to work out an original classification of astrocytes and to reveal the neurono-glio-vascular complexes consisting of the neuronal base and two glial-vascular links. Three main varieties of protoplasmic astrocytes are determined: short-rayed with a long dendrite-like process, short-rayed cap-like and long-rayed with a double bush of branchings. In the latter forms axon-like processes are revealed, some of them make complex basket-like branchings and each of them surrounds a group of neuronal bodies, predominantly the pyramidal ones in the layer III. Distribution of the marginal glia and the three mentioned varieties of astrocytes is subjected to a single plan. The raws of gliocytes along the horizontal and vertical lines are connected with each other and with the neuronal elements. Peculiar receptive apparatuses performing interrelation are ball-like formations revealed on the apical dendrites of the pyramidal neurons. The information that gets into them is processed automatically. Problems concerning the importance of the ball-like formations in integration of the layer I is discussed, and the role of the glial cells with axon-like processes in the active transport of various substances and in regulating metabolism of the pyramidal cells of the layer III is also dealt with.

Animals↗
PubMed1984

[New electrophysiologic data on localizing visual representation in the limbic area of the neocortex].

In the limbic part of the rat neocortex, afferents from the retino-geniculo-cortical and retino-tecto-thalamo-cortical visual subsystems converge to the area 29. A specific feature of the area 29 responses to stimulation of thalamic visual nuclei (the LGB and the postero-lateral nucleus) involves gradualness of their appearance during rhythmic stimulation. The responses have an initial negative phase, are resistant against nembutal, have a short and stable latency, their neuronal reaction being phasic in nature and showing dependence on physical parameters of stimulation. These intermediate type reactions possess features of both specific and unspecific responses of the neocortex which seems to be characteristic of the area 29 function.

Afferent Pathways↗
PubMed1980

[Orientation of nerve fiber systems in the tangential plane of layer I of the rat neocortex].

The orientation of nerve fibers in the tangential plane of layer I has been studied in silver impregnated paraffin sections and in frozen sections of rat cerebral cortex. The neocortex was divided into 4-6 pieces which were embedded separately and serially cut tangentially to the surface. In these serial sections the orientation of the nerve fibers running parallel to the cortical surface was studied. A system of parallel fibers was revealed which form a distinct pattern in layer Ib that changes in a characteristic way from one region to the next. Diagrams of preferential fiber directions have been drawn into a reconstruction of the entire neocortex. It is assumed that the orientation of the tangential fibers is indicative of associative connections between primary thalamo-cortical projection areas.

Animals↗
PubMed1981

[Quantitative examinations of stellate cell types of the regio cingularis mesoneocorticalis in comparison to the adjacent regions (mesoarchicortex and neocortex) after deafferentation in the rat].

Stellate cells of three adjacent subregions of the cingulate cortex (neocortex, mesoneocortex, mesoarchicortex) in the rat were analyzed quantitatively. The parameters of the dendritic tree and the spine distribution show some regional differences in the subregions. These results provide evidence for differences in the phylogenetical differentiation level of the subregions. For the characterization of this level dendritic parameters are more valuable than spine values. Isodendritic stellate cells without spines (I/OS)--which represent a phylogenetical older type--in the lower layers of the mesoneocortex are endowed with widely branched dendritic trees and with numerous varicosities (multisynaptic contacts). In the neocortex small, highly branched spiny stellate cells dominate in upper layers. Due to lesions of thalamic afferences to the cingulate cortex the isodendritic stellate cells without spines in the mesoneocortex show a significant decrease of synaptic contacts and of the size of pericarya and dendritic trees.

Afferent Pathways↗
PubMedDate not supplied

[Effect of entopeduncular nucleus and reticular part of substantia nigra on the antiepileptic activity of the caudate nucleus in the neocortex].

Experiments carried out on rats show that inhibiting influences from striatal electrostimulation on the cortical epileptic activity are removed under conditions of destruction of entopeduncular nucleus (EPN). They decrease under conditions of lesion of substantia nigra pars retieulata (SNR). It is found that both EPN and SNR destruction resulted in antiepileptic effect on the development of the neocortex epileptic activity complexes. Possible mechanisms realizing inhibition of the caudate nucleus effects on the neocortex epileptic activity are discussed.

