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At least 937 records · Page 52Linked to original sources
PubMed1995

Abnormalities of gyration, heterotopias, tuberous sclerosis, focal cortical dysplasia, microdysgenesis, dysembryoplastic neuroepithelial tumour and dysgenesis of the archicortex in epilepsy. Clinical, EEG and neuroimaging features in 100 adult patients.

Cerebral cortical dysgenesis (CD) is a heterogeneous disorder of cortical development and organization commonly associated with epilepsy, with a variety of subtypes. We reviewed the clinical, EEG and neuroimaging features in 100 adult patients with CD. There were 39 men and 61 women with a median age of 27 years (range 15-63 years). All patients were referred because of medically refractory epilepsy. Median age at seizure onset was 10 years (range 3 weeks to 39 years); in 30 patients, onset was in adulthood. The epilepsy was classified as generalized in 16 patients and localization-related in 84. Of the latter, the epileptic syndromes in decreasing frequency were frontal (32%), temporal (31%), parietal (14%) and occipital (7%). Only 15% of patients had a history of status epilepticus. Prenatal/perinatal problems were reported in 32 patients but these were severe in only four: exposure to drugs (three) and infection (one) during the first trimester. Delayed developmental milestones were seen in 10%, mental retardation in 9%, additional congenital abnormalities in 4% and neurological deficits in 14% of patients. Diagnosis of CD was based on neuroimaging in 70, pathology in four and both methods in the remaining 26. The following subcategories were identified: agyria/diffuse macrogyria (four patients), focal macrogyria (16), focal polymicrogyria (one), focal macrogyria/polymicrogyria associated with a cleft (11), minor gyral abnormalities (seven), subependymal grey matter heterotopia (20), bilateral subcortical laminar grey matter heterotopia (eight), tuberous sclerosis (five), focal cortical dysplasia/microdysgenesis (seven) and dysembryoplastic neuroepithelial tumours (DNT) (21). Sixty-eight percent of patients had normal CT and 19 out of 36 patients had normal previous conventional MRI. MRI-based hippocampal volume measurements in 47 patients revealed ratios (smaller: larger hippocampus) of < 0.90 in 16, 0.90-0.94 in 14 and > or = 0.95 in 17 patients. EEGs were normal in only five patients. Alpha rhythm was preserved in 78 patients, including one patient with bilateral posterior macrogyria. Localized polymorphic slow activity was present in 43 patients. Five of 68 patients with focal/unilateral CD had only bilateral independent/synchronous spiking and 14 out of 32 with diffuse/bilateral CD only focal/unilateral spiking. In 60 patients with nondiffuse CD or with abnormal gyration or DNT, the epileptiform abnormalities were less extensive than coextensive with the lesion in 28, more extensive than and overlapped the lesion in 18 and remote from the lesion in five; nine patients did not have epileptiform abnormalities. There was poor correlation between the epileptic syndromes and EEG abnormalities and the location/extent of CD as defined by MRI and pathology.(ABSTRACT TRUNCATED AT 400 WORDS)

Adolescent↗
PubMed2000

Handedness and professional tennis.

Based on the hypothesis that as a group left-handed (LH) people have better developed right hemispheres and therefore have better developed motor, attentional, and spatial functions than right-handed people (Geschwind, 1982; Geschwind and Galaburda, 1985a, 1985b; Nass and Gazzaniga, 1987), several studies have examined a possible association between left-handedness and superior tennis ability (cited in Annett, 1985; Azemar et al., 1983; Wood and Aggleton, 1989). The conflicting findings of these studies are due to flawed research designs, very limited data, and inadequate data analyses. In this study an estimated population rate of left-handedness for racket use (8.1%) was compared with rates found among professional tennis players; and highly successful competitors over a 32-year period were analyzed for handedness frequency. Results revealed that from 1968 through 1999 LH competitors were significantly over-represented among top ranking players (World Number One and Top Ten) and among Grand Slam finalists, including champions. Rates of left-handedness ranged from two to five times higher than expected in these highly successful players. However, no difference was found in the rate of left-handedness for racket use among male (N = 1,904; LH = 6.98%) or female (N = 533; LH = 7.69%) professional tennis players compared to the general population. These findings indirectly support the notion that LH people have neuroanatomically-based advantages in performing certain neurocognitive tasks, such as visuospatial and gross (whole body) visuomotor tasks. The present findings are also consistent with a nature/nurture model of cortical development and functioning (Casey, 1996).

