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PubMed2000

[Features of the development of homo- and heterotopic allotransplants of rat embryonal neocortex].

Mechanisms of regulation of cell division in the developing neocortex are largely unknown. The aim of the present study was to investigate the influence of a microenvironment on the fetal neocortex histogenesis. The fetal neocortex from 15-day old Wistar rat embryo was grafted into the neocortex, crushed sciatic nerve and anterior chamber of eye of adult rats. A comparative study of graft development was carried out on 1, 3, 7, 10, 30 days using histological (Nissl stain, hematoxylin-eosin) and immunohistochemical (monoclonal antibody to proliferating cell nuclear antigen, and to glial fibrillary acidic protein) methods. Grafted neuroepithelial cells proliferated in grafts that developed in the neocortex and the anterior chamber of eye for 7 days, and in the sciatic nerve for 10 days. In all grafts differentiating neuroblasts, young neurons and mature neurons were observed 7, 10 and 30 days later, respectively. In 10 days, transplants in the nerve have a glial capsule, in contrast to other sites of grafting. The capsule consists of ependymocytes with microvilli and cilia 30 days later. These cells are GFAP-positive. Our results indicate epigenetic influence on the development of neuroepithelial precursors. The microenvironment of the peripheral nerve is suggested to promote glyogenesis in developing grafts. Afferent inputs do not influence the proliferative potency of brain cell precursors.

Animals↗
PubMed1999

Parametric PET imaging of 5HT2A receptor distribution with 18F-setoperone in the normal human neocortex.

UNLABELLED: Because of 5HT2A receptor's (5HT2AR) putative role in several neuropsychiatric diseases, studying it in vivo is an important goal. 18F-setoperone is a well-validated and widely used PET radioligand for the study of neocortical 5HT2AR. We have previously developed and validated in baboons a method to generate parametric maps of the binding potential (i.e., the k3-to-k4 ratio) on a pixel-by-pixel basis, based on a single-dose tracer amount dynamic 18F-setoperone PET paradigm, and with the receptor-poor cerebellum as reference structure. However, previous semiquantitative PET human studies suggested that nonspecific (NS) binding in the neocortex might not be identical to that in the cerebellum. METHODS: As a first step in the development of k3:k4 parametric mapping in humans, we therefore estimated directly the NS binding of 18F-setoperone in the neocortex of four young healthy volunteers who were studied with PET both before and after 2 wk of daily therapeutic oral doses of sertindole, an atypical neuroleptic possessing strong 5HT2AR antagonistic activity. RESULTS: Visual analysis of the dynamic PET data obtained over 120 min confirmed that virtually full receptor saturation had indeed been achieved; however, the late neocortical time-activity curves (TACs) progressively fell to lower uptake values than corresponding cerebellar TACs and could not be fitted according to a four-compartment (four-Cpt) nonlinear model, indicating lack of specific binding. The cerebellum TACs for both the control and the challenge conditions, as well as the challenge neocortical TACs, were fitted according to three-Cpt modeling, providing the k/k6 ratio and in turn the f2 fraction for both structures. Despite the small sample of only four subjects, the f2 fraction for the neocortex was significantly larger (i.e., NS binding was smaller) than that estimated for the cerebellum. This allowed us to determine the k3-to-k4 ratio for the control neocortex using the challenge neocortex as reference structure, that is, without using the cerebellum at all. This "assumption-free" approach was also successfully used to generate k3:k4 maps for these four subjects, which showed highest values for the temporal cortex. CONCLUSION: This study shows that, for every new PET or SPECT radioligand and when estimation of specific binding is based on a reference structure, it is important to determine the uniformity of nonspecific binding before proceeding with human investigations.

Adult↗
PubMed1992

Ontogenesis of the pyramidal cell of the mammalian neocortex and developmental cytoarchitectonics: a unifying theory.

