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At least 739 records · Page 41Linked to original sources
PubMed2003

Beta-amyloid regulation of presynaptic nicotinic receptors in rat hippocampus and neocortex.

Alteration by beta-amyloid (Abeta) of signaling via nicotinic acetylcholine receptors (nAChRs) has been implicated in the early stages of Alzheimer's disease. nAChRs function both post- and presynaptically in the nervous system; however, little is known about the functional consequence of the interaction of Abeta with these receptors, particularly those on presynaptic nerve terminals. In view of the strong correlation between loss of synaptic terminals and dementia, together with the reduction in nAChRs in Alzheimer's disease, the possibility exists that presynaptic nAChRs may be targets for Abeta. To explore this possibility, we assessed the effect of Abeta peptides on nicotine-evoked changes in presynaptic Ca2+ level via confocal imaging of isolated presynaptic nerve endings from rat hippocampus and neocortex. Abeta1-42 appeared to inhibit presynaptic nAChR activation by nicotine. Surprisingly, picomolar Abeta1-42 was found to directly evoke sustained increases in presynaptic Ca2+ via nAChRs, revealing that the apparent inhibitory action of Abeta1-42 was the result of an occlusion of nicotine to further stimulate the receptors. The direct effect of Abeta was found to be sensitive to alpha-bungarotoxin, mecamylamine, and dihydro-beta-erythroidine, indicating involvement of alpha7-containing nAChRs and non-alpha7-containing nAChRs. Prior depolarization strongly attenuated subsequent Abeta-evoked responses in a manner dependent on the amplitude of the initial presynaptic Ca2+ increase, suggesting that nerve activity or Ca2+ channel density may control the impact of Abeta on presynaptic nerve terminal function. Together, these results suggest that the sustained increases in presynaptic Ca2+ evoked by Abeta may underlie disruptions in neuronal signaling via nAChRs in the early stages of Alzheimer's disease.

Amyloid beta-Peptides↗
PubMed2003

Different mechanisms promote astrocyte Ca2+ waves and spreading depression in the mouse neocortex.

Cortical spreading depression (CSD) is thought to play an important role in different pathological conditions of the human brain. Here we investigated the interaction between CSD and Ca2+ waves within the astrocyte population in slices from mouse neocortex (postnatal days 10-14). After local KCl ejection as a trigger for CSD, we recorded the propagation of Ca2+ increases within a large population of identified astrocytes in synchrony with CSD measured as intrinsic optical signal (IOS) or negative DC-potential shift. The two events spread with 39.2 +/- 3.3 mum/sec until the IOS and negative DC-potential shift decayed after approximately 1 mm. However, the astrocyte Ca2+ wave continued to propagate for up to another 500 microm but with a reduced speed of 18.3 +/- 2.5 microm/sec that is also typical for glial Ca2+ waves in white matter or culture. While blocking CSD using MK-801 (40 microm), an NMDA-receptor antagonist, the astrocyte Ca2+ wave persisted with a reduced speed (13.2 +/- 1.5 microm/sec). The specific gap junction blocker carbenoxolon (100 microm) did not prevent CSD but decelerated the speed (2.9 +/- 0.9 microm/sec) of the astrocyte Ca2+ wave in the periphery of CSD. We also found that interfering with intracellular astrocytic Ca2+ signaling by depletion of internal Ca2+ stores does not affect the spread of the IOS. We conclude that CSD determines the velocity of an accompanying astrocytic Ca2+ response, but the astrocyte Ca2+ wave penetrates a larger territory and by this represents a self-reliant phenomenon with a different mechanism of propagation.

Animals↗
PubMed2003

Sleep-dependent theta oscillations in the human hippocampus and neocortex.

Hippocampal theta waves recorded during rapid eye movement (REM) sleep are thought to play a critical role in memory consolidation in lower mammals, but previous attempts to detect similar theta oscillations in the human hippocampus have been unsuccessful. Using subdural and depth recordings from epileptic patients, we now report the first evidence of state-dependent hippocampal theta waves (4-7 Hz) in humans. Unlike the continuous theta in rodents, however, these oscillations were consistently observed during REM sleep in short (approximately 1 sec) bursts and during transitions to wake in longer epochs. Theta waves were also observed in the basal temporal lobe and frontal cortex during transitions from sleep to wake and in quiet wakefulness but not in REM, and they were not coherent with hippocampal theta oscillations. The absence of functional coupling between neocortex and hippocampus during theta periods indicates that multiple theta generators exist in the human brain, and that they are dynamically regulated by brain state. Gamma oscillations were also present during REM theta bursts, but the fluctuations in gamma power were not associated with theta phase, pointing out another significant difference between rodent and human theta properties. Together, these findings suggest that the generation mechanisms of theta oscillations in humans might have evolved from tonic to phasic in hippocampus during REM sleep and extended from hippocampus to cortex, where they appear in certain wakefulness-related states.