Brain↗
PubMed2004

Differential gene expressions in the visual cortex of postnatal day 1 versus day 21 rats revealed by suppression subtractive hybridization.

The neonatal visual cortex is a highly plastic structure and its development is guided by visual experience during early postnatal life. Rats do not open their eyes until the end of the second postnatal week. We hypothesized that the expression of genes in the visual cortex would differ before and after eye opening. As a first step in uncovering these differences, we compared gene expressions in the visual cortex of postnatal days (PND) 1 and 21 rats. Suppression subtractive hybridization was performed using PND1 samples as the tester and PND21 as the driver. More than 30 genes were expressed at a higher level in PND1 than PND21 samples, but 5 fragments showed higher copies than others. PCR product of the five fragments was gel-purified and cloned into pCRII vectors. They showed significant homology to cDNA of genes: (A). clone MGC: 19375; (B). Type II iodothyronine 5'-deiodinase (D2); (C). reduced expression 3 gene; (D). lactosylceramide synthase; and (E). septin 4, respectively. Functions of A, C and E are unknown. By means of RACE PCR, three full-length cDNAs not reported previously in the rat were obtained for A, C and E, and we named them "expression genes 1, 2 and 3, respectively, in the rat visual cortex (EG1RVC, EG2RVC and EG3RVC)". EG1RVC was further characterized by Northern blots, in situ hybridization and in vitro transfection. These approaches confirmed that EG1RVC was expressed at a significantly higher level in PND1 than in PND21 visual cortical samples, and that transfected PC12 cells and primary neuronal cultures showed expression mainly in neuronal cell bodies. Our data indicate that genes expressed more abundantly on PND1 are associated with various metabolic pathways and enzymatic changes, and may play an important role in visual cortical development, growth and/or plasticity.

Animals↗
PubMed1998

Long-term evolution of excitotoxic cortical dysgenesis induced in the developing rat brain.

Cortical dysplasias are frequently caused by excitotoxic brain damage due to hypoxia or ischemia during development. Ibotenate, a glutamatergic agonist, was injected in the neopallium of rat pups at day of birth. The resulting cytoarchitectonic pattern includes neuronal depopulation in deep cortical layers, sulcus formation, and molecular ectopias, mimicking human polymicrogyria and disorders of neuronal migration. These cortical dysplasias persist until adulthood, providing a rat model to investigate the long-term functional consequences of cortical malformations.

Abnormalities, Drug-Induced↗
PubMed1999

Adult-onset MELAS presenting as herpes encephalitis.