The prenatal development of the mammalian neocortex has been analyzed, with the rapid Golgi method, in a variety of experimental animals (hamster, mouse, rat, and cat) and in humans. A new developmental conception of the structural organization of the mammalian neocortex is discussed. Neocortical development begins with the establishment of the primordial plexiform layer (PPL) which precedes and is a prerequisite for the subsequent formation of the cortical plate (CP). The formation of the CP occurs, in its entirety, within the PPL. During its development, three fundamental neuronal events occur: migration, early differentiation, and late maturation. All migrating neurons, travelling on radial glial fibers, reach layer I, develop an apical dendrite, and establish contacts with its elements. These newly differentiated neurons assume similar morphology resembling embryonic pyramidal cells. As such, an early differentiation stage common to all neurons of the CP is established. During the late maturation stage, all CP neurons acquire their specific phenotypic structural and functional features. Only pyramidal neurons retain and expand their original connections with layer I while other neuronal types lose these connections. The pyramidal cell is redefined in developmental terms: the neocortex's pyramidal cell is both structurally and functionally locked into position between layer I and the cortical depth of its soma. During mammalian evolution pyramidal cells are forced to structurally and functionally elongate their apical dendrite outwardly to accommodate an increasing amount of information without losing either their original anchorage to layer I or their cortical depth. This unique property of pyramidal neurons is considered to be a mammalian innovation. Based on these observations, a unifying developmental cytoarchitectonic theory applicable to all mammals is proposed. The theory considers the CP to be a mammalian innovation and to represent a single, stratified, and expanding telencephalic nucleus. The theory envisions the mammalian neocortex as an open biological system capable of progressive expansion by the recruitment and transformation of primitive neurons from upper layer II into pyramidal cells. Hence, the number of pyramidal cell strata increases over the course of mammalian phylogeny. The developmental roles of layer I in the migration of neurons, formation of the CP, unique morphology of pyramidal cells, and overall structural organization of the mammalian neocortex are emphasized.

Animals↗
PubMed1994

The neocortex. An overview of its evolutionary development, structural organization and synaptology.

By way of introduction, an outline is presented of the origin and evolutionary development of the neocortex. A cortical formation is lacking in amphibians, but a simple three-layered cortex is present throughout the pallium of reptiles. In mammals, two three-layered cortical structures, i.e. the prepiriform cortex and the hippocampus, are separated from each other by a six-layered neocortex. Still small in marsupials and insectivores, this "new" structure attains amazing dimensions in anthropoids and cetaceans. Neocortical neurons can be allocated to one of two basic categories: pyramidal and nonpyramidal cells. The pyramidal neurons form the principal elements in neocortical circuitry, accounting for at least 70% of the total neocortical population. The evolutionary development of the pyramidal neurons can be traced from simple, "extraverted" neurons in the amphibian pallium, via pyramid-like neurons in the reptilian cortex to the fully developed neocortical elements designated by Cajal as "psychic cells". Typical mammalian pyramidal neurons have the following eight features in common: (1) spiny dendrites, (2) a stout radially oriented apical dendrite, forming (3) a terminal bouquet in the most superficial cortical layer, (4) a set of basal dendrites, (5) an axon descending to the subcortical white matter, (6) a number of intracortical axon collaterals, (7) terminals establishing synaptic contacts of the round vesicle/asymmetric variety, and (8) the use of the excitatory aminoacids glutamate and/or aspartate as their neurotransmitter. The pyramidal neurons constitute the sole output and the largest input system of the neocortex. They form the principal targets of the axon collaterals of other pyramidal neurons, as well as of the endings of the main axons of cortico-cortical neurons. Indeed, the pyramidal neurons constitute together a continuous network extending over the entire neocortex, justifying the generalization: the neocortex communicates first and foremost within itself. The typical pyramidal neurons represent the end stage of a progressive evolutionary process. During further development many of these elements have become transformed by reduction into various kinds of atypical or aberrant pyramidal neurons. Interestingly, none of the six morphological characteristics, mentioned above under 1-6, has appeared to be unassailable; pyramidal neurons lacking spines, apical dendrites, long axons and intracortical axon collaterals etc. have all been described. From an evolutionary point of view the typical pyramidal neurons represent not only the principal neocortical elements, but also the source of various excitatory local circuit neurons. The spiny stellate cells, which are abundant in highly specialized primary sensory areas, form a remarkable case in point.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1994

Disruption of neuronal migration in the neocortex of the dreher mutant mouse.

