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PubMed1991

Planar differences in nuclear area and orientation in the subventricular and intermediate zones of the rat embryonic neocortex.

Nuclear area and orientation in the subventricular and intermediate zones was studied quantitatively in coronal vs. sagittal sections of the dorsomedial neocortex. Nissl-stained methacrylate-embedded normal rat embryos were studied between embryonic days (E) 13 and E22. The area of nuclear profiles and the degrees their long axes (defined as a straight line through the two most distant points in the nuclear profile) deviated from the horizontal (defined as parallel to the pial membrane) were determined with a computer-graphics program. Because the nucleus is the most clearly outlined structure in embryonic cells, the area and orientation of the nucleus was taken to reflect the overall size and orientation of the cell body. Nuclear area is larger in the coronal plane than it is in the sagittal plane, especially between E17 and E20. Cell body orientation in the subventricular and lower intermediate zones is predominantly horizontal in the coronal plane and predominantly vertical in the sagittal plane. In the upper intermediate zone, cell body orientation is predominantly vertical in both planes, but more so in the sagittal plane. These data indicate that the majority of cell bodies in the subventricular and lower intermediate zones have a horizontally oriented, flattened elliptical shape with their larger diameters lying within the coronal plane and their smaller diameters in the sagittal plane. Because of the flattening, the cell bodies falsely appear to be vertically oriented in the sagittal plane. Qualitative observations in horizontal sections confirmed the quantitative computer analysis. These results are related to other findings with [3H]thymidine autoradiography concerning cell migration and the sojourn of cells in the subventricular and intermediate zones.

Animals↗
PubMed1991

GABAergic interneurons containing calbindin D28K or somatostatin are major targets of GABAergic basal forebrain afferents in the rat neocortex.

The arborization pattern and postsynaptic targets of the GABAergic component of the basal forebrain projection to neo- and mesocortical areas have been studied by the combination of anterograde tracing and pre- and postembedding immunocytochemistry. Phaseolus vulgaris leucoagglutinin (PHAL) was iontophoretically delivered into the region of the diagonal band of Broca, with some spread of the tracer into the substantia innominata and ventral pallidum. A large number of anterogradely labelled varicose fibres were visualized in the cingulate and retrosplenial cortices, and a relatively sparse innervation was observed in frontal and occipital cortical areas. Most of the labelled axons were studded with large en passant varicosities (Type 1), whereas the others (Type 2) had smaller boutons often of the drumstick type. Type 1 axons were distributed in all layers of the mesocortex with slightly lower frequency in layers 1 and 4. In the neocortex, layer 4, and to a smaller extent upper layer 5 and layer 6 contained the largest number of labelled fibres, whereas only a few fibres were seen in the supragranular layers. Characteristic type 2 axons were very sparse but could be found in all layers. Most if not all boutons of PHAL-labelled type 1 axons were shown to be GABA-immunoreactive by immunogold staining for GABA. Altogether 73 boutons were serially sectioned and found to make symmetrical synaptic contacts mostly with dendritic shafts (66, 90% of total targets), cell bodies (6, 8.2% of total), and with one spine. All postsynaptic cell bodies, and the majority of the dendritic shafts (44, 60.3% of total targets) were immunoreactive for GABA. Thus at least 68.5% of the total targets were GABA-positive, but the majority of the dendrites not characterized immunocytochemically for technical reasons (15.1%) also showed the fine structural characteristics of nonpyramidal neurons. The target interneurons included some of the somatostatin- and calbindin-containing subpopulations, and a small number of parvalbumin-containing neurons, as shown by double immunostaining for PHAL and calcium-binding proteins or neuropeptides. We suggest that the innervation of inhibitory interneurons having extensive local axon arborizations may be a mechanism by which basal forebrain neurons-most notably those containing GABA--have a powerful global effect on the majority of principal cells in the entire cortical mantle.

