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PubMed1995

Preservation of the structural integrity of a freshly lesioned or transplanted mouse neocortex and the immunoreactivity of cell-specific marker proteins in demineralized histological material.

Analysis of superficially lesioned or grafted brains poses the problem that their removal from the skull prior to histological processing often causes damage to the operated area and may lead to loss of the graft. Here, we propose an original approach to this problem, developed on mice whose cortices have been surgically lesioned and some grafted with fetal neural tissue. The experimental animals were killed 1, 3 or 6 days after operation. Our procedure was based on the softening of skulls by demineralization in Gendre's picric solution, followed by solidification of the wounded region by embedding in polyester wax. This permitted the preparation of serial sections from brains together with neurocrania. To check their immunoreactivity, the sections were later reacted with specific antisera for glial fibrillary acidic protein (GFAP), microtubule-associated protein 2 (MAP2), calbindin, and the thermolabile cell-surface glycoprotein Thy-1. The histological material revealed excellent structural integrity and cytoarchitecture. In transplanted animals, the tiny graft, protected by the overlying bone, was found in the host cavity. Immunostaining showed typical localization of the chosen marker proteins. The anti-Thy-1 antibody enabled us to distinguish between graft and host tissues, which differed, in our experiments, in their expression of two distinct allelic forms of the Thy-1 molecule. The method lends itself perfectly to histochemical study of the earliest stages of freshly operated superficial brain regions in small laboratory animals, and should also be applicable to the evaluation of other brain structures which are difficult to gain access to without being damaged.

Animals↗
PubMed1981

Adjustment of connectivity in rat neocortex after prenatal destruction of precursor cells of layers II-IV.

Prenatal administration of cytotoxic drugs during proliferation of precursor cells of neurons in granular and supragranular layers of the rat cerebral cortex prevents these layers from forming and causes malformations of some cells in the surviving layers. But it does not prevent the surviving layers from establishing normal efferent connections, nor does it prevent afferent fibers from colonizing the cortex and establishing a bilaminar pattern of synaptic connections, partly in an abnormal position.

Animals↗
PubMed1985

An immunocytochemical study of the distribution of some plasma proteins within the developing forebrain of the pig with special reference to the neocortex.

The distributions of 4 plasma proteins (fetuin, transferrin, alpha-fetoprotein and albumin) have been studied by means of immunocytochemistry in the forebrain of the pig from 20 to 109 days of gestation, term being at 114 days. These proteins are present in plasma, cerebrospinal fluid, meninges, some epithelial cells of choroid plexus and some neural cells and processes. The most striking observation is that these proteins are excluded from the brain to a large extent even at the earliest ages. Fetuin is present early in gestation in a few cells bordering the ventricle. Fetuin-positive cells are subsequently seen principally in the newly formed cortical plate and later in the subplate zone. This suggests that fetuin may be acting as a signal for the early migrating cells of the cortex and that its presence is necessary to these cells, particularly as there appears to be an increase in the amount of fetuin in these same cells in mid-gestation at a time when many fibres are arriving in this region to make cortical connections. Late in gestation after connectivity, it has been established that there are few fetuin-positive neurons remaining. However, at this late stage many neurons are strongly positive for transferrin, for which they have been negative earlier. This appearance may be related to the onset of activity. Alpha-fetoprotein has a distribution similar to that of fetuin. Albumin, although present transiently in the cerebrospinal fluid in the middle of gestation, is not seen in neural cells within the cortex. There has been some controversy as to whether these proteins which have been reported to be present in the brains of other species have been synthesized by neural cells or been taken up by specific mechanism. This study suggests that during the course of brain development, both processes may play their part.

Animals↗
PubMed1987

Deviations in brain development due to caloric undernutrition and scope of their prevention by rehabilitation: alterations in the power spectra of the EEG of areas of the neocortex and limbic system.