OBJECTIVE: To report an unusual presentation of mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes (MELAS) manifested in late life with a clinical picture of herpes simplex encephalitis. DESIGN: Case report. SETTING: Clinical neurology department in a tertiary care hospital. CASE DESCRIPTION: A 55-year-old woman developed aphasia and delirium during ophthalmic herpes zoster infection treated with oral prednisone and ophthalmic steroids, which was followed by progressive cognitive decline without acute neurologic events for 5 years. At age 60, the patient presented with new onset of seizures, hemiparesis, and hemianopsia. Subsequently she developed cortical blindness, multiple traumatic soft tissue injuries from falls, acute psychosis, and severe dementia with periods of agitation. She died in a nursing home in March 1997, 6 years after initial presentation. RESULTS: Magnetic resonance imaging scan of the brain showed hyperintensity on T2-weighted images involving temporal, parietal, and occipital lobes bilaterally as well as mild atrophy of brainstem and cerebellum. Single photon emission computed tomographic imaging showed hypoperfusion of temporal, parietal, and occipital lobes. Results of video electroencephalographic monitoring showed periodic lateralizing epileptiform discharges in temporal and occipital areas. The serum lactate level was normal in May 1996 and elevated in October 1996. The creatine kinase level was elevated with a 100% MM fraction in August 1991 and normal in March 1996. Results of repeated cerebrospinal fluid analyses indicated elevated protein levels. Analysis of DNA was diagnostic of MELAS by mitochondrial DNA point mutation at position 3243. The results of autopsy showed moderate cerebral, cerebellar, and brainstem atrophy with signs of infarction in temporal and parietal lobes bilaterally. CONCLUSIONS: The clinical presentation as well as age at onset of MELAS are highly variable. Onset of mitochondrial disorders can be provoked by febrile illness when there is mismatch between energy requirements and availability. In the differential diagnosis of herpes encephalitides, MELAS syndrome should be considered.

Age of Onset↗
PubMed1997

Disrupted pattern of D2 dopamine receptors in the temporal lobe in schizophrenia. A postmortem study.

BACKGROUND: Anatomical substrates for the clinical efficacy of D2 dopamine receptor antagonism in ameliorating positive symptoms, including auditory hallucinations, in schizophrenia are not fully known. We previously identified a modular organization of D2 receptors unique to the temporal lobe. The dense bands of D2 receptors showed highest frequency in auditory and speech association cortices (Brodmann areas 22, 39, and 42) and auditory-visual association areas (Brodmann areas 20 and 37) but were rarely found in somatosensory association regions (Brodmann area 21). Since the anatomical localization of these bands mirrors the presumed sites underlying hallucinations in schizophrenia, the modular and laminar distribution of D2 receptors was studied in the temporal cortex in the brains of schizophrenic and control subjects. METHODS: Tissue obtained post mortem from 12 elderly schizophrenic subjects and 13 controls matched for age and postmortem interval was examined by quantitative receptor autoradiography for D2 receptor binding with [125I]epidepride. All regions of the temporal lobe were sampled in all cases. RESULTS: Schizophrenia cases exhibited significantly disrupted patterns of D2 receptors in the perirhinal, superior, and inferior temporal cortices, including disrupted patterns in the modular D2 receptor bands. The schizophrenic cases had reduced concentrations of D2 receptors in the supragranular layers and elevated concentrations of D2 receptors in the granular layer in isocortical regions of the temporal lobe. This disruption does not appear to be due to long-term treatment of antipsychotic drugs and is regionally specific as there were no differences between groups for concentrations or patterns of expression in the hippocampal complex. CONCLUSIONS: Blockade of the disrupted distribution of D2 receptors in auditory and auditory-visual association cortices is a likely mechanism for the clinical efficacy of D2 antagonists in reducing hallucinations. The regionally specific, aberrant pattern of D2 receptors may be a symptom of anomalous cortical development in these regions.

Adult↗
PubMed1999

Layer VI in cat primary auditory cortex: Golgi study and sublaminar origins of projection neurons.