Animals↗
PubMed1994

Complete and selective cholinergic denervation of rat neocortex and hippocampus but not amygdala by an immunotoxin against the p75 NGF receptor.

The immunotoxin 192 IgG-saporin, produced by coupling the ribosome-inactivating protein saporin to the monoclonal 192 IgG antibody against the low-affinity p75 NGF receptor (NGFr), was injected into the cerebral ventricle, septal area, and substantia innominata of adult rats. Injections into the cerebral ventricle induced a complete loss of NGFr-positive basal forebrain neurons and their axons. Extensive loss of cholinergic neurons was found in the septum, diagonal band, and magnocellular preoptic nucleus but not in the nucleus basalis-substantia innominata complex, where many cholinergic, presumably NGFr-negative, neurons remained intact. Cholinergic fibers were completely lost in the neocortex and hippocampus, showed some preservation in allocortical areas, and showed only minor loss in the amygdala. The NGFr-positive cholinergic basal forebrain neurons progressively degenerated during the first 5 d and did not recover after 180 d. The effect of intraventricular 192 IgG-saporin injections on NGFr-positive basal forebrain neurons could be blocked by simultaneous intraventricular injection of colchicine. Intraparenchymal injections into the septal area or substantia innominata damaged cholinergic neurons mainly around the injection sites and reduced their respective cortical and hippocampal projections. Noncholinergic septal neurons containing parvalbumin and noncholinergic neurons containing calbindin-D28k or NADPHd, which were adjacent to cholinergic nucleus basalis-substantia innominata neurons, were not affected by 192 IgG-saporin. The ChAT immunoreactivity in cortical interneurons, habenula, and brainstem was unchanged. Dopaminergic and noradrenergic cortical afferents remained intact. 192 IgG-saporin damaged two neuronal groups outside the basal forebrain that express the p75 NGF receptor: NGFr-positive cerebellar Purkinje cells after intraventricular injection and cholinergic striatal interneurons after injections into the substantia innominata. These results indicate that the immunotoxin 192 IgG-saporin induces a complete and selective lesion of NGFr-positive cholinergic basal forebrain neurons projecting to hippocampus and neocortex.

Acetylcholinesterase↗
PubMed1993

Selective distribution of kainate receptor subunit immunoreactivity in monkey neocortex revealed by a monoclonal antibody that recognizes glutamate receptor subunits GluR5/6/7.

A monoclonal antibody (4F5) was generated against a portion of the putative extracellular domain of glutamate receptor subunit GluR5. Western blot analyses and immunocytochemistry of transfected human embryonic kidney 293 cells confirmed that monoclonal antibody 4F5 was specific for GluR5, -6, and -7 (the three identified members of the kainate receptor subunit class), but did not recognize GluR1, -2, or -3 (the AMPA/kainate receptor subunit class). The antibody was subsequently used to examine immunocytochemically the regional, laminar, and cellular distribution of GluR5/6/7 receptor subunits at the light and electron microscopic levels in monkey neocortex. Receptor subunit immunoreactivity was present throughout all cortical areas examined, but exhibited marked cellular, laminar, and regional specificity. Typically, pyramidal cell somata and apical dendrites were well stained. Electron microscopy revealed an extensive cytoplasmic localization of GluR5/6/7 immunoprecipitate, with intense staining of many postsynaptic densities, all of which were associated with asymmetric synapses located on dendritic shafts or dendritic spines. There was no evidence of stained glial cells or presynaptic axon terminals. In most areas, labeled cells and dendrites were concentrated in layers II, III, and V while layers I, IV, and VI typically possessed the fewest and/or least intensely stained elements. A consistent feature in many areas was groups of clustered layer V pyramidal cells and bundles of ascending apical dendrites. Regionally, motor areas and higher-order association areas of the frontal, parietal, and occipital lobes were more densely stained than primary sensory areas (somatic sensory and visual cortex), which was confirmed quantitatively. These data indicate a high degree of selectivity in the distribution of kainate receptors composed of GluR5/6/7 subunits, and suggest that functional specificity and diversity in the ubiquitous excitatory amino acid-utilizing axonal systems in neocortex are achieved in part by the differential association of particular glutamate receptor subunits with specific cortical circuits. In addition, the regional, laminar, and morphological characteristics of GluR5/6/7-immunoreactive neurons bear a strong similarity to those of the neocortical neurons with heightened vulnerability in certain neurodegenerative disorders.

