Development of interhemispheric cortical connections.
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Aging↗
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[Conditions for development of spreading cortical depression during application of direct current].
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Animals↗
The development of topography in the hamster geniculo-cortical projection.
Precise point-to-point connectivity is the basis of ordered maps of the visual field. The immaturity of the newborn hamster's visual system has allowed us to examine emerging topography in the geniculo-cortical projection well before thalamic axons have reached their cortical target, layer IV. Using anterograde transneuronal labeling with wheat germ agglutinin conjugated to horseradish peroxidase (WGA-HRP), we visualized the ingrowth of the whole population of geniculate fibers in the neonatal hamster. Two days after birth (P2), the bulk of the fibers is in the deep cortical layers and the subplate. At the same age, injections of paired retrograde tracers (red and green fluorescent latex microspheres) into area 17 reveal an unordered projection from the dorsal lateral geniculate nucleus (dLGN) to cortex. Individual labeled cells are found throughout the dLGN, and quantitative analysis reveals no segregation of the red and the green populations. At P6, when the pattern of geniculate back label appears ordered and essentially adult-like, geniculate fibers have reached layer IV. The role of selective cell death in this process was investigated by making a tracer injection at P2 and allowing the animals to survive to P6 or P12, when the map is mature. The results show early labeled neurons that made inappropriate connections when the projection was scattered surviving through the period of geniculate cell death. We conclude that the geniculo-cortical map develops from an initially unordered projection to the subplate and the lower cortical layers. Selective cell death appears not to contribute significantly to this process.
Animals↗
[Development of evoked cortical activity and its inducement (author's transl)].
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Animals↗
The development of somatostatin immunoreactive neurons in cat visual cortical areas.
The development of somatostatin immunoreactive (SOM-ir) neurons in cat striate and extrastriate cortex was studied to determine whether temporal changes in the morphology, distribution and density of SOM-ir neurons during development would provide clues to the emergence of specific cortical areas. The visual cortical areas examined included areas 17-19 and 7, posteromedial lateral suprasylvian, posterolateral lateral suprasylvian cortex and splenial visual area. We observed that the pattern of SOM-ir neurons in the cortical plate reflects the maturation of the cortical plate. At 1 week of age, SOM-ir neurons were only found in layers V and VI of the developing cortex; by 2 weeks of age, SOM-ir neurons were found in layer IV; and by 3 weeks of age, SOM-ir neurons were located in all layers of the cortex except layer I. SOM-ir neurons in the subplate were much more numerous under lateral cortical areas than under medial areas. This difference decreased over the first 2 postnatal weeks and by the 14th day after birth (P14), the distribution and numbers of SOM-ir neurons in the subplate/white matter had reached the adult pattern. The timing of exuberant SOM expression in the subplate suggests a function in the formation of visual corticocortical connections which begin to develop during the first postnatal week in the kitten.
Animals↗
Initial development of gamma-aminobutyric acid immunoreactivity in the human cerebral cortex.
The development of cortical cells immunoreactive for gamma-aminobutyric acid (GABA) was studied in human cerebral cortex in the first trimester of gestation (from 4 to 13 gestational weeks; g.w.). The first GABA-immunoreactive (IR) cells were observed at 6.5 g.w., i.e., before the appearance of the cortical plate, which gives rise to a majority of the adult cortical layers. GABA-IR cells were found initially in the telencephalic wall, where a lateromedial gradient in the density of GABA-positive cells was observed at this early developmental time point, but not at later stages. At 7 g.w., as the cortical plate emerged in the ventrolateral region of the cerebral vesicle, GABA-immunoreactive cells were found dorsal and ventral to the developing cortical plate. At this stage, immunoreactivity was also observed in the other transient developmental zones of the cortical anlage: in the subplate layer and in the intermediate, subventricular and ventricular zones. From 8 to 9 g.w. and continuing throughout the end of the studied period (13 g.w.), GABA-IR cells were distributed throughout the full width of the telencephalic wall, and, at 13 g.w., the newly formed subpial granular layer contained GABA-immunoreactive cells, as well. However, the predominant sites for GABA immunoreactivity remained the prospective layer I and the subplate. The population of GABA-positive cells described here was not immunoreactive for glial fibrillary acidic protein (GFAP) at any gestational age examined and, therefore, probably represents GABA-containing neurons. The observation that GABA-IR neurons appear in human developing cortex slightly before the cortical plate formation and beginning of synaptogenesis (6.5 g.w.) suggests that GABA plays an important role in the initial organization of the developing human cerebral cortex.