The organization of layer VI in cat primary auditory cortex (AI) was studied in mature specimens. Golgi-impregnated neurons were classified on the basis of their dendritic and somatic form. Ipsilateral and contralateral projection neurons and the corticogeniculate cells of origin were labeled with retrograde tracers and their profiles were compared with the results from Golgi studies. Layer VI was divided into a superficial half (layer VIa) with many pyramidal neurons and a deeper part (layer VIb) that is dominated by horizontal cells. Nine types of neuron were identified; four classes had subvarieties. Classical pyramidal cells and star, fusiform, tangential, and inverted pyramidal cells occur. Nonpyramidal neurons were Martinotti, multipolar stellate, bipolar, and horizontal cells. This variety of neurons distinguished layer VI from other AI layers. Pyramidal neuron dendrites contributed to the vertical, modular organization in AI, although their apical processes did not project beyond layer IV. Their axons had vertical, intrinsic processes as well as corticofugal branches. Horizontal cell dendrites extended laterally up to 700 microm and could integrate thalamic input across wide expanses of the tonotopic domain. Connectional experiments confirmed the sublaminar arrangement seen in Nissl material. Commissural cells were concentrated in layer VIa, whereas corticocortical neurons were more numerous in layer VIb. Corticothalamic cells were distributed more equally. The cytological complexity and diverse connections of layer VI may relate to a possible role in cortical development. Layer VI contained most of the neuronal types found in other layers in AI, and these cells form many of the same intrinsic and corticofugal connections that neurons in other layers will assume in adulthood. Layer VI, thus, may play a fundamental ontogenetic role in the construction and early function of the cortex.

Animals↗
PubMed1998

Sexually dimorphic responses to neonatal basal forebrain lesions in mice: I. Behavior and neurochemistry.

The nucleus basalis magnocellularis (nBM) provides the primary source of cholinergic input to the cortex. Neonatal lesions of the nBM produce transient reductions in cholinergic markers, persistent abnormalities in cortical morphology, and spatial navigation impairments in adult mice. The present study examined sex differences in the effects of an electrolytic nBM lesion on postnatal day 1 (PND 1) in mice on behavior and neurochemistry in adulthood. Mice were lesioned on PND 1 and tested at 8 weeks of age on a battery of behavioral tests including passive avoidance, cued and spatial tasks in the Morris water maze, simple and delayed nonmatch to sample versions of an odor discrimination task, and locomotor activity measurements. Following behavioral testing, mice were sacrificed for either morphological assessment or neurochemical analysis of a cholinergic marker or catecholamines. There were no lesion or sex differences in acquisition or retention of passive avoidance, performance of the odor discrimination tasks, or activity levels. Control mice showed a robust sex difference in performance of the spatial water maze task. The lesion produced a slight cued but more dramatic spatial navigation deficit in the water maze which affected only the male mice. Neurochemical analyses revealed no lesion-induced changes in either choline acetyltransferase activity or levels of norepinephrine or serotonin at the time of testing. The subsequent report shows a sex difference in lesion-induced changes in cortical morphology which suggests that sexually dimorphic cholinergic influences on cortical development are responsible for the behavioral deficits seen in this study.

Aging↗
PubMed2002

Drug resistance in epilepsy: human epilepsy.

The basis of drug resistance in human epilepsy is not understood. Parallels with resistance in cancer suggest that drug resistance proteins may have a role. To examine this possibility, we have studied human brain tissue containing pathologies capable of causing refractory epilepsy. Using immunohistochemistry for P glycoprotein (Pgp) and multidrug resistance-associated protein 1 (MRP1), we examined both pathological tissue and control tissue. We demonstrate expression of Pgp and MRP1 in glia from cases of malformation of cortical development studied both before and after the onset of epilepsy, as well as in cases of hippocampal sclerosis and dysembryoplastic neuroepithelial tumours. In one particular type of malformation, we also demonstrate that dysplastic neurons express MRP1. The pattern of immunolabelling suggests overexpression is concentrated particularly around vessels in most of the pathologies. The timing shows that expression may be constitutive in some pathologies. These findings suggest that drug resistance proteins may contribute to drug resistance in refractory epilepsy.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed2001

Causes of epilepsies: insights from discordant monozygous twins.