Wistar rats underwent caloric undernutrition so as to produce undernourished pups (F1, both male and female), which were put on a reduced diet throughout life, causing deficits in body weight of 40-70%, and in brain weight of 14-20% by adulthood. These chronic undernourished rats were mated and their progeny (F2), which had suffered gestational and postnatal undernutrition, were undernourished, like their parents, throughout life until the moment of use in this study. At this degree of chronic undernutrition, rats do not appear to be sick or morbid, but only small-for-age, they are active and can reproduce. The computer-generated power spectra of the EEG of two neocortical areas (visual and motor) and of 3 regions of the limbic system (cingulate, hippocampus and olfactory bulb) of the chronically undernourished pups were obtained at different ages from birth to adulthood, and compared with the normal ontogenetic patterns of corresponding areas obtained from age-matched controls. In another group of rats, the undernutrition was imposed on normal pups from the day of weaning (21st day), i.e., after the major part of the brain growth spurt is over. Finally, the effect of restituting normal rehabilitatory nutrition from the day of weaning on the chronic group was also studied. The results show that all brain regions studied were affected by the chronic caloric undernutrition. The deviations from the normal consist of: (1) an initial lag or delay in the development of the EEG amplitude and activity by several days, (2) a later development of an abnormally high amplitude or power in the EEG power spectra by about the weaning age, and (3) an imbalance in the occurrence of the characteristics of the EEG of the respective areas of the brain (the low and high frequency spindles of slow sleep, the slow and fast theta activities of paradoxical sleep of the hippocampus, the delta rhythm, etc.). While the chronic undernutrition was continuing there was also a certain degree of spontaneous reduction in the magnitude of abnormality after about 80 days of age, instead of worsening with age, perhaps due to an intrinsic adaptational readjustment to the stress of the nutritional deprivation. The results reveal a variation in the susceptibility of development to these abnormalities. Typical examples of the range of variation of the effects are presented in the results showing that there can be nearly normal EEG patterns in some undernourished subjects (about 14-22%), and also that there can be abnormal EEG power spectra in a proportion of normals (up to about 20%).(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1988

Ontogeny and afferent connections of corticotropin releasing factor-like immunoreactivity in the rat neocortex.

The first set of the present experiments was designed to investigate the postnatal development of corticotropin releasing factor-like immunoreactivity (CRFI) in the rat cerebral cortex by means of cobalt-enhanced immunohistochemistry. Results showed the occurrence of CRFI fibres before cells in the developing rat cerebral cortex with and without colchicine treatment, suggesting that some CRFI cells in subcortical regions may project to the cerebral cortex. In the second set of experiments, ipsilateral double-labelled cells which contained both retrogradely transported horseradish peroxidase (HRP) and CRFI were observed in the zona incerta, subincertal nucleus, lateral hypothalamic area, perifornical hypothalamic area, and in the dorsal hypothalamic area after unilateral HRP injections into the cerebral cortex. These findings indicate the existence of corticopetal CRFI-containing projections arising from the above areas.

Animals↗
PubMed1988

Control of cell number in the developing neocortex. I. Effects of early tectal ablation.

Target availability is an important factor in the early control of neuron number in many structures in the developing vertebrate nervous system. In early neocortical development, the role of target availability in the survival of subcortically projecting neurons is not yet understood, particularly because these cells' axons are widely distributed and highly branched. In this study, we have looked for alterations in the pattern of early cell death, adult cell density and adult morphology of pyramidal cells in layer V of visual cortex consequent to removal of one of their principal targets, the ipsilateral superior colliculus. After neonatal tectal ablation, there was no difference in the incidence of pyknotic cells in the cortex overall, or in layer V during the period of normal cell death in the cortex. Neither in adulthood, nor at any point in development did the density of layer V cells or cortical cell density overall differ from normal in Nissl material. Soma size of cells in layer V overall did not differ from normal in Nissl material. In addition, the soma size of the subpopulation of cells labelled with horseradish peroxidase (HRP) from midbrain injections was unaltered. In summary, this cell population appears unresponsive in both number and morphology to deletions of a major component of its target pool. This observation has some interesting implications for reasons of constancy of cell number in layer V across cytoarchitectonic areas.