Cerebral Cortex↗
Widespread programmed cell death in proliferative and postmitotic regions of the fetal cerebral cortex.
A key event in the development of the mammalian cerebral cortex is the generation of neuronal populations during embryonic life. Previous studies have revealed many details of cortical neuron development including cell birthdates, migration patterns and lineage relationships. Programmed cell death is a potentially important mechanism that could alter the numbers and types of developing cortical cells during these early embryonic phases. While programmed cell death has been documented in other parts of the embryonic central nervous system, its operation has not been previously reported in the embryonic cortex because of the lack of cell death markers and the difficulty in following the entire population of cortical cells. Here, we have investigated the spatial and temporal distribution of dying cells in the embryonic cortex using an in situ endlabelling technique called 'ISEL+' that identifies fragmented nuclear DNA in dying cells with increased sensitivity. The period encompassing murine cerebral cortical neurogenesis was examined, from embryonic days 10 through 18. Dying cells were rare at embryonic day 10, but by embryonic day 14, 70% of cortical cells were found to be dying. This number declined to 50% by embryonic day 18, and few dying cells were observed in the adult cerebral cortex. Surprisingly, while dying cells were observed throughout the cerebral cortical wall, the majority were found within zones of cell proliferation rather than in regions of postmitotic neurons. These observations suggest that multiple mechanisms may regulate programmed cell death in the developing cortex. Moreover, embryonic cell death could be an important factor enabling the selection of appropriate cortical cells before they complete their differentiation in postnatal life.
Animals↗
Role of renal cortical sulfhydryl groups in development of mercury-induced renal toxicity.
The effect of lowering renal cortical sulfhydryl concentration on development of acute renal failure (ARF) was evaluated in rats receiving HgCl2 (15 mg/kg body weight, im). Within 90 min after HgCL2 injection urine flow rate and fractional excretion of sodium (FENa) were significantly elevated above control levels, and they remained elevated throughout the 3-h experimental period. Urine flow rate and FENa were not significantly elevated above control levels in animals injected with diethyl maleate (3 mmol/kg, ip) 30 min before and 90 min after HgCl2 (DEM/HgCl2). Administration of DEM alone did not alter renal function. Although lower than control levels, concentrations of protein-bound sulfhydryl groups (PBSH) were comparable in HgCl2- and DEM/HgCl2-treated animals. In contrast, concentrations of nonprotein sulfhydryl groups (NPSH) were 62% lower in DEM/HgCl2 animals than in those treated with HgCl2 alone. Similarly, Hg accumulation was 54% lower in DEM/hgCl2-treated animals than in animals treated with HgCl2 alone. These results suggest that NPSH play an important role in Hg uptake and subsequent development of Hg toxicity.
Acute Kidney Injury↗
Absence of interhemispheric connections of area 17 during development in the monkey.