Adolescent↗
PubMed2004

Early development of the neocortex in human foetuses aged 9 weeks.

A study was made of human embryos at the end of 8 weeks and foetuses aged 9 weeks. It was shown that at the beginning of the foetal period the cortical plate, which is the primordium of the neocortex, covers the whole surface of the cerebral hemisphere. The plate consists of 8-12 rows of densely packed cells. Below the cortical plate is the subplate.

Gestational Age↗
PubMedDate not supplied

Multiple system atrophy: laminar distribution of the pathological changes in frontal and temporal neocortex--a study in ten patients.

OBJECTIVE: To determine the distribution of the pathological changes in the neocortex in multiple-system atrophy (MSA). METHOD: The vertical distribution of the abnormal neurons (neurons with enlarged or atrophic perikarya), surviving neurons, glial cytoplasmic inclusions (GCI) and neuronal cytoplasmic inclusions (NI) were studied in alpha-synuclein-stained material of frontal and temporal cortex in ten cases of MSA. RESULTS: Abnormal neurons exhibited two common patterns of distribution, viz., density was either maximal in the upper cortex or a bimodal distribution was present with a density peak in the upper and lower cortex. The NI were either located in the lower cortex or were more uniformly distributed down the cortical profile. The distribution of the GCI varied considerably between gyri and cases. The density of the glial cell nuclei was maximal in the lower cortex in the majority of gyri. In a number of gyri, there was a positive correlation between the vertical densities of the abnormal neurons, the total number of surviving neurons, and the glial cell nuclei. The vertical densities of the GCI were not correlated with those of the surviving neurons or glial cells but the GCI and NI were positively correlated in a small number of gyri. CONCLUSION: The data suggest that there is significant degeneration of the frontal and temporal lobes in MSA, the lower laminae being affected more significantly than the upper laminae. Cortical degeneration in MSA is likely to be secondary to pathological changes occurring within subcortical areas.

Aged↗
PubMedDate not supplied

[Suppression of gamma EEG activity as an index of a spreading depression wave in the neocortex of a waking rabbit].

A spreading depression (SD) can spontaneously develop in seizures, attacks of migraine, vascular disorders and other pathological states of the brain. However, problems in technique of recording the DC-potential in the neocortex of humans and waking animals substantially restrict the possibilities of studying functional consequences of the SD. In this article, the EEG pattern was studied in detail at the moment of the SD development. Specific features were revealed, which make it possible to detect the SD without recording shifts of the DC-potential. At the moment of the SD arrival, the interhemispheric balance drastically disturbs because of a strong decrease in the high-frequency activity. By the time indices, the course of the suppression of the gammal and gamma2 EEG frequencies is the most reliable symptom of the SD wave development. The EEG spectral power in the delta band increases with a certain delay in reference to the deep depression of the high-frequency activity and is, in essence, an SD aftereffect. The found EEG signs of an SD wave can substantially simplify the identification of this phenomenon both in experiment and clinical conditions in certain pathological states of the brain.

Animals↗
PubMed2005

[Neocortex formation in mice developing after prenatal serotonin depletion].

The objective of this study was a detailed investigation of structural changes taking place in murine neocortex during its formation and stratification after prenatal serotonin depletion. The study was carried out in murine embryos of F1 (C58BL/CBA) hybrid strain. For depletion of endogenous serotonin in mice, pchlorophenylalanin, an inhibitor of tryptophan hydroxylase - a key enzyme of serotonin synthesis, was used. Brain of the offspring was studied on postnatal days 1, 5 and 10 (n = 10-15 for each time point). Intact animals of respective developmental stages were used as a control. The study demonstrated that prenatal inhibition of serotonin synthesis resulted in malformation of all neocortical layers, disorders of neuronal growth, development and differentiation, changes in their shape and dimensions. During postnatal development, the loss of a significant numbers of cells was observed in the brain structures studied of serotonin-depleted animals.