Aging↗
PubMed1988

Immunohistochemical analysis of the development of somatostatin in the reeler neocortex.

The development of somatostatin (SS) neurons and fibers has been examined in the dorsolateral cortex of the mouse mutant reeler. Immunohistochemistry was performed using antisera directed primarily against SS28 or SS28(1-12). In the normal mouse at postnatal day 5 (P5), somatostatin (SS) neurons are concentrated in the ventral half of the cortex, in the developing layers V and VI. In the reeler mutant, SS neurons are scattered throughout the radial extent of the cortex, being concentrated in the dorsal half of the cortex in the polymorphic and large pyramidal cell layers. By P20, when the adult pattern of SS neuron distribution is evident in the normal mouse cortex, the distribution of similar neurons in the reeler appears inverted: immunoreactive neurons are concentrated in the dorsal half of the cortex. Immunoreactive fiber distribution follows a developmental pattern similar to that observed for SS neurons. At P5, SS fibers are most dense in layer I and V-VI of the normal cortex, while in the reeler, fibers are predominant in the polymorphic and large pyramidal cell layers. By P10, many fewer immunoreactive fibers can be detected in either normal or reeler mice than at P5. Nevertheless, while SS fibers in the normal cortex are most dense in layers I and V-VI, the reeler cortex exhibits little laminar heterogeneity in the distribution of these fibers. Thus, the SS fiber distribution appears less organized in the reeler cortex. These results suggest that whatever the nature of the genetic alteration resulting in cortical cellular developmental malposition in the reeler, SS cells and fibers, representing a completely intrinsic neocortical cellular system, behave as do all other cortical elements.

Aging↗
PubMed1990

Ontogeny of substance P-immunoreactive structures in the primate cerebral neocortex.

The distribution and the ontogeny of substance P (SP)-immunoreactive structures were investigated in the various cortical areas of macaque monkey cerebrum at embryonic day 120 (E120), embryonic day 140 (E140), newborn (Nb), postnatal day 30, postnatal day 60 (P60) and adult stages, using an immunohistochemical method. SP-immunoreactive cell bodies and fibers were detectable at E120 and the cell number increased until Nb stage. At E140, many immunoreactive cells were present in the upper part of layer V. Some of them seemed to be developing pyramidal cells which ascended their fibers toward layer I. After Nb stage, the number of immunoreactive structures decreased. By P60, the distribution patterns of SP-immunoreactive structures reached the adult level. Between Nb and P60, we occasionally observed structures which were presumably degenerated neurons and fibers. The distribution and developmental ontogeny of immunoreactivities were different among the various cortical areas. In areas OC and FA (von Bonin and Bailey), we observed the high densities of immunoreactive fibers and terminals, in spite of low numbers of cell somatas. While, in the association areas (areas FD, PE, TA and TE), there existed larger numbers of immunoreactive cells at E140 and newborn stages, following the decrease of cell number until P60. Our present study shows the transient increase and the following decrease of the numbers of SP-immunoreactive cells. Since we observed SP-immunoreactive pyramidal cells and degenerating cells during development, the decrease of immunoreactivities may be due to both cell death and change in phenotype.

Animals↗
PubMed1993

Strychnine-sensitive glycine receptors in cultured primary neurons from rat neocortex.

After 1 day in vitro (DIV) glycine (1 mM) evoked chloride-dependent membrane currents in about 50% of primary cultured rat neocortical neurons and more than 98% of the cells were glycine-sensitive after 2 DIV lasting for at least up to 12 DIV which was similar to GABA chemosensitivity. Strychnine (IC50 40 nM) and picrotoxin (30 microM) but not bicuculline (50 microM) blocked the glycine-evoked currents. The results provide evidence for a very early expression of glycine receptors on cortical neurons leading to a powerful chloride channel-operating capacity during early development.

Animals↗
PubMed1994

Developmental expression of a 56 kDa protein isolated from rat neocortex.