To analyze developmental abnormalities related to neuronal migration in the dreher mutant mouse, the neocortical cytoarchitecture of dreher and control mice were examined in Nissl-stained serial sections by light microscopy. In general, the dreher neocortex has six layers which are similar in size and thickness to those observed in normal mouse neocortex. However, in dreher neocortex, three types of abnormalities were found: (1) an increase in the number of diffusely distributed neurons in layer I, (2) small, ectopic collections of neurons in layer I, and (3) isolated disturbances of local cytoarchitecture characterized by neuron-free space distributed in areas between layer II to IV. The occurrence of small, punctate deficits in the dreher neocortex may be secondary to disruptions of the radial glial fiber system and neuronal migration. The fact that cytoarchitectonic abnormalities of several types were found in the dreher neocortex may be useful in analyzing the relationship between radial glial fibers and migrating young neurons, the synaptic connections which are formed by ectopically situated neurons, and the mechanism of formation of sporadically distributed neocortical abnormalities.

Animals↗
PubMed1995

Morphological changes in the thalamus and neocortex of the cat brain after a restricted unilateral fetal neocortical lesion.

In order to study the response of the brain to injury during early development, the neocortex of ten fetal kittens was lesioned at age E43-48, in either the frontal (n = 8) or parieto-occipital (n = 2) areas. The thalamus and neocortex of the lesioned animals were analyzed using quantitative morphometry and compared to intact control cats (n = 10). Ipsilaterally, the volumes of the remaining neocortex and of the thalamus were 26.5% and 25.7% smaller, respectively (P < 0.05). Contralaterally, the neocortex did not change in volume, whereas the thalamus tended to be smaller by a mean of 11.1%. Ipsilaterally, in all four thalamic nuclei studied, the neuronal and glial cell packing densities (NCPD and GCPD) and the cross sectional area of neuronal somata did not differ between lesioned and intact animals except for the principal ventromedial nucleus, where the GCPD was significantly lower (P < 0.05) in lesioned animals. Contralaterally, the NCPD and GCPD did not show any differences between groups, except for the principal ventromedial nucleus, in which the GCPD was lower in lesioned cats (P < 0.05). Furthermore, in the contralateral basal ventromedial nucleus, the cross sectional area of the neuronal somata was smaller in lesioned than in intact animals (P < 0.01). These results indicate loss of neurons and glia in the ipsilateral thalamus and probably in the neocortex. Since, at the time of the cortical resection, transient reciprocal thalamosubplate connections have been established in the cat, the lesion-induced deprivation of subplate target neurons and cortical inputs probably precluded the survival of a substantial number of developing thalamic neurons. In the cortex the hypothetical loss of neurons may, at least partly, be attributed to lesion-induced elimination of target neurons before establishment of corticocortical connections.

Animals↗
PubMed1997

Parvalbumin- and calbindin-containing neurons express c-fos protein in primary and secondary (mirror) epileptic foci of the rat neocortex.

The present experiments aimed at the description and further immunocytochemical characterization of activated neocortical neurons expressing the c-fos gene. Focal seizures were induced by the topical application of isotonic, isohydric 4-aminopyridine solution to the frontal neocortex of adult anesthetized Wistar rats. The EEG of both hemispheres was recorded from the surface of the skull. The animals were perfused with fixative, coronal plane vibratome sections were cut and stained with cocktails containing polyclonal c-fos and monoclonal calbindin or parvalbumin antibodies. The polyclonal c-fos antibody was tested with Western blotting and the diffusion of 4-aminopyridine investigated with autoradiography of [3H]4-aminopyridine. The c-fos protein was detected in every layer of the neocortex (primary focus) and in some allocortical areas of the treated hemisphere. Scattered immunostained nuclei were observed in layers II, III, IV and VI of the contralateral neocortex (mirror focus). Several parvalbumin- and calbindin-positive neurons contained the c-fos protein in both foci. The medium-sized non-pyramidal parvalbumin neurons were found in layers II-IV and VI of the neocortex and in stratum multiforme of the prepiriform cortex. The c-fos protein was colocalized with calbindin mainly in layers II and III in small and medium-sized non-pyramidal neurons. The results prove that focal epileptiform activity of the neocortex activates diverse inhibitory neuronal populations. As concluded, the inhibitory control is probably more effective in the contralateral hemisphere (mirror focus) than on the side of 4-APY treatment (primary focus).