Afferent Pathways↗
PubMed1991

Developmental expression of neural cell adhesion molecules in the mouse neocortex and olfactory bulb.

Polyclonal antibodies to N-CAM and L1 and monoclonal antibodies to epitopes of N-CAM (designated 12F11, 8A2, and 12F8) were used to investigate the spatial and temporal distribution of these neural cell adhesion molecules during the development of mouse cortex and olfactory bulb. The aim of the study was to correlate developmental events such as cell migration, dendritic and axonal outgrowth, and synaptogenesis with the appearance and disappearance of specific molecules involved in cell-cell interactions. Western transfer studies indicated that 12F8 antibody recognized polysialic acid found on embryonic N-CAM; 8A2 antibody primarily recognized the 140 kD component of N-CAM while the 12F11 antibody recognized the 180 and the 140 kD forms. The study demonstrates a high degree of cell surface molecular specialization of different compartments in developing neocortex and olfactory bulb. L1 is found on a variety of unmyelinated fiber tracts including thalamocortical fibers, olfactory nerve, and inner plexiform layer of the olfactory bulb. In contrast, N-CAM epitope recognized by 12F11 antibody is present on olfactory nerve fibers but appears later and is much weaker than L1 on thalamocortical fibers and is absent from the olfactory lobe inner plexiform layer. Dendritic regions are best labeled by 12F8 antibody; the epitope becomes faint in adult cortex but remains strongly expressed in olfactory bulb. This study reveals that widespread N-CAM expression in the central nervous system is constituted by a diversity of local expression of different molecular forms of N-CAM; their different anatomical distributions suggest they may each have unique roles.

Aging↗
PubMed1992

Development of GABA-immunoreactivity in the neocortex of the mouse.

The prenatal and postnatal development of GABAergic elements in the neocortex of the mouse was analyzed by GABA-immunocytochemistry. Radial distribution of cells and laminar numerical densities were calculated at each developmental stage to substantiate qualitative observations. The first immunoreactive neurons were observed in the cortical anlage at embryonic day 12-embryonic day 13 (E12-E13) in the primitive plexiform layer. At following prenatal stages (E14-E19), most GABA-positive neurons were present in the marginal zone, subplate, and subventricular zone. GABA-immunoreactivity in the cortical plate appeared early (E14), although the complete maturation of its derivatives was achieved postnatally. At prenatal stages we noted a well-developed system of immunopositive fibers in the subplate. As indicated by the direction of growth cones, most of these fibers had an extracortical origin and invaded the cortex laterally through the internal capsule and striatum. In rostral and middle telencephalic levels, fibers originating in the septal region contributed to the cingulate bundle. Presumably corticofugal fibers and callosal axons were also noticed. At postnatal stages the maturation of GABA-immunoreactivity appeared to be a complex, long-lasting process, in which the adult pattern was produced at the same time as the appearance of certain regressive phenomena. Thus, between postnatal day 0 and postnatal day 8 (P0-P8), GABA-positive populations disappeared from the subventricular zone, marginal zone and to a lesser extent from the subplate. At the same ages we noticed the presence of morphologically abnormal, GABA-immunoreactive neurons in the subventricular zone and subplate which are interpreted as correlates of neuronal degeneration. Most GABA-positive subplate fibers also disappeared whereas GABA-immunoreactive axons were seen in the cingulate bundle until the adult stage. In the derivatives of the cortical plate, the maturation of GABA-immunoreactive elements progressed according to the "inside-out" gradient of cortical development, with the important exception of layer IV, which was the last layer to exhibit an adult-like appearance. Within each layer deriving from the cortical plate (layers VIa to II-III), GABA-immunoreactivity showed a protracted maturation in which the first GABA-positive cells were detected a few days after cell birth but substantial numbers of neurons began to express GABA considerably later. The later phase occurred concurrently with the maturation of GABA-positive axonal plexuses. These results suggest that different GABA-positive populations show different developmental regulation of GABA expression during cortical ontogenesis.