The expression of ALZ-50 immunoreactivity in the immature rat cortex was assessed using a variety of immunochemical techniques. The antigen recognized by ALZ-50 was isolated using immunoaffinity column chromatography. Unlike the ALZ-50-positive antigen found in the brains of people with Alzheimer's Disease (mol. wt. 68 kDa), the principal antigen expressed in the immature rat had a molecular weight of 56 kDa. The temporal expression of ALZ-50-positive antigens was determined with immunoblotting techniques. The expression of the 56 kDa protein appeared during the last prenatal week, increased to a peak during the second postnatal week and waned in the third postnatal week. Immunohistochemically, neonatal cortex contained many ALZ-50-positive neurons in the cortical subplate and the intermediate zone and a smattering of neurons in the cortical plate. The temporal expression of the ALZ-50-positive 56 kDa antigen was similar to that for fetal tau (tau-1); however, the principal protein identified by the anti-tau-1 antibody was considerably larger (being about 68-70 kDa). In contrast to ALZ-50, tau-1-immunoreactive elements were distributed in the subplate, the deep cortical plate, the intermediate zone and the subventricular zone. tau-1-positive axons passing through the superficial intermediate zone were conspicuous. Thus, the biochemical and anatomical evidence show that ALZ-50 and tau-1 recognize distinct proteins.

Animals↗
PubMed1987

Cross-modal recognition of familiar and unfamiliar objects by the monkey: the effects of ablation of polysensory neocortex or of the amygdaloid complex.

Nine rhesus monkeys were trained to a standard level of cross-modal recognition (CMR) in the directions vision to touch and touch to vision. Their level of performance remained essentially unchanged with unfamiliar objects. Five then received bilateral removals of frontal, temporal and parietal polysensory cortex in one stage or successively, and 4 underwent removal of the amygdaloid complex in one stage. All animals were retrained to criterion with familiar objects and then again tested with unfamiliar objects. Postoperatively, the monkeys with extensive neocortical removals were unimpaired or slightly impaired with familiar objects, and slightly impaired (in only one direction) with unfamiliar objects. The animals with amygdaloid ablations showed a different pattern of change: with familiar objects they were unimpaired (if removals were less extensive), or were severely but transiently impaired (if the removals of the amygdala were more extensive and/or other structures were involved); with unfamiliar objects they were unimpaired, tending to improve. The neocortical polysensory areas may be necessary for generating new visual representations during learning--a performance required only for the CMR of unfamiliar objects.

Afferent Pathways↗
PubMed1996

Suppression of synaptic transmission may allow combination of associative feedback and self-organizing feedforward connections in the neocortex.

Selective suppression of synaptic transmission during learning is proposed as a physiological mechanism for combining associative memory function at feedback synapses with self-organization of feedforward synapses in neocortical structures. A computational model demonstrates how selective suppression of feedback transmission allows this combination of synaptic function. During learning, sensory stimuli and the desired response are simultaneously presented as input to the network. Feedforward connections form self-organized representations of input, while suppressed feedback connections learn the transpose of the feedforward connectivity. During recall, suppression of transmission is removed, input activates the self-organized representation, and activity settles into a learned solution to the problem. This computational model can be used for learning of problems which are not linearly separable, including the negative patterning task (the XOR problem). Experiments in brain slice preparations of the rat somatosensory cortex tested whether the combination of self-organization and associative memory function could be provided by cholinergic suppression selective for feedback versus feedforward synapses. The cholinergic agonist carbachol selectively suppressed synaptic potentials elicited by stimulation of layer I (which contains a high percentage of feedback synapses), while having no effect on synaptic potentials elicited by stimulation of layer IV (with a high percentage of afferent and feedforward synapses).

Animals↗
PubMed1989

Developmental aspects of the neocortex of the bat.