Animals↗
PubMed1999

Cell migration from the ganglionic eminence to the neocortex investigated by labeling nuclei with UV irradiation via a fiber-optic cable.

Recent studies have shown that the ganglionic eminence is one of the sources of tangentially migrating cells in the developing neocortex. Since the migration of the DiI-labeled cells from the ganglionic eminence to the neocortex was not monitored by videomicroscopy in these reports, we devised a novel method to study cell migration in vitro and in vivo. The new method involves ultraviolet (UV) irradiation of the cells through a fiber-optic cable and subsequent identification of the irradiated cells on the basis of the formation of thymine dimers in the nuclei. First, we tested the new method (UV-thymine dimer-labeling method) by applying it to monitor the cell migration of neuronal precursor cells in the rostral migratory stream in the neonatal rat telencephalon. In vitro, UV irradiation for 1 s through the fiber-optic cable resulted in the formation of sufficient thymine dimers as to allow immunohistochemical detection after 6 h of incubation; a significant proportion of the irradiated cells continued to migrate in the same direction and at the same speed as those before irradiation. There was no significant difference in the cell migration distance over 6 h between cells exposed and not exposed to the UV irradiation in vitro. In vivo, this method revealed that three times as many cells in the subventricular zone of the olfactory bulb migrated rostrally as caudally. The new method also allowed us to measure the speed of cell migration, which was estimated to be about 70 microm/h at the maximum in the rostral direction. After these examinations of reliability of the method, we applied it to the rat embryo brain. One day after UV irradiation of the ganglionic eminence, labeled migrating cells were found in the striatum, in the internal capsule, and in the intermediate zone of the neocortex. The observation period of cell migration to the neocortex was extended by the use of a xeroderma pigmentosum group A gene mutant mouse, which lacked an ability to remove thymine dimer from the UV-irradiated nuclei. Two days after the UV irradiation, labeled migrating cells from the ganglionic eminence of the mutant mouse embryos were found both in the cortical plate and in the intermediate zone of the neocortex.

Animals↗
PubMed1997

Effects of combined ventral forebrain grafts to neocortex and amygdala on behavior of rats with damage to the nucleus basalis magnocellularis.

In rats with damage to the nucleus basalis magnocellularis, transplantation of the embryonic ventral forebrain to the neocortex improves behavioral performance in some behavioral tasks. The present investigation focuses on improvement of behavioral performance by combined graft placement to both neocortex and amygdala. Male rats received unilateral microinjections of quisqualate to the nucleus basalis magnocellularis to produce cell damage. Embryonic ventral forebrain cell suspensions were placed in one group of rats in the frontal and parietal neocortex, in a second group in the amygdala, and in a third group in the frontal and parietal neocortex and in the amygdala. These groups were compared to a group of nonoperated rats and a group of rats with damage but with no grafts. Quisqualate-induced damage to the nucleus basalis magnocellularis reduced cholinergic innervation in the ipsilateral cortical hemisphere, impaired performance in the one-trial training version of passive avoidance, an increased motility and time spent in the open arms of the elevated plus maze. Combined graft placement to neocortex and amygdala normalized performance of passive avoidance and restored the normal time spent in the open arms of an elevated plus maze. These results suggest that after damage to the nucleus basalis magnocellularis, modulation of function in multiple brain regions may be necessary for optimization of adaptive behavior in situations involving induction of fear.

Amygdala↗
PubMed1998

Gyri of the human neocortex: an MRI-based analysis of volume and variance.

This magnetic resonance imaging (MRI)-based morphometric analysis of cortical topography in the human brain is based upon the segmentation and parcellation of volumetric T1-weighted MRI data for a set of 20 young adult brains including 10 males and 10 females. For the most part, each parcellation unit (PU) of the neocortex corresponds to a single or a portion of a single gyrus. The volumes of each PU were computed for each brain. Subsets of PUs were also grouped so as to represent the neocortex for the frontal, temporal, parietal and occipital lobes. The coefficient of variation of the mean volume of total neocortex and that of the neocortex assigned to individual lobes cluster around 10%, whereas that of neocortex assigned to the individual gyri (PU) is more than twice that value. Approximately 80% of the total variance in gyral volume arises from determinants interactive for individual and specific gyri, while only approximately 10% of the total variance appears to be a reflection of uniform scaling to total neocortical volume. Sexual dimorphism contributes a pervasive though relatively small component of this variance. These results have implications for the study of structure-function correlation, and the proper statistical methods of handling volumetric data in morphometric studies. In addition, the nature of the covariance structure of the data will lead to future hypotheses regarding the relationships between the various potential genetic and epigenetic gyral influencing factors.