Our understanding of the development of cortical connectivity largely stems from studies of the ontogeny of interhemispheric pathways in carnivores, rodents and lagomorphs. Early in development, cortical neurons projecting to the contralateral hemisphere through the corpus callosum (callosal projection neurons) have a widespread distribution. As maturation proceeds, callosal projection neurons become restricted to those cortical regions that are connected in the adult. In newborn cats and rats, for example, callosal projection neurons are not restricted to the 17-18 border as in the adult, but are found throughout areas 17 and 18. The macaque monkey is an exception, because at birth it has an adult-like distribution of callosal projection neurons in area 18, with practically none in area 17. Here we show that whereas area 17 is devoid of interhemispheric connections throughout prenatal development, the distribution of callosal projection neurons in area 18 shows the common sequence of an early widespread distribution followed by regression. The absence of callosal projection neurons in area 17 throughout ontogeny may well be a feature unique to Old World primates.
Animals↗
Cell migration along the lateral cortical stream to the developing basal telencephalic limbic system.
During embryogenesis, the lateral cortical stream (LCS) emerges from the corticostriatal border (CSB), the boundary between the developing cerebral cortex and striatum. The LCS is comprised of a mix of pallial- and subpallial-derived neural progenitor cells that migrate to the developing structures of the basal telencephalon, most notably the piriform cortex and amygdala. Using a combination of in vitro and in vivo approaches, we analyzed the timing, composition, migratory modes, origin, and requirement of the homeodomain-containing transcription factor Gsh2 (genomic screened homeobox 2) in the development of this prominent migratory stream. We reveal that Pax6 (paired box gene 6)-positive pallial-derived and Dlx2 (distal-less homeobox 2)-positive subpallial-derived subpopulations of LCS cells are generated in distinct temporal windows during embryogenesis. Furthermore, our data indicate the CSB border not only is comprised of separate populations of pallial- and subpallial-derived progenitors that contribute to the LCS but also a subpopulation of cells coexpressing Pax6 and Dlx2. Moreover, despite migrating along a route outlined by a cascade of radial glia, the Dlx2-positive population appears to migrate primarily in an apparent chain-like manner, with LCS migratory cells being generated locally at the CSB with little contribution from other subpallial structures such as the medial, lateral, or caudal ganglionic eminences. We further demonstrate that the generation of the LCS is dependent on the homeodomain-containing gene Gsh2, revealing a novel requirement for Gsh2 in telencephalic development.
Animals↗
Somatosensory evoked cortical potentials indicating impaired motor development in infancy.
Somatosensory evoked cortical potentials were performed on 120 infants between one and 10 months of age because impaired development was suspected on the basis of their histories or clinical findings. All but two had a follow-up examination after their first birthday. Of the 120 infants, 47 presented with only minor perinatal risks: these had normal neurological and developmental findings in infancy and at follow-up and they formed the control group. 73 infants initially had developmental delay or abnormal neurological findings: at follow-up 35 were normal and 38 had pathological conditions (16 general psychomotor retardation, 15 cerebral palsy, four degenerative and three neurometabolic diseases of the CNS). Marked prolongation of N1 peak latencies (greater than 2ms) above the two-sigma border, or absence of potentials on one or both sides, indicated handicap after their first birthday in all 19 infants showing such alterations. The author concludes that these marked alterations have a high prognostic value.
Developmental Disabilities↗
Early development of the SI cortical barrel field representation in neonatal rats follows a lateral-to-medial gradient: an electrophysiological study.
Development of the barrel field in layer IV of SI cortex of neonatal rats was studied in vivo using electrophysiological recording techniques. This study was designed to determine (a) the earliest time SI cortex is responsive to peripheral mechanical and/or electrical stimulation and (b) whether the development of the SI cortical barrel field map of the body surface follows a differential pattern of development similar to the pattern previously demonstrated using peanut agglutinin (PNA) binding (McCandlish et al. 1989). Carbon fiber microelectrodes were used to record evoked responses from within the depth of the cortex in neonatal rats between postnatal day 1. (PND-1), defined as the day of birth, and PND-14. Evoked responses were first recorded approximately 12 h after birth. These responses in the youngest animals were of low amplitude, monophasic waveshape, and long latency, with long interstimulus intervals necessary to drive the cortex. Increases in amplitude and complexity of waveshape and decreases in latency were observed over subsequent postnatal days. The earliest responses recorded on middle PND-1 were evoked by stimulation of the face and/or mystacial vibrissae. The next responses were evoked approximately 24 h after birth (late PND-1) by stimulation of the forelimb. The last responses were evoked approximately 36 h after birth (middle PND-2), by stimulation of the hindlimb. The physiological map of the representation of the body surface follows a developmental gradient similar to the gradient observed using PNA histochemistry; however, the lectin-generated morphological map lagged approximately 48 h behind the physiological map.(ABSTRACT TRUNCATED AT 250 WORDS)
Aging↗
The development of neuropeptide Y immunoreactive neurons in cat visual cortical areas.