Animals↗
PubMed1997

NR2A subunit expression shortens NMDA receptor synaptic currents in developing neocortex.

NMDA receptors play important roles in learning and memory and in sculpting neural connections during development. After the period of peak cortical plasticity, NMDA receptor-mediated EPSCs (NMDAR EPSCs) decrease in duration. A likely mechanism for this change in NMDA receptor properties is the molecular alteration of NMDA receptor structure by regulation of NMDA receptor subunit gene expression. The four modulatory NMDAR2A-D (NR2A-D) NMDA receptor subunits are known to alter NMDA receptor properties, and the expression of these subunits is regulated developmentally. It is unclear, however, how the four NR2 subunits are expressed in individual neurons and which NR2 subunits are important to the regulation of NMDA receptor properties during development in vivo. Analysis of NR2 subunit gene expression in single characterized neurons of postnatal neocortex revealed that cells expressing NR2A subunit mRNA had faster NMDAR EPSCs than cells not expressing this subunit, regardless of postnatal age. Expression of NR2A subunit mRNA in cortical neurons at even low levels seemed sufficient to alter the NMDA receptor time course. The proportion of cells expressing NR2A and displaying fast NMDAR EPSCs increased developmentally, thus providing a molecular basis for the developmental change in mean NMDAR EPSC duration.

Aging↗
PubMed1997

Instantaneous perturbation of dentate interneuronal networks by a pressure wave-transient delivered to the neocortex.

Whole-cell patch-clamp recordings and immunocytochemical experiments were performed to determine the short- and long-term effects of lateral fluid percussion head injury on the perisomatic inhibitory control of dentate granule cells in the adult rat, with special reference to the development of trauma-induced hyperexcitability. One week after the delivery of a single, moderate (2.0-2.2 atm) mechanical pressure wave to the neocortex, the feed-forward inhibitory control of dentate granule cell discharges was compromised, and the frequency of miniature IPSCs was decreased. Consistent with the electrophysiological data, the number of hilar parvalbumin (PV)- and cholecystokinin (CCK)-positive dentate interneurons supplying the inhibitory innervation of the perisomatic region of granule cells was decreased weeks and months after head injury. The initial injury to the hilar neurons took place instantaneously after the impact and did not require the recruitment of active physiological processes. Furthermore, the decrease in the number of PV- and CCK-positive hilar interneurons was similar to the decrease in the number of the AMPA-type glutamate receptor subunit 2/3-immunoreactive mossy cells, indicating that the pressure wave-transient causes injurious physical stretching and bending of most cells that are large and not tightly packed in a cell layer. These results reveal for the first time that moderate pressure wave-transients, triggered by traumatic head injury episodes, impact the dentate neuronal network in a unique temporal and spatial pattern, resulting in a net decrease in the perisomatic control of granule cell discharges.

Animals↗
PubMedDate not supplied

[The connection between ultrastructural synaptic plasticity and the number of ribosomes in the dendritic terminals studied in a cell model of conditioning in the rat neocortex].

The dependence was studied of the ultrastructural changes in postsynaptic densities of axodendritic synapses on the size of postsynaptic ribosomal aggregates. A positive correlation was established between the thickness of postsynaptic densities and the number of ribosomes. The role of dendritic mRNA is discussed and the possible mechanisms underlying rapid local protein synthesis in a modification of postsynaptic components which have been observed in case of combined application of two neurotransmitters to the neocortex of rats.

Animals↗
PubMedDate not supplied

[Differentiation of neurons and synapses of mossy fibers in transplants of fascia dentata developing in the rat neocortex].