Adult↗
PubMed1989

Timing of expression of tau and its encoding mRNAs in the developing cerebral neocortex and cerebellum of the mouse.

The expression of tau mRNA and of the corresponding encoded protein variants was studied during postnatal development in two brain regions differing in their timing of differentiation: the cerebral neocortex and the cerebellum. (a) The expression of tau mRNA was different in the two regions. Maximal contents were found at early stages in the cerebral neocortex, with a 10-fold decrease at later stages. In the cerebellum, two peaks of tau mRNA were observed soon after birth and in adulthood, with minimal values at postnatal day 6. (b) The expression of total tau proteins was similar to that of their encoding mRNAs in the cerebral neocortex, i.e., high concentrations after birth and low contents at later stages. In contrast, two peaks of tau proteins were observed in the cerebellum: the first perinatally and the second with a maximum at postnatal day 15. (c) Both in the cerebral neocortex and especially in the cerebellum, increasing concentrations of mature tau variants were expressed at late developmental stages, i.e., when total tau protein contents were decreased. In conclusion, the fluctuations in expression of tau and of its encoding mRNA seen in the cerebellum seem to reflect differences in the timing of differentiation of the various cell types, i.e., the macroneurons and the interneurons, present in this brain region. The adult tau variants appear in both the neocortex and the cerebellum only at late developmental stages, i.e., when most of the circuitry has been established, although these two regions markedly differ in their timing of differentiation.

Animals↗
PubMed1991

Homology and evolutionary origins of the 'neocortex'.

The telencephalon of mammals is characterized by the presence of a hexalaminated structure on its external surface, with specific auditory, visual, somatosensory and motor regions. Due to its seeming unique presence in mammals, it is frequently designated as the neocortex. The evolutionary origins of the so-called neocortex have long puzzled comparative neuroanatomists, in view of the seeming absence of a neocortical-like anlage in nonmammalian amniotes. The resolution of this puzzle requires analysis of both adult and embryonic brains. Experimental neuroanatomical, physiological and behavioral methods applied to adult avian and reptilian brains have finally clarified several fundamental questions regarding the origins of 'neocortex' and have indicated that these origins can be viewed as consequent to two separate events: (1) The elaboration of constituent neuronal populations and their associated connections that are common to the telencephalae of both nonmammalian and mammalian amniotes. In mammals these populations are found within the so-called neocortex. In birds and reptiles, most of these neurons are found within the dorsal and dorsolateral ventricular ridges (DVR and DLVR). (2) In mammals, the components of the DVR and DLVR are incorporated into the thin overlying pallium to form a laminated 'neocortex'. Analysis of development in domestic chicks suggests that the DVR is one of several prosencephalic neuromeres ('Prosomeres') that contribute to the ontogeny of comparable structures in birds. Perhaps in mammals, as well, cortical development is consequent to incorporation of these several prosomeres into proliferative ependyma of the pallial mantle.

Animals↗
PubMed1987

Regional heterogeneity in the distribution of somatostatin-28- and somatostatin-28(1-12)-immunoreactive profiles in monkey neocortex.