Whereas some patients with epilepsy have known acquired or genetic causes, in many the cause is unknown. By analyzing monozygotic twins, discordant for epilepsy, subtle etiological factors may be detected. We analyzed 12 monozygotic, discordant twins for factors explaining discordancy. These factors were presence of major clinical risk factors, presence of possibly epileptogenic lesions on brain magnetic resonance imaging (MRI), and quantitative brain volume abnormalities. Major risk factors, with associated acquired lesions were found in 4 of 12 twins. An MRI lesion without a major risk factor was found in a further 4 of 12 twins. Two of these had unilateral malformations of cortical development, 1 had bilateral periventricular heterotopia, and 1 had focal atrophy. Significant twin-twin differences in MRI volumes without obvious MRI lesions or major risk factors were found in 2 of 12 twins. Both had larger volumes than their co-twins, and idiopathic generalized epilepsy. No clinical or MRI findings accounting for discordance for epilepsy were found in 2 of 12 twins. In 10 of 12 pairs a clinical or MR correlate of epilepsy was found; some of those were subtle and only apparent by twin-twin comparison. They may be due to occult acquired factors, such as prenatal insults, or to genetic abnormalities resulting from postfertilization genetic processes.

Adult↗
PubMed2006

Additional chromosomal abnormalities in patients with a previously detected abnormal karyotype, mental retardation, and dysmorphic features.

The detection of chromosomal abnormalities in patients with mental retardation (MR) and dysmorphic features increases with improvements of molecular cytogenetic methods. We report on six patients referred for detailed characterization of chromosomal abnormalities (four translocations, one inversion, one deletion) detected by conventional cytogenetics, in whom metaphase CGH revealed imbalances not involved in the initially detected rearrangements. The detected abnormalities were validated by real-time PCR. Parents were investigated by CGH in four cases. The genomic screening revealed interstitial deletions of 2q33.2-q34, 3p21, 4q12-q13.1, 6q25, 13q22.2-q31.1, and 14q12. The estimated minimum sizes of the deletions ranged from 2.65 to 9.27 Mb. The CGH assay did not reveal imbalances that colocalized with the breakpoints of the inversion or the translocations. The deletion of 6q included ESR1, in which polymorphisms are associated with variation of adult height. FOXG1B, known to be involved in cortical development, was located in the 14q deletion. The results illustrate that whole-genome molecular cytogenetic analysis of phenotypically affected patients with abnormal conventional karyotypes may detect inapparent molecular cytogenetic abnormalities in patients with microscopic chromosomal abnormalities and that these data provide additional information of clinical importance.

Adolescent↗
PubMed2007

The role of RELN in lissencephaly and neuropsychiatric disease.

Reelin is an extracellular matrix-associated protein important in the regulation of neuronal migration during cerebral cortical development. Point mutations in the RELN gene have been shown to cause an autosomal recessive human brain malformation termed lissencephaly with cerebellar hypoplasia (LCH). Recent work has raised the possibility that reelin may also play a pathogenic role in other neuropsychiatric disorders. We sought, therefore, to define more precisely the phenotype of RELN gene disruption. To do this, we performed a clinical, radiological, and molecular study of a family in whom multiple individuals carry a chromosomal inversion that disrupts the RELN locus. A 6-year-old girl homozygous for the pericentric inversion 46,XX,inv7(p11.2q22) demonstrated the same clinical features that have been previously described in association with RELN point mutations. The girl's brain magnetic resonance imaging (MRI) findings, including pachygyria and severe cerebellar hypoplasia, were identical to those seen with RELN point mutations. Fluorescence in situ hybridization confirmed that one of the breakpoints of this inversion mapped to within the RELN gene, and Western blotting revealed an absence of detectable serum reelin protein. Several relatives who were heterozygous for this inversion were neurologically normal and had no signs of psychotic illness. Our findings demonstrate the distinctive phenotype of LCH, which is easily distinguishable from other forms of lissencephaly. Although RELN appears to be critical for normal cerebral and cerebellar development, its role, if any, in the pathogenesis of psychiatric disorders remains unclear.

Brain↗
PubMed2003

Neuroimaging studies in the evaluation of developmental delay/mental retardation.