Analysis of Variance↗
PubMed1996

Reversible signal abnormalities in the hippocampus and neocortex after prolonged seizures.

PURPOSE: To investigate the phenomenon of reversible increased signal intensity of medial temporal lobe structures and cerebral neocortex seen on MR images of six patients with recent prolonged seizure activity. METHODS: After excluding patients with known causes of reversible signal abnormalities (such as hypertensive encephalopathy), we retrospectively reviewed the clinical findings and MR studies of six patients whose MR studies showed reversible signal abnormalities. MR pulse sequences included T2-weighted spin-echo coronal views or conventional short-tau inversion-recovery coronal images of the temporal lobes. RESULTS: All six MR studies showed increased signal intensity within the medial temporal lobe, including the hippocampus in five studies. All follow-up MR examinations showed partial or complete resolution of the hyperintensity within the medial temporal lobe and the neocortex. In one patient, results of a brain biopsy revealed severe cerebral cortical gliosis. Temporal lobectomy performed 4 years later showed moderate cortical gliosis and nonspecific hippocampal cell loss and gliosis. CONCLUSION: Significant hyperintensity within the temporal lobe is demonstrable on MR images after prolonged seizure activity, suggestive of seizure-induced edema or gliosis. Damage to medial temporal lobe structures by prolonged seizure activity indicates a possible mechanism of epileptogenic disorders.

Adolescent↗
PubMed1997

Fates of the earliest generated cells in the developing murine neocortex.

In mammalian species studied to date, the first-born neocortical cells normally form two layers, one above and one below the cortical plate, called the marginal zone (future layer 1) and the subplate. In primates and carnivores, many of these first-born cells die early in postnatal life. Whether this also occurs in rodents is highly controversial. In this study, we injected pregnant mice with bromodeoxyuridine on embryonic days (E) 11-14 to label the earliest generated neocortical cells, and examined their fates between birth and postnatal day 21. At birth, most cells born on embryonic day 11 were below the cortical plate, and a smaller proportion were above it. Very few of these cells remained by postnatal day 3 and there were none at any depth in the neocortex at older ages. At birth, the largest proportion of cells born on embryonic days 12 and 13 were in the subplate and smaller proportions were in the cortical plate and marginal zone. At older ages, almost all of these cells had disappeared from the marginal zone and from below the cortical plate, although some were retained in the cortical plate. The density of the remaining E12- and E13-born cells decreased more than could be explained by neocortical expansion alone. As a control, we studied cells born on embryonic day 14. These cells were restricted to the cortical plate at birth. By postnatal day 21, their density had decreased by an amount that could be explained by neocortical expansion alone. We conclude that, as in other species, many of the earliest generated cells of the murine neocortex die.

Age Factors↗
PubMed1997

Functional and pharmacological properties of GABA-mediated inhibition in the human neocortex.

This paper describes some functional and pharmacological properties of GABA-mediated mechanisms in the human neocortex maintained in vitro in a slice preparation. Neocortical neurons recorded intracellularly under normal conditions generate stimulus-induced and spontaneous potentials that are mediated by the activation of postsynaptic GABAA and GABAB receptor subtypes. As reported in other species, pharmacological blockade of the GABAA receptor makes epileptiform bursts appear in response to extracellular focal stimuli, thus indicating that inhibition mediated through the activation of the GABAA receptor exerts an important role in controlling neuronal excitability in the human neocortex. Spontaneous, prolonged epileptiform discharge are recorded when slices are bathed in Mg(2+)-free medium. Under these experimental conditions GABAA receptor mediated potentials occur between epileptiform events; moreover their rate of occurrence decreases shortly before the onset of each discharge. Blockade of GABAA receptor mediated potentials during application of Mg(2+)-free medium (i) prolongs the epileptiform discharges, (ii) increases the amplitude of their field potential DC shifts, and (iii) augments the concomitant decreases in [Ca2+]0 and increases in [K+]0. These findings indicate therefore that GABAA receptor mediated inhibitory potentials are operant during Mg(2+)-free epileptiform activity, and modulate the occurrence of epileptiform discharges. Moreover, they may also play a role in controlling the changes in [Ca2+]0 and [K+]0 that accompany each epileptiform event.