Aging↗
PubMed1993

Developmental changes in layer I of the human neocortex during prenatal life: a DiI-tracing and AChE and NADPH-d histochemistry study.

The development of fetal layer I (marginal zone, MZ) was studied in the human neocortex by using DiI tracing and AChE and NADPH-d histochemistry, and examining the Nissl-stained material of the Yakovlev Collection. We describe the sequential maturation of the Cajal-Retzius (CR) cells and the granule cells of the subpial granular layer (SGL), and the close relationship between both. The first CR cells appear in the primordial plexiform layer, at 6 gestational weeks (GW). After the formation of the cortical plate, they settle under the pial surface. At 13 GW, the SGL begins to form around the CR cells. The horizontal members of a polymorphic population of CR cells begin to mature at 13 GW, and the intermediate and vertical forms differentiate at 16 and 18 GW, respectively. All CR cells project into an axonal plexus in the lower third of the MZ. From 18 GW, CR cells and SGL become segregated, and the polymorphic CR cells lie now below the SGL, with which they remain connected by ascending processes. Granule cells invade the lower MZ contacting somata and processes of CR cells. The somata of vertical CR cells elongate until 23/24 GW when they show degenerative signs. After 24 GW, all polymorphic CR cells die. Granule cells degenerate after 24 GW; the SGL disappears at 28/30 GW. A population of persisting CR cells, morphologically different from the transient polymorphic forms, appears in a subpial position and survives in small numbers throughout life. Small non-CR neurons differentiate first in the lower half of layer I, thereafter also in the upper half. Histochemically, all CR cells are AChE-positive; they contain NADPH-d only transiently at 20 GW. We propose that CR cells and SGL provide a transient innervation network for the developing cortical plate at a time when the definitive fiber systems of the molecular layer are not yet established.

Acetylcholinesterase↗
PubMed1994

A quantitative analysis of parvalbumin neurons in rabbit auditory neocortex.

Parvalbumin (PV) is a calcium-binding protein present in GABAergic cells in the cerebral cortex and in thalamic relay neurons. In the present study, parvalbumin immunocytochemistry (PVi) and stereological methods were used to obtain estimates of cortical volume, total neuron number, laminar density, and the percentage of PV-immunoreactive neurons in auditory neocortex. PVi clearly delineated the primary auditory cortex (AI), which was characterized by two PV+ bands: dense terminal-like labeling within lamina III/IV and PV+ somata in lamina VIa. Stereological analysis of Nissl-stained sections revealed that the total number of neurons in rabbit AI was 1.48 x 10(6) with a mean neuronal density of 55 x 10(3)/mm3. Based on a mean cortical thickness of 1.92 mm, there are approximately 106,000 neurons in a 1 mm2 column of auditory cortex. PVi yields an extraordinary Golgi-like staining of nonpyramidal cells in all cortical layers. PV+ nonpyramidal cells constitute approximately 7.0% of the neurons in AI. There were significant differences in the morphology and density of PV+ neurons across layers. Although only 5% of cells in lamina I were PV+, three nonpyramidal cell types were present. Lamina II had the highest numerical density within AI but the lowest percentage of PV+ neurons (3.3%). Lamina II, however, contained the greatest diversity of PV+ nonpyramidal cell types, which included small multipolar cells, bipolar cells, and, less frequently, large cells of the bitufted, bipolar, and stellate varieties. Lamina IV had one of the highest numerical densities (67.6 x 10(3) neurons/mm3) and contributed nearly 27% of the total neuron number in AI. The numerical density of PV+ nonpyramidal cells was also greatest within lamina IV (7.1 x 10(3)/mm3) where they formed 10.4% of the neuronal population. PV+ nonpyramidal cells in lamina IV and lamina III were predominantly large basket-type cells with bitufted dendritic domains and tangentially oriented local axonal plexuses. The terminal-like label within lamina III/IV derived in part from the basket-cell axons, which formed pericellular arrays around unstained somata. Cell-sparse lamina V contained the largest PV+ nonpyramidal cells in AI. These cells, which formed 11% of the neuron population in lamina V, were notable for their tangentially oriented dendritic fields and local axonal arbors. PVi partitioned lamina VI into VIa and VIb. Large multipolar nonpyramidal cells were distributed throughout lamina VI and made up approximately 6% of the total population. Lamina VIa contained a band of lightly labeled PV+ pyramidal neurons that formed 15% of the neuronal population.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1995