The development of NPY-ir neurons and fibers in cat striate and extrastriate cortex was studied to determine whether temporal changes in the morphology, distribution and density of NPY-ir neurons during development would provide clues to the emergence of specific cortical areas. No differences in the number or distribution of NPY-ir neurons were observed at any age among the five visual cortical areas examined, area 17, 18, 19, posteromedial lateral suprasylvian and posterolateral lateral suprasylvian cortex. The number of NPY-ir neurons in cat visual cortical areas was higher in adult animals than in kittens. The proportion of NPY-ir neurons found in layer VIb was constant throughout life, suggesting that NPY immunoreactivity is not a marker for the transient neurons of the subplate. NPY-ir neuronal morphology was seen to 'flatten' in older animals with the development of sulci and increasing density of the brain. In contrast to the pattern observed with NPY-ir neurons, NPY-ir processes exhibited area-dependent differences during development. NPY-ir fibers grew into area 17 earlier and with a radial orientation which was not consistently observed laterally. This radial orientation was still apparent in adult brains in layer IV of area 17, though there was no orientation of fibers in the other laminae or other visual areas of the adult.
Aging↗
Development of motion-specific cortical responses in infancy.
The development of visual motion mechanisms has been studied in infants with a visual evoked potential (VEP) technique which isolates responses from directionally-selective mechanisms. In adults, the amplitude of this directional VEP increased with velocity up to a maximum at 15-20 deg/sec, and then declined with further increases in velocity. In a group of infants tested longitudinally, directional responses were first found at a median age of 74 days with a stimulus velocity of 5 deg/sec, and 90 days with a velocity of 20 deg/sec; this age difference was statistically significant. Initially, VEP amplitudes were significantly greater at 5 deg/sec than at 20 deg/sec. By the end of the longitudinal study, there was no significant difference in amplitudes at the two velocities. In a second group of infants, simultaneous recording of VEPs and electrooculograms indicated that eye movements tracking the stimulus were not a significant factor in the development of the directional VEP. It is concluded that the development of directional selectivity starts at low velocities, and extends to higher velocities with age.
Adult↗
NMDA and glutamate evoke excitotoxicity at distinct cellular locations in rat cortical neurons in vitro.
The development of cortical neurons in vivo and in vitro is accompanied by alterations in NMDA receptor subunit expression and concomitant modifications in the pharmacological profile of NMDA-activated ionic currents. For example, we observed that with decreasing NR2B/NR2A subunit expression ratio, the block of NMDA receptor-mediated whole-cell responses by the NR2B-selective antagonist haloperidol was also decreased. In mature cultures (>22 d in vitro), however, NMDA responses obtained from excised nucleated macropatches, which comprised a large portion of the soma, remained strongly antagonized by haloperidol. These results suggest that in more mature neurons NR1/NR2B receptors appear to be preferentially expressed in the cell body. As predicted from the whole-cell recording pharmacological profile, NMDA-induced toxicity was largely unaffected by haloperidol in mature cultures. However, haloperidol effectively blocked glutamate toxicity in the same cultures, suggesting that the neurotoxic actions of this amino acid were mostly due to the activation of somatic NMDA receptors. In experiments in which the potency of glutamate toxicity was increased by the transport inhibitor l-trans-pyrrolidine-2,4-dicarboxylic acid, the neuroprotective effects of haloperidol were significantly diminished. This was likely because of the fact that glutamate, now toxic at much lower concentrations, was able to reach and activate dendritic receptors under these conditions. These results strongly argue that exogenous glutamate and NMDA normally induce excitotoxicity at distinct cellular locations in mature mixed neuronal cultures and that NR1/NR2B receptors remain an important component in the expression of glutamate, but not NMDA-induced excitotoxicity.