Bicuculline↗
PubMed1997

Cellular-synaptic generation of sleep spindles, spike-and-wave discharges, and evoked thalamocortical responses in the neocortex of the rat.

Thalamocortical neuronal oscillations underlie various field potentials that are expressed in the neocortex, including sleep spindles and high voltage spike-and-wave patterns (HVSs). The mechanism of extracellular current generation in the neocortex was studied in the anesthetized and awake rat. Field potentials and unit activity were recorded simultaneously along trajectories perpendicular to the cortical layers at spatial intervals of 100 microm by multiple-site recording silicon probes. Current source density (CSD) analysis revealed that the spatial positions of sinks in layers IV, V-VI, and II-III and of the accompanying sources were similar during sleep spindles, HVSs, and thalamic-evoked responses, although their relative strengths and timings differed. The magnitude and relative timing of the multiple pairs of sinks and sources determined the amplitude variability of HVSs and sleep spindles. The presence of temporally shifted dipoles was also supported by the time distribution of unit discharges in different layers. Putative interneurons discharged with repetitive bursts of 300-500 Hz. The spike component of HVSs was associated with fast field oscillations (400-600 Hz "ripples"). Discharges of pyramidal cells were phase-locked to the ripples. These findings indicate that the major extracellular currents underlying sleep spindles, HVSs, and evoked responses result from activation of intracortical circuitries. We hypothesize that the fast field ripples reflect summed IPSPs in pyramidal cells resulting from the high frequency barrage of interneurons.

Animals↗
PubMed1997

Microglial and macrophage reactions mark progressive changes and define the penumbra in the rat neocortex and striatum after transient middle cerebral artery occlusion.

Transient middle cerebral artery occlusion in rats leads to infarction of the lateral part of the striatum and adjacent neocortex, with selective neuronal necrosis in the bordering penumbral zones. Administration of glutamate, cytokine, and leukocyte antagonists have rescued mainly neocortical neurons, indicating differences in the degenerative processes. The aim of this study was, therefore, to describe the microglial/macrophage activation and polymorphonuclear leukocyte recruitment patterns and to correlate these with the ischemia-induced degenerative processes. The analysis showed significant differences in the characteristics and timing of the microglial/macrophage responses between the caudate putamen and neocortical infarct zones, the infarct zones and their associated penumbral zones, as well as between the striatal and the neocortical penumbral zone. Infiltrations with polymorphonuclear leukocytes into the infarct zones were limited and shortlasting and confined to the acutely degenerating striatum and piriform cortex. A delayed, massive infiltration with lipid phagocytes into the caudate putamen infarct markedly contrasted an early recruitment and activation of microglia/macrophages in the adjacent penumbra. Within the neocortex, a later onset of degeneration along the insular-parietal axis was marked by neuronal expression of heat shock protein and a progressive microglial activation with induction of the full repertoire of microglial activation markers, including a widespread microglial major histocompatibility complex (MHC) class II antigen expression. We interpret the present results as delineating two differentially progressing penumbral zones, which are likely to reflect differences in the underlying degenerative processes. Differences in the microglial/macrophage activation pattern attract special attention, as these cells may constitute specific targets for therapeutic intervention.

Animals↗
PubMedDate not supplied

[An analysis of changes in the background electrical activity of the dog neocortex during elaboration of food-getting conditioned reflexes].

Background electrical activity of different areas of the neocortex was studied at interstimuli periods during elaboration of food-procuring (instrumental) conditioned reflexes in dogs. By using the complex of EEG parameters obtained after a correlation-spectral analysis, it was possible to provide differentiated EEG characteristics of such externally similar conditions as rest in a situation of food-procuring and in an indifferent situation. Further, it has been found that the background activity parameters significantly differ in one and the same situation of food-procuring, depending on the functional state (passive rest and activation of attention). The data obtained point to the informative nature of background electrical activity of the neocortex, whose parameters reflect the peculiarities of specific functional conditions.