Golgi studies on the cerebral cortex (central region) of newborn and adult bats (Myotis myotis) have shown that (a) extraverted cells in layer II-III are the source of a rich horizontal plexus originating from large numbers of long, proximal axonic collaterals, and (b) significantly greater numbers of basilar and apical dendrites (Student's t-test, P less than 0.001) of extraverted pyramidal cells are found in the newborn than in the adult bat, indicating an overproduction of dendrites during the early stages of development.

Animals↗
PubMed1991

In situ hybridization reveals VIP precursor mRNA-containing neurons in monkey and rat neocortex.

The cDNAs encoding monkey vasoactive intestinal polypeptide (VIP) and PHM-27 and rat VIP and PHI-27 were cloned and used to generate antisense RNA probes. Using in situ hybridization, neurons expressing the VIP/PHM or VIP/PHI precursor mRNAs were localized in monkey and rat somatic sensory and visual cortex. In both neocortical areas of both species, labeled cells were observed in all 6 layers as well as the subcortical white matter.

Amino Acid Sequence↗
PubMed1992

Transient ischemia stimulates glial fibrillary acid protein and vimentin gene expression in the gerbil neocortex, striatum and hippocampus.

Astrocytic activation plays a major role in homeostatic maintenance of the central nervous system in response to neuronal damage. To assess the reactivity of astrocytes in transient cerebral ischemia of the gerbil, we studied the levels of glial fibrillary acidic protein (GFAP) and its mRNA. GFAP mRNA increased by 4 h after carotid artery occlusion, reached peak levels by 72 h with a 12-fold increase over control and then started declining as early as 96 h postischemia. An examination of the specific regions of the brain revealed an increase in GFAP mRNA associated with the forebrain, midbrain, hippocampus and striatum. GFAP mRNA in the non-ischemic cerebellum however, remained expressed at constitutively low levels. Immunoblot analysis with anti-GFAP antibodies demonstrated a 2- to 3-fold increase in the protein after 24 and 48 h of reperfusion. Pretreatment with pentobarbital and 1-(5'-oxohexyl)-3-methyl-7-propyl xanthine (HWA 285), the drugs that have been shown to protect against ischemic damage, prevented the increase in GFAP mRNA in the cortex following ischemic injury. Forebrain ischemia also induced vimentin mRNA and protein quantities by 12 h of reperfusion in the cortex. The levels of c-fos and preproenkephalin mRNA increased rapidly within 1 h after ischemic injury, demonstrating a temporal difference in mRNA changes following ischemia. These results indicate that an increase in GFAP and vimentin, the two glial intermediate filament proteins in the area of the ischemic lesion may be associated with a glial response to injury.

Animals↗
PubMed1994

Protein-DNA interactions in the promoter region of the amyloid precursor protein (APP) gene in human neocortex.

We have investigated protein-DNA interactions in the proximal promoter of the human amyloid precursor protein (APP) gene in temporal lobe neocortical nuclei isolated from control and Alzheimer disease (AD) affected brains. We report that the human APP 5' promoter sequence from -203 to +55 bp, which has been previously reported to contain essential regulatory elements for APP gene transcription, lies in a deoxyribonuclease I, micrococcal nuclease- and restriction endonuclease-sensitive, G+C-rich nucleosome-free gap flanked both 5' and 3' by typical nucleosome structures. As analyzed by electrophoretic mobility shift assay, this extended internucleosomal linker DNA is heavily occupied by nuclear protein factors, and interacts differentially with nuclear protein extracts obtained from HeLa and human brain neocortical nuclei. This suggests that the chromatin conformation of the APP gene promoter may vary in different cell types, and may correlate with differences in APP gene expression. Human recombinant transcription factors AP1, SP1 and TFIID (but not AP2 or brain histones H1, H2B and H4) interact with the -203 to +55 bp of the human APP promoter sequence. Only minor differences were observed in the chromatin structure of the immediate APP promoter between non-AD and AD affected neocortical nuclei, suggesting either that post-transcriptional processes, or that regulatory elements lying elsewhere in the APP gene may be important in the aberrant accumulation of the APP gene product.

Aged↗