ATP-Binding Cassette Transporters↗
Elevated AP-1 transcription factor DNA binding activity at the onset of functional plasticity during development of rat sensory cortical areas.
The patterns of three transcription factor DNA binding activities, namely AP-1, Octamer and CREB, were examined in barrel and visual cortices of rat brain during early postnatal development, when activity-dependent plasticity of neuronal responses and connectivity was described. Main peak levels of AP-1 DNA binding activity have been observed at 21 days postnatally in both cortical areas. In addition, slightly elevated AP-1 levels were detected at 3-7 postnatal days in the barrel and in the visual cortex. In contrast, Octamer DNA binding activities were at the highest levels in both areas at 7 days postnatally, and CREB DNA binding activities were not appreciably modulated throughout the development. The AP-1 protein complex at 21 days postnatally was composed of JunD, JunB, Fra-2, FosB and to much lesser extent of c-Fos in both cortical areas. Treatment of 21 day old rats with MK-801, an NMDA receptor antagonist, provoked a dramatic decrease in AP-1 DNA binding activities in the barrel cortex, but not in the visual cortex. Elevated AP-1 DNA binding activity can be taken as a good correlate of an onset of functional plasticity in the rat sensory cortex, although in the two primary sensory cortices examined it seems to be regulated in different ways.
Aging↗
Postnatal development of the striate cortical projection onto the extrageniculate visual thalamus in the cat: an HRP study.
The postnatal development of the striate cortical projection onto the extrageniculate visual thalamus was examined by using the orthograde and retrograde HRP methods. At birth, the projection is present, and fibres of the projection terminate in the lateral part of the lateral posterior nucleus. A rough topographical arrangement of the projection is already established. Neurones that give rise to the projection are located exclusively in layer V from birth onward. However, the neurones are much more densely packed at birth than in adult cats. The packing density of the neurones decreases rapidly during the second postnatal week, and afterwards continues to become gradually lower. In the meantime, the cross sectional area of the neurones increases sharply during the second postnatal week. These findings suggest that striate cortical neurones projecting onto the lateral posterior nucleus rapidly complete the final stages of their maturation shortly after the normal opening of the eyelids, and during this time some of these neurones undergo axonal elimination or neuronal death, or both.
Animals↗
The early differentiation of the neocortex: a hypothesis on neocortical evolution.
During development, a cerebral cortex appears in the wall of the telencephalic vesicle in reptiles and mammals. It arises from a cell-dense cortical plate, which develops within a primordial preplate. The neurons of the preplate are essential for cortical development; they regulate the neuronal migration of the cortical plate neurons and form the first axonal connections. In the reptilian cortex and in the hippocampus of the mammalian cerebral cortex, most ingrowing afferent axons run above the cortical plate, in the zone where the receptive tufts of apical dendrites of the cortical pyramidal neurons branch extensively. In the mammalian neocortex, however, axons enter mainly from below the cortical plate where they do not encounter the apical tufts of these pyramidal neurons. In this paper, we discuss the idea that this difference in cortical development has relieved a functional constraint in the expansion of the cortex during evolution. We hypothesize that the entrance of axons below the cell-dense cortical plate, together with the inside-out migration of cortical neurons, ensures that the neocortex remains an "open" system, able to differentiate into new (sub)layers and more cortical areas.
Animals↗