Tempo of neurogenesis and synaptogenesis in the primate cingulate mesocortex: comparison with the neocortex.

In the neocortex, the onset of the rapid phase (phase 3) of synaptogenesis occurs after the end of neurogenesis. However, we still do not know whether or not these two developmental events are causally related. The present study compares the time-course and tempo of neurogenesis and synaptogenesis in the anterior cingulate cortex (area 24 of Brodmann) and in the primary visual cortex (area 17) in a series of pre- and postnatal rhesus monkeys. Autoradiographic analysis of animals fetally injected with 3H-thymidine showed that all neurons destined for area 24 are generated by embryonic day 70, which is 30 days earlier than in area 17. The rapid phase of synaptogenesis in area 24 starts during the third embryonic month and continues at the same rate through the remainder of gestation and the first 2 months after birth, as has been seen in neocortical areas examined previously. Statistical analysis of the linear portions of the rapid phase indicates that, although neurogenesis in area 24 is completed 1 month earlier than in area 17, the rapid phase of synaptogenesis occurs 41 days later. Moreover, the tempo of synaptic accretion was remarkably similar to that in motor, somatosensory, visual, or associational areas. All were grouped within the same time window of about 40 days, centered at birth. After the second postnatal month, synaptic density in area 24 remains at a high level until sexual maturity. This work shows that the rapid phase of synaptogenesis in the cingulate mesocortex is not linked temporally to the end of neurogenesis. We suggest that it is regulated by the same genetic or humoral factors that control synaptogenesis in the phylogenetically newer neocortical areas.

Animals↗
PubMed1995

Development of calretinin immunoreactivity in the neocortex of the rat.

The prenatal and postnatal development of calretinin (CR)-containing elements in the neocortex of the rat was analyzed using immunohistochemistry. CR immunoreactivity in the cortical anlage appeared early at embryonic day 14 (E14), with CR-positive neurons located in the primitive plexiform layer and in the emerging subplate and marginal zones. At later prenatal and early postnatal stages, these two layers showed the highest CR immunostaining in the cortex, and large numbers of cell bodies and fibers were immunostained. From postnatal day 3 (P3) onwards, CR immunostaining disappeared progressively from the subplate-layer VIb and the marginal zone-layer I, so that very few cells remained stained in these layers in the adult. In the cortical plate and prospective layers VIa to II-III, CR-positive neurons were seen at prenatal stages, their numbers increasing markedly during the first postnatal week. Most neurons showed undifferentiated nonpyramidal shapes, and matured during the second and third postnatal weeks, when the adult pattern of CR immunostaining was achieved. In addition, some pyramidal-like neurons in the infragranular layers and in layer II-III transiently expressed CR during the postnatal period, most notably between P3 and P12. Colocalization experiments performed at P0-P3 with antibodies against the neurotransmitter gamma-aminobutyric acid (GABA) showed that most nonpyramidal CR-positive neurons in the derivates of the cortical plate were also GABAergic during development. In contrast, large numbers of CR-containing neurons in the subplate and marginal zone were GABA-negative. The present results show that in addition to recording the early development of a subset of nonpyramidal neurons, CR is transiently expressed in certain GABA-negative populations of the subplate and marginal zone, and most likely in pyramidal neurons.

Animals↗
PubMed2006

Genetic targeting of principal neurons in neocortex and hippocampus of NEX-Cre mice.