Animals↗
PubMed1998

Nicotine selectively enhances NMDA receptor-mediated synaptic transmission during postnatal development in sensory neocortex.

The neurotransmitters acetylcholine (ACh) and glutamate have been separately implicated in synaptic plasticity during development of sensory neocortex. Here we show that these neurotransmitters can, in fact, act synergistically via their actions at nicotinic ACh receptors (nAChRs) and NMDA receptors, respectively. To determine how activation of nAChRs modifies glutamatergic EPSPs, we made whole-cell recordings from visualized pyramidal neurons in slices of rat auditory cortex. Pulsed (pressure) ejection of nicotine onto apical dendrites selectively enhanced EPSPs mediated by NMDA receptors without affecting AMPA/kainate (AMPA/KA) receptor-mediated EPSPs. The enhancement occurred during a transient, postnatal period of heightened cholinergic function [neurons tested on postnatal day 8-16 (P8-16)], and not in the mature cortex (>P19). Three related findings indicated the mechanism of action: (1) The specific alpha7 nAChR antagonist methyllycaconitine citrate (MLA) blocked the effect of nicotine; (2) pulsed nicotine did not enhance postsynaptic depolarizations induced by iontophoretically applied NMDA; and (3) bath exposure to nicotine for several minutes produced apparent nAChR desensitization and precluded enhancement of EPSPs by pulsed nicotine. Together, the data suggest that nicotine acts at rapidly desensitizing, presynaptic alpha7 nAChRs to increase glutamate release onto postsynaptic NMDA receptors. The synergistic actions mediated by alpha7 nAChRs and NMDA receptors may contribute to experience-dependent synaptic plasticity in sensory neocortex during early postnatal life.

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed1998

Parvalbumin is expressed in a reciprocal circuit linking the medial geniculate body and auditory neocortex in the rabbit.

Recent studies of the rabbit auditory forebrain have shown that antibodies directed against the calcium-binding protein parvalbumin (PV) specifically demarcate auditory neocortex and the ventral division of the medial geniculate body (MGV). The auditory cortex is characterized by two PV- immunoreactive bands: dense terminal-like labeling within layer III/IV and a prominent band of PV+ somata in the upper half of layer VI. In some cases, there are distinct patches of PV immunoreactivity within layers III/IV of auditory cortex that appear similar to the patchy termination of thalamocortical axons labeled by the injection of anterograde tracers into MGV. The presence of PV+ patches in III/IV, PV+ somata in layer VI, and the high density of PV+ neurons and terminals in the MGV suggest the existence of a reciprocal PV+ circuit linking primary auditory cortex (AI) and the MGV. In the present study, double-labeling experiments in adult rabbits were carried out to provide evidence for this circuit. Focal injections of the tracers biocytin or biotinylated dextran amine (BDA) into the MGV labeled thalamocortical afferent patches within layer III/IV and retrogradely labeled corticothalamic neurons in layer VIa of the ipsilateral auditory cortex. Adjacent sections stained with antibodies against PV revealed terminal-like PV-immunoreactive patches in III/IV and PV+ somata in VIa that were in register with those labeled by BDA injections into the MGV. Serial section reconstruction of BDA-labeled corticothalamic neurons in VIa revealed pyramidal cells with tangentially oriented basal dendrites and sparsely branched apical dendrites that ascended to layer I. Fluorescent double-labeling studies demonstrated that a subpopulation of corticothalamic neurons also express PV. PV-negative corticothalamic neurons were also found. Discrete injections of BDA into auditory cortex labeled bands of neurons in the ipsilateral MGV, whose orientation paralleled the fibrodendritic laminae characteristic of this subdivision. Retrograde double-labeling experiments showed that most MGV relay neurons also express PV. Small numbers of PV-negative relay neurons were also found. These studies provide evidence for the existence of multiple, chemically coded pathways linking primary auditory cortex and the MGV.