The distribution of the prosomatostatin-derived peptides (PSDP), somatostatin-28 and somatostatin-28(1-12), in the cynomolgus monkey (Macaca fascicularis) neocortex was characterized in quantitative immunohistochemical studies of 3 visual areas (V1, primary visual cortex; V2, the adjacent visual association area; and AIT, a visual association area in anterior inferior temporal cortex), 2 auditory areas (AI, primary auditory cortex; and T1, an adjacent auditory association area) and anterior cingulate cortex (Area 24). The results of similar quantitative analyses in 3 homologous areas in rat neocortex (primary visual, primary auditory, and anterior cingulate) are also presented. Primate cortical areas differed significantly in both density and laminar distribution of PSDP-immunoreactive profiles. Area 24, the most densely labeled area, had nearly 6 times as many PSDP-immunoreactive neurons as V1. Both auditory areas contained approximately two-thirds the number of PSDP-immunoreactive neurons found in Area 24; however, both had nearly 4 times as many immunoreactive neurons as V1. The 3 visual areas showed incremental increases in the number of PSDP-immunoreactive neurons; V2 contained nearly twice and AIT nearly 3 times the number of immunoreactive neurons present in V1. Both the supra- and infragranular layers were densely labeled in Area 24 and Area T1, however, in AI, V1, V2, and AIT the infragranular layers were relatively sparsely labeled. In contrast to the regional heterogeneity found in the primate neocortex, the distribution of immunoreactive neurons was quite uniform across the 3 rat cortical areas. The rat cortical areas contained substantially fewer immunoreactive neurons than most of the monkey cortical areas, and a majority of these immunoreactive neurons were located in the infragranular layers. These findings suggest that the regional specialization of primate neocortex involves the selective distribution of PSDP-immunoreactive neurons. They also suggest that chemically specified intrinsic organization of neocortex is not likely to be uniform across species or across cortical areas in the primate. The distinctive regional distribution patterns of PSDP-immunoreactive profiles appear to parallel that of the long corticocortical projections (contralateral and distant ipsilateral projections), suggesting an association between these presumed inhibitory interneurons and this important extrinsic system.

Animals↗
PubMed1980

The brain of the mammal-like reptile Probainognathus jenseni (Therapsida, Cynodontia). A correlative paleo-neoneurological approach to the neocortex at the reptile-mammal transition.

A natural endocranial cast of the South American cynodont Probainognathus jenseni is studied, and an evaluation of the probable nature of the neocortex at the level of certain cynodonts of the Middle Triassic is made, based in the available paleo-neoneurological information. The endocast of Probainognathus shows well developed olfactory bulbs, long cerebral hemispheres, small anterior colliculi and well represented cerebellum and flooculi. The pineal gland may have been located between the caudal hemispheric poles. No parietal foramen exists. The dorsal surface of the cerebral hemispheres shows a slope at the level of the anterior edge of the caudal fourth part, which is interpreted as the posterior limit of the neocortical plate. At the level of the olfactory peduncles, it is visible a stem vessel; one of its branches distributes on the anterior part of the lateral border of the hemisphere. It is advanced the interpretation that this latter vessel could indicate the paleo-neocortical boundary. The analysis of the neoneurological information led the author to suppose that the neocortex of Probainognathus, and surely of other cynodonts of the Middle Triassic, has shown supplementary somatic sensory and motor, visual and auditory representations, and perhaps incipient primary somati sensory and motor ones, advancing a "polymodal cortex", as it is supposed had stem mammals. Moreover, the histostructure of the neocortex at this state of the evolution may have been in a proisocortical-isocortical stage, that is, in the beginnings of the true neocortex. The confrontation of the paleoneurologic with the neoneurologic information led the author to suppose that Triconodon and Ptilodus have had a neocortex, surely more developed than Probainognathus, but that it is not seen in the endocasts at present studied. The quantitative analysis of Probainognathus' endocast, as well as those of other cynodonts, suggest that certain cynodonts of the Middle Triassic were in an advanced state toward endothermy.

Animals↗
PubMed1997

TGF-beta receptor type II and fetuin in the developing sheep neocortex.