Conditional mutagenesis permits the cell type-specific analysis of gene functions in vivo. Here, we describe a mouse line that expresses Cre recombinase under control of regulatory sequences of NEX, a gene that encodes a neuronal basic helix-loop-helix (bHLH) protein. To mimic endogenous NEX expression in the dorsal telencephalon, the Cre recombinase gene was targeted into the NEX locus by homologous recombination in ES cells. The Cre expression pattern was analyzed following breeding into different lines of lacZ-indicator mice. Most prominent Cre activity was observed in neocortex and hippocampus, starting from around embryonic day 11.5. Within the dorsal telencephalon, Cre-mediated recombination marked pyramidal neurons and dentate gyrus mossy and granule cells, but was absent from proliferating neural precursors of the ventricular zone, interneurons, oligodendrocytes, and astrocytes. Additionally, we identified formerly unknown domains of NEX promoter activity in mid- and hindbrain. The NEX-Cre mouse will be a valuable tool for behavioral research and the conditional inactivation of target genes in pyramidal neurons of the dorsal telencephalon.

Animals↗
PubMed1989

Size and density of glial and neuronal cells within the cerebral neocortex of various insectivorian species.

Morphometric measurements were done on frontal sections through the somatosensory neocortex of various insectivorian species. All measured parameters varied with the size of animals; there was a better correlation with the ventriculartopial brain wall thickness than with the brain weight. The following rules were evaluated: with increasing brain wall thickness, 1) lamina I becomes thinner; 2) the nuclei of both neuronal and glial cells become larger; 3) the volume density of neuronal cells decreases greatly; 4) the volume density of glial cells increases slightly; and 5) as a result, the glia:neuron index increases markedly. There was no equal number of neurons under a unit surface area in the cortices of any species studied. Developmental processes that might account for the above-mentioned rules are discussed in this report.

Animals↗
PubMed1995

Disruption of the blood-brain interface in neonatal rat neocortex induces a transient expression of metallothionein in reactive astrocytes.

Exposure of the adult rat brain parenchyma to zinc induces an increase in the intracerebral expression of the metal-binding protein, metallothionein, which is normally confined to astrocytes, ependymal cells, choroid plexus epithelial cells, and brain endothelial cells. Metallothionein is expressed only in diminutive amounts in astrocytes of the neonatal rat brain, which could imply that neonatal rats are devoid of the capacity to detoxify free metals released from a brain wound. In order to examine the influence of a brain injury on the expression of metallothionein in the neonatal brain, PO rats were subjected to a localized freeze lesion of the neocortex of the right temporal cortex. This lesion results in a disrupted blood-brain interface, leading to extravasation of plasma proteins. From 16 h, reactive astrocytosis, defined as an increase in the number and size of cells expressing GFAP and vimentin, was observed surrounding the neocortical lesion site. Astrocytes and pial cells situated adjacent to the area of injury also became positively stained for metallothionein. At 3-6 days post-lesion, the highest level of reactive astrocytes expressing metallothionein was observed. Neo-Timm staining revealed that histochemically reactive zinc had disappeared from the lesion site. Extracellular albumin and metallothionein-positive astrocytes were absent approximately 2 weeks after the lesion, whereas reactive astrocytosis was still observed. These results show that a lesion of the neonatal rat brain induces a transient expression of metallothionein in reactive astrocytes, probably as a response to metals released from the site of the brain injury.

Animals↗
PubMed1981

Laminar distribution of cholinergic markers in neocortex: effects of lesions.