The employment of neuroimaging studies in the evaluation of individuals with developmental delay/mental retardation (DD/MR) is still highly debated. The Consensus Conference of the American College of Medical Genetics has suggested that "neuroimaging appears to have an especially important role in patients with microcephaly or macrocephaly, seizures, loss of psychomotor skills and neurologic signs," whereas the value of neuroimaging investigations "in the normocephalic patient without focal neurological signs is unclear" [Curry et al., 1997]. However, recent literature reports show how the latest neuroimaging techniques (in vivo proton magnetic resonance spectroscopy [H-MRS]) may prove to be useful in the diagnostic process of those individuals with DD/MR and no neurological signs/symptoms. The use of these techniques can, in addition, help in monitoring treatment in distinct metabolic disorders. This review will focus on the usefulness of neuroimaging studies in some of the newer metabolic disorders. This paper will also cover those recognizable patterns of human malformation where neuroimaging findings seem to be relevant both toward diagnosis and management, and add to our understanding of the related behavior phenotype. The essential role of magnetic resonance imaging (MRI) on the progress in the diagnostic recognition of malformations of cerebral cortical development is stressed.

Cerebral Cortex↗
PubMed1995

Precursor cell types in the germinal zone of the cerebral cortex.

Retroviral lineage tracing experiments suggest that the cortical ventricular zone is composed of a mixture of precursor cell types. The majority generate a single cell type (neurones, astrocytes or oligodendrocytes) and the remainder generate neurones and a single type of glial cell. Pluripotential precursor cells, that have the ability to generate all three cell types, are not observed. A recent paper, however, reports that when single ventricular zone cells are cultured in isolation, a small percentage of these cells are pluripotential. This review will discuss what this knowledge tells us about cortical development.

Animals↗
PubMed2007

Magnetic resonance imaging and histological studies of corpus callosal and hippocampal abnormalities linked to doublecortin deficiency.

Mutated doublecortin (DCX) gives rise to severe abnormalities in human cortical development. Adult Dcx knockout mice show no major neocortical defects but do have a disorganized hippocampus. We report here the developmental basis of these hippocampal abnormalities. A heterotopic band of neurons was identified starting at E17.5 in the CA3 region and progressing throughout the CA1 region by E18.5. At neonatal stages, the CA1 heterotopic band was reduced, but the CA3 band remained unchanged, continuing into adulthood. Thus, in mouse, migration of CA3 neurons is arrested during development, whereas CA1 cell migration is retarded. On the Sv129Pas background, magnetic resonance imaging (MRI) also suggested abnormal dorsal hippocampal morphology, displaced laterally and sometimes rostrally and associated with medial brain structure abnormalities. MRI and cryosectioning showed agenesis of the corpus callosum in Dcx knockout mice on this background and an intermediate, partial agenesis in heterozygote mice. Wild-type littermates showed no callosal abnormalities. Hippocampal and corpus callosal abnormalities were also characterized in DCX-mutated human patients. Severe hippocampal hypoplasia was identified along with variable corpus callosal defects ranging from total agenesis to an abnormally thick or thin callosum. Our data in the mouse, identifying roles for Dcx in hippocampal and corpus callosal development, might suggest intrinsic roles for human DCX in the development of these structures.

Aborted Fetus↗
PubMed1976

Areal changes in mouse cortical barrels following vibrissal damage at different postnatal ages.