Fetuin shows a characteristic pattern of distribution in the developing neocortex in many mammalian species. Its expression is confined to early-appearing cortical-plate and later subplate neurons. A short 19 amino-acid sequence of fetuin shows a degree of homology to an 18 amino-acid sequence of the TGF-beta type II receptor (TbetaR-II) and in vitro fetuin binds to members of the TGF-beta family of cytokines. It has been suggested that fetuin is the biologically significant antagonist of these cytokines. We have compared, using immunocytochemistry, the distribution pattern of TbetaR-II and fetuin in the developing neocortex of foetal sheep. TbetaR-II immunoreactivity first appears at around 40 days of gestation in the fetal sheep (E40, term in sheep is 150 days from conception), localised in two discreet bands: one just outside the cortical plate in the inner part of the marginal zone and one deep in the cortical plate in what becomes the transient subplate zone. By E70-E80, TbetaR-II is prominent in a population of subplate cells, whereas, by E120 only small patches of TbetaR-II-positive cells are visible, principally in pyramidal cells in layer VI. The developmental sequence of the staining pattern for TbetaR-II in the neocortex is complementary to that for fetuin, rather than overlapping with it. Double-labelling of fetuin and TbetaR-II shows some cellular co-localisation, especially at E60, but most fetuin-positive cells are not immunoreactive for TbetaR-II. Thus, fetuin's proposed role as an antagonist of TGF-beta cytokines and mimic of TbetaR-II is not consistent with the observed distribution of these two molecules in the developing neocortex of the foetal sheep.

Animals↗
PubMed2001

Biogenic amines in the human neocortex in patients with neocortical and mesial temporal lobe epilepsy: identification with in situ microvoltammetry.

Biogenic amines in well defined subtypes of human temporal lobe epilepsy (TLE) have not been well characterized. Specimens from five patients with neocortical TLE (NTLE) and nine with mesial TLE (MTLE) were immediately placed in Ringer's lactate; stearate indicator microelectrodes were placed in temporal gray matter, Ag/AgCl reference microelectrodes and auxiliary microelectrodes were placed 3-7 mm contralaterally to the indicator microelectrode. Dopamine (DA), ascorbic acid (AA), norepinephrine (NE) and serotonin (5-HT) were identified by their characteristic oxidative potentials in vitro. Four of five patients with NTLE had NE depletion in temporal neocortex while eight of nine patients with MTLE had high concentrations of NE (chi-square P<0.01). Significant concentrations of DA were present in the temporal lobes of three of five NTLE patients but in only one of the nine MTLE patients (chi-square P<0.05). 5-HT was present in the neocortex of both NTLE and MTLE patients in similar concentrations. AA was found in the neocortex of one NTLE patient. These data support an association between NE depletion and NTLE. The relative NE deficiency along with the consistent presence of DA in NTLE patients suggest an impairment in the catecholamine pathway. The presence of AA, a co-factor in NE synthesis, in the neocortex of one NTLE patient may also be related since AA is a cofactor in NE synthesis.

Biogenic Amines↗
PubMed1999

Differential expression of c-fos mRNA in the rat neocortex by in situ hybridization.

The c-fos mRNA expression pattern in rat neocortex, was determined in the rat kept in a 12:12 light/dark cycle, in constant dark, or in constant light by in situ hybridization. At the beginning of the light period, c-fos mRNA was induced both in the neocortex and suprachiasmatic nucleus (SCN). Transiently increased c-fos mRNA expression was detected from 0830 to 0900 and soon declined to basal levels. Immediately prior to the beginning of the dark period, c-fos mRNA expression also increased and remained elevated in the neocortex following the dark period. In the constant dark group, c-fos mRNA expression showed no transient elevation at the beginning of the light period. On the other hand, c-fos mRNA expression in the constant light group increased during their subjective dark period as well as normal light/dark cycle. These results demonstrate a circadian pattern of c-fos mRNA expression in the neocortex which is similar to that observed previously in the inner and outer nuclear layers of the retina.

Animals↗
PubMed1999

Ultra-miniature headstage with 6-channel drive and vacuum-assisted micro-wire implantation for chronic recording from the neocortex.

We describe a head-stage, with precision microtranslators for the chronic placement of micro-wire electrodes in the neocortex, that minimizes compressive damage to the brain. The head-stage has a diameter of 5.8 mm and allows six electrodes, separated by 450 microm on a hexagonal grid, to be individually and continuously positioned throughout a depth of approximately 3 mm. Suction is used to transiently support the dura against a curved array of tubes that guide and stabilize the electrodes as a means to prevent compression of the neocortex as the electrodes breach the dura. With this headstage we recorded extracellular signals in a rat immediately after surgery. Single-unit waveforms at a given electrode position were stable for at least several hours in the freely behaving animal and were obtained throughout the depth of the neocortex for at least 2 months. Electrophysiological records and histological examination showed that the upper layers of the neocortex were intact and minimally damaged after the implantation.

Animals↗