Animals↗
PubMed1999

Mouse Dac, a novel nuclear factor with homology to Drosophila dachshund shows a dynamic expression in the neural crest, the eye, the neocortex, and the limb bud.

Dac is a novel nuclear factor in mouse and humans that shares homology with Drosophila dachshund (dac). Alignment with available sequences defines a conserved box of 117 amino acids that shares weak homology with the proto-oncogene Ski and Sno. Dac expression is found in various neuroectodermal and mesenchymal tissues. At early developmental stages Dac is expressed in lateral mesoderm and in neural crest cells. In the neural plate/tube Dac expression is initially seen in the prosencephalon and gets gradually restricted to the presumptive neocortex and the distal portion of the outgrowing optic vesicle. Furthermore, Dac transcripts are detected in the mesenchyme underlying the Apical Ectodermal Ridge (AER) of the extending limb bud, the dorsal root ganglia and chain ganglia, and the mesenchyme of the growing genitalia. Dac expression in the Gli 3 mutant extra toes (Xt/Xt) shows little difference compared to the expression in wild-type limb buds. In contrast, a significant expansion of Dac expression are observed in the anterior mesenchyme of the limb buds of hemimelic extra toes (Hx/+) mice. FISH analysis reveals that human DAC maps to chromosome 13q22.3-23 and further fine-mapping defined a position of the DAC gene at 54cM or 13q21.1, a locus that associates with mental retardation and skeletal abnormalities.

Amino Acid Sequence↗
PubMed1998

Strong nuclear factor-kappaB-DNA binding parallels cyclooxygenase-2 gene transcription in aging and in sporadic Alzheimer's disease superior temporal lobe neocortex.

Cyclooxygenase-2 (COX-2; EC 1.14.99.1) RNA message abundance in 25 control and Consortium to Establish a Registry for Alzheimer's Disease (CERAD)-confirmed sporadic Alzheimer's disease (AD) brains is remarkably heterogeneous when compared with 55 other AD brain RNA message levels that were previously characterized (Lukiw and Bazan: J Neurosci Res 50:937-945, 1997). Examination of nuclear protein extracts (NPXTs) that were derived from control and AD-affected brain neocortical nuclei (n = 20; age range, 60-82 years; postmortem interval, 0.5-6.5 hours) by using gel shift, gel supershift, and cold oligonucleotide competition assay revealed a highly significant relationship between the extent of inflammatory transcription factor, nuclear factor (NF)-kappaB: DNA binding and the abundance of the COX-2 RNA signal (P < 0.0001; analysis of variance). No strong correlation with AP-1-DNA binding was noted (P > 0.045). These data are the first linking inflammation-related transcription factor NF-KB-DNA binding to up-regulation of transcription from a key inflammatory gene, COX-2, in both normally aging brain and in AD-affected neocortex. Systematic deletion of NF-KB-DNA binding sites in human COX-2 promoter constructs attenuates COX-2 transcriptional induction by mediators of inflammation. Strong NF-kappaB-DNA binding has been reported previously to temporally precede COX-2 gene transcription in human epithelial (A549), hamster B-cell (HIT-T15), human endothelial (HUVEC), human lymphoblast (IM9), human fibroblast (IMR90), rat glioma/mouse neuroblastoma (NG108-15), human keratinocyte (NHEK), mouse fibroblast (NIH 3T3), rat neuroblastoma (SH-SY5Y) cell lines and in mouse and rat brain hippocampus, indicating a highly conserved inflammatory signaling pathway that is common to diverse species and cell types. The mouse, rat, and human COX-2 immediate promoters, despite 7.5 x 10(7) years of DNA sequence divergence, each retain multiple recognition sites specific for NF-kappaB-DNA binding. These data suggest that basic gene induction mechanisms, which have been conserved over long periods of evolution, that increase NF-kappaB-DNA binds ing may be fundamental in driving transcription from inflammation-related genes, such as COX-2, that operate in stressed tissues, in normally aging cell lines, and in neurodegenerative disorders that include AD brain.

Aged↗
PubMed2000

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.

Acetylcholinesterase↗