The distribution of presynaptic markers for cholinergic and GABAergic neurons in the various layers of the lateral neocortex was determined with a technique in which sections of increasing depth horizontal to the pial surface were obtained on a frozen-stage microtome and analyzed for the markers. The specific activities of choline acetyltransferase and acetylcholinesterase had an uneven distribution in the cortex with lowest levels of activity associated with lamina II and III, whereas glutamate decarboxylase activity was highest in lamina II, III, and IV. Fetally-induced hypoplasia of the cortex resulted in an enrichment in both choline acetyltransferase and acetylcholinesterase activity in all layers with no significant change in the activity of glutamate decarboxylase. Lesion of the nucleus basalis-cortical cholinergic pathway resulted in marked reductions in the activities of acetylcholinesterase and choline acetyltransferase in all cortical layers and an elimination of the uneven distribution of these markers within the cortex. These results provide further evidence that acetylcholinesterase activity is specifically associated with cortical cholinergic afferents and support the existence of cortical intrinsic cholinergic neurons.

Acetylcholinesterase↗
PubMed1993

Platelet-activating factor antagonists reduce excitotoxic damage in cultured neurons from embryonic chick telencephalon and protect the rat hippocampus and neocortex from ischemic injury in vivo.

The neuroprotective effects of the platelet-activating factor (PAF) antagonists BN 52020 and BN 52021 were determined in a temperature-controlled model of transient forebrain ischemia in the rat (occlusion of both common carotid arteries combined with lowering of the mean arterial blood pressure to 40 mm Hg for 10 min). After 7 days of recirculation, the ischemic neuronal damage was evaluated histologically within the hippocampus and neocortex. Combined pre- and post-treatment with the PAF antagonists (2 x 25 mg/kg, s.c.) significantly reduced the resulting neuronal damage of the CA1 and CA3 hippocampal subfields and of the occipital and parietal cerebral cortex. The two PAF antagonists were also tested for their neuroprotective activity in primary neuronal cultures isolated from embryonic chick telencephalon. Since an excessive activation of excitatory amino acid receptors is discussed to be of importance for the ischemic brain damage, the cultured neurons were exposed to the excitatory amino acid L-glutamate (1 mM) for a period of 60 min. Twenty hours after the excitotoxic insult, BN 52020- and BN 52021-treated cultures (1-100 microM) showed both a better preserved morphology, as well as a dose-dependent increase in cell viability and protein content compared to the control cultures. Our results demonstrate that the PAF antagonists BN 52020 and BN 52021 have the capacity to protect brain tissue against ischemic neuronal damage independent of hypothermic effects and are also capable of reducing excitotoxic damage of telencephalic neurons from chick embryos cultured in the absence of glial or endothelial cells. We thus propose that PAF plays an important role in the pathophysiology of ischemic/excitotoxic neuronal injury via a direct action on neurons.

Animals↗
PubMed1990

GABA and glutamate receptor development of cultured neurons from rat hippocampus, septal region, and neocortex.

The early development of functionally active GABA and glutamate receptors on neurons from hippocampus, septal region, and neocortex of embryonic rats were studied using primary dissociated serum-free cell cultures. The responses to GABA and glutamate, applied to individual neurons by pressure ejection, were tested at different developmental stages, starting at 1 day in vitro (DIV) until 3 weeks. In all three types of neuronal cultures, the GABAA-receptor developed prior to the glutamate receptors, and after 9 DIV most of the neurons were sensitive to both GABA and glutamate. N-methyl-D-aspartate (NMDA) and non-NMDA receptor subtypes of the glutamate receptors could be distinguished in hippocampal cultures. The development of GABA and glutamate receptors on septal region neurons appeared to be delayed as compared to hippocampal neurons. In neocortical cultures the majority of neurons was sensitive to GABA just after plating, whereas the sensitivity to glutamate was retarded. The differences in GABA and glutamate receptor development among these three neuronal cultures provide evidence that the appearance of transmitter receptors on cultured neurons is predominantly determined by intrinsic mechanisms rather than by environmental conditions. The proportion of spontaneously active networks in these cultures increased with a time course very similar to the rise in glutamate-sensitive neurons suggesting that functional active glutamate receptors may be involved in the generation of spontaneous activity.