The normal cytoarchitectonic pattern of barrels in layer IV of mouse SmI face cortex is altered by early damage to the mystacial vibrissae (Van der Loos and Woolsey, '73). In the present study, the middle row of vibrissae (row-C) on one side of the face in groups of Swiss mice was cauterized on the day of birth (postnatal day [PND] -1)or on PND's - 2, 3, 4, 5, 7, 10, 12, 15, 20 and 30; littermates in each group served as controls. All animals were perfused on PND-60 and the brains sectioned parallel to SmI layer IV. For each specimen, the posteromedial barrel subfields (PMBSF) of the two hemispheres were reconstructed with a camera lucida and the cross-sectional areas of individual barrels measured using a small computer. The findings are: (1) The hemispheres ipsilateral to the vibrissal damage are quantitatively indistinguishable from the littermate controls indicating that the ipsilateral hemispheres in lesioned animals can serve as controls for observations of the type reported in this paper. (2) There are no consistent differences in the cross-sectional areas of the PMBSF's as a whole in the hemispheres ipsi- and contralateral to the peripheral damage, suggesting that there is no net loss of cortex as a result of the lesions. (3) The contralateral row-C barrels are reduced in size. Expressed as a percentage of normal values; row-C is reduced to 17% for animals lesioned on PND-1, 16% on PND-2, 38% on PND-3, 52% on PND-4 and 79% on PND-5; on PND-7 and later the cross-sectional areas of row-C barrels are normal. This implies that the barrel field of the SmI face cortex becomes progressively refractory to the effects of peripheral damage during the first postnatal week and in the period prior to PND-6, an intact periphery is necessary for normal cortical development. (4) In every case, the decreased cross-sectional area of row-C is accompanied by precisely increased cross-sectional areas of the barrels in adjacent rows-B and D. in the case of the restricted peripheral damage which we produced, there is a "compensation" in the contralateral hemisphere, which can be correlated with patterns of the specific thalamocortical projections.

Age Factors↗
PubMed1977

The effect of cortical lesions upon visual discriminations in binocularly deprived cats.

Four cats were raised with binocular eyelid suture and, after their eyes were opened, were trained on a series of discrimination tasks. They performed at normal rates on the brightness task but indicated some difficulty with the pattern tasks. They then received large, bilateral occipito-temporal cortex ablations. Postoperatively, this in no observable way affected their visually guided orienting behavior, but it did destroy their capacity to perform the preoperatively learned pattern tasks. Postoperative performance on the brightness task remained good. These data indicate that, in these deprived cats, there is little or no cortical development for visual orienting, but cortex is necessary for visual discrimination learning.

Animals↗
PubMed1981

The site of origin and route and rate of migration of neurons to the hippocampal region of the rhesus monkey.

The site of origin and route and rate of migration of neurons in the developing hippocampal region of the rhesus monkey were studied with tritiated thymidine (3H-TdR) autoradiography. Analysis of specimens sacrificed approximately 1 hour after exposure to 3H-TdR shows that the neurons destined for the hippocampus and subiculum are generated exclusively in the ventricular zone lining the medial wall of the lateral cerebral ventricle. In contrast, neurons of the parahippocampal formation are generated in two proliferative zones: The majority of neurons destined for the lamina principalis interna arise from the ventricular zone, whereas most of those destined for the lamina principalis externa originate from the subventricular zone. The neurons of the dentate gyrus are also generated in two locations: in the ventricular zone (between E38 and E85) and within the prospective hilus of the dentate gyrus (from E58 up to approximately 3 months after birth). Analysis of specimens sacrificed at progressively longer intervals after exposure to 3H-TdR indicates that neurons destined for all of the subdivisions of the hippocampal region (except those cells generated in the hilus of the dentate gyrus) migrate through the intermediate zone, bypassing previously generated neurons on their way to the superficial limits of the developing cortical plate. Estimated migration rates are approximately 15 micrometer/day in the sector of the hippocampal formation, about 100 micrometer/day in the parahippocampal formation, and about 15 micrometer/day in the region of adjacent neocortex. Thus simultaneously generated neurons destined for three distinct cytoarchitectonic areas have significantly different rates of cell migration. These differences are unrelated to the length of cell trajectories and may depend on the mechanism of cell translocation and/or the timing of signals that initiate cell movement. The differential rate of migration indicates that the fate of postmitotic cells may be determined before they have reached their final destination.

Aging↗