Animals↗
PubMed1991

Distribution of somatostatin-immunoreactive cell bodies and fibers in the neocortex of Macaca fuscata.

The distribution of somatostatin-immunoreactive cell bodies and processes was studied in the cerebral cortex of the macaque monkey (Macaca fuscata), by applying an immunohistochemical technique with a monoclonal antibody raised against somatostatin tetradecapeptide. Many somatostatin-immunoreactive cell bodies and processes were observed in all regions of the cerebral cortex, i.e., frontal, parietal, temporal, insular, occipital, and cingulate cortices, and also in the underlying white matter. Three types of somatostatin-containing cell bodies were distinguished in the cerebral cortex. These cell bodies were distributed in layers II to VI of the cortex, and also in the underlying white matter. There were dense deposits of somatostatin-containing granular structure in layers I and II, and many somatostatin-containing processes in layers IV and V. The present observations demonstrate that in the primate neocortex somatostatin 14-containing neuronal systems are as highly developed as other prosomatostatin-derived peptides but differ from the latter systems in terms of cell morphology and fiber distribution.

Animals↗
PubMed1983

Effects of the cytostatic drug cis-platinum on the developing neocortex of the mouse.

The effects of the new cytostatic drug cis-diamminedichloroplatinum(II) (cis-platinum) on the developing neocortex of NMRI mouse embryos or fetuses were investigated using light- and electron-microscopic methods. Single doses of 20 mg cis-platinum/kg were applied intraperitoneally on day 10, 11, . . ., or 16 of gestation. After treatment on day 10 or 11-i.e., during the phase of organogenesis-no morphological alterations could be detected in the neuroepithelium. However, after treatment on day 12 or later, the mitotic activity was markedly reduced and a great number of cells had become necrotic within 12-24 h after application of the drug. At the ultrastructural level, the development of necroses began with a condensation of the chromatin, culminating in the formation of large condensation plaques and shrinkage and fragmentation of the cytoplasm. The observed necroses can be classified according to Schweichel and Merker as type I necroses. It is argued that the apparent teratogenic inefficiency of cis-platinum on days 10 and 11 of murine pregnancy is caused by the inability of cis-platinum to pass the placental barrier at this stage of pregnancy.

Animals↗
PubMed1997

Coordination of neuronal activity by gap junctions in the developing neocortex.

During embryonic development, gap junctions link cells into functional communication compartments characterized by a common development fate. Increasing evidence for gap junctions between immature neurons suggest that similar mechanisms may also be at work in the developing vertebrate brain, where gap junction-coupled neuronal assemblies often precede synaptically-linked functional networks. Recent experiments in the developing mammalian neocortex demonstrated the presence of gap-junction mediated second messenger waves, similar to those in non-neuronal cells. The primary function of neuronal gap junctions, therefore, might be to coordinate biochemical activity, rather than to act as purely electrical synapses. Thus, gap junctions may serve to amplify neuronal activity produced by weak synaptic stimulation.

Journal Article↗
PubMed1996

Distribution of glutamate receptor subunit GluR1 and GABA in human cerebral neocortex: a double immunolabelling and electron microscopic study.

Specimens of human cerebral neocortex were obtained during neurosurgical operations and studied by immunocytochemistry and electron microscopy, using antibodies to the glutamate receptor subunit GluR1 and gamma-aminobutyric acid (GABA). Many GluR1-positive pyramidal neurons and fewer GluR1-positive non-pyramidal neurons were present in the cortex. Non-pyramidal neurons were more heavily labelled for GluR1 than pyramidal neurons. Most GABAergic neurons were labelled for GluR1. The white matter was unstained, except for occasional labelled neurons. This pattern of GluR1 immunostaining is similar to that in rat cerebral cortex, but is different from that in the hippocampus and amygdala, where large numbers of pyramidal or projection neurons, but few non-pyramidal or GABAergic neurons, were labelled for GluR1.

Adolescent↗