Embryonic fascia dentata tissue isolated from the hippocampus was transplanted heterotopically into the neocortex of adult rats. Ultrastructural characteristics of neurons and synapses in transplants were studied nine months later. It has been found that the main types of neurons present in fascia dentata undergo differentiation in the transplants, and a dense neuropile containing various types of synapses is produced. A characteristic feature of the transplanted neurons is the presence of additional microspines on somatic and dendrite surfaces; this appears to be due to a deficiency of external and internal afferents. Gigantic synaptic terminals of granule cell axons (mossy fibers) in transplants possess unique morphological characteristics, which allow their identification in a complex neuropile. Just as in situ, they form two types of contacts: chemical asymmetric contacts with dendrite spines and desmosome-like ones with dendrite surface characteristics. However, accumulations of large vesicles with electron-dense centers can often be observed near the active zones of the synapses, and desmosome-like connections are more prominent. The most important feature is that gigantic synapses in transplants use midsize and small dendrites as postsynaptic targets up to terminal branches, and they contact with spines of the usual shape and size, whereas in situ terminal synaptic contacts of mossy fibers are formed only with gigantic processes of initial segments of the large apical dendrites. Thus, in the absence of normal synaptic targets, mossy fibers can produce contacts having all features of functional synapses, but with atypical postsynaptic structures.

Animals↗
PubMed1996

Development of spinal cord projections from neocortical transplants heterotopically placed in the neocortex of newborn hosts is highly dependent on the embryonic locus of origin of the graft.

Previous experiments based on heterotopic transplantation paradigms have indicated that the distribution of efferents developed by layer V pyramidal cells seems to be related to where in the neocortex the cells develop and not to where they were generated. The present study was undertaken in an attempt to obtain a quantitative estimation of the weight of extrinsic factors in the development of neocortical efferents. Fragments of embryonic (E15-E19) frontal or occipital cortex were grafted homotopically or heterotopically into the frontal or occipital cortex of newborn rats. As adults, the hosts received an injection of a retrograde tracer into the pyramidal tract decussation, and the distribution of the subsequent cell labeling was examined in each category of transplant. The mean numbers of labeled cells were 725 in frontal-to-frontal transplants and 250 in frontal-to-occipital transplants. In occipital-to-frontal transplants, the numbers of labeled cells were extremely low, ranging from 0 to 14. Finally, as expected, practically no cell labeling was found in occipital-to-occipital transplants. Thus, transplants of presumptive frontal origin systematically develop and maintain in adulthood a spinal cord projection even though they are placed in the host occipital cortex. Conversely, transplants of presumptive occipital origin are practically incapable of maintaining a spinal cord projection in adulthood even though they are placed in the host frontal cortex. It seems, therefore, that the generation of regional differences in efferent connectivity found in the mature cortex depends on early regional specification within the neocortical neuroepithelium.

Animals↗
PubMed1996

GluR1-immunopositive interneurons in rat neocortex.

Recent in vitro studies suggest that inhibitory interneurons in cortex may express the GluR1 glutamate receptor subunit in the absence of GluR2, leading to calcium-permeable alpha-amino-3-hydroxy-5-methylisoxazole-4-propionate (AMPA) channels. We performed a study of rat somatic sensory cortex to confirm and extend these observations, using quantitative immunocytochemistry for multiple antigens. A morphologically distinct subpopulation of nonpyramidal neurons in neocortex was intensely immunoreactive for GluR1. Electron microscopic analysis of these cells revealed somatic staining for GluR1, mainly in the rough endoplasmic reticulum. Dendritic staining was concentrated at the synaptic active zone and in the adjacent subsynaptic cytoplasm. Double immunostaining revealed that the large majority of intensely GluR1-positive cells contained gamma-aminobutyric acid or its synthetic enzyme, glutamic acid decarboxylase, but little or no GluR2. Thus, AMPA receptors on a subpopulation of inhibitory interneurons in cortex are likely to be calcium permeable. This calcium permeability is likely to influence functional properties of these neurons; it may underlie the high levels of calcium-binding proteins they contain; and may render them liable to excitotoxic injury

Animals↗
PubMed1996

Morphological properties of intracellularly labeled layer I neurons in rat neocortex.

The morphology of neurons in layer I of rat neocortex, including Cajal-Retzius (CR) cells, was studied by using intracellular biocytin staining in brain slices obtained from rats during the first 22 postnatal days. Within the first postnatal week, horizontal bipolar neurons or CR cells were prominent in layer I. Typically, CR cells had one main dendrite and one axon originating from opposite poles of the somata. Even though the main dendrites and axons could be quite long, complex dendritic or axonal arbors were not observed. Starting around postnatal day 6 (PN 6), CR cells were less frequently observed. From PN 10 to PN 21, nonpyramidal neurons with diverse morphologies became the main neuronal component in layer I. The somata of layer I nonpyramidal neurons were quite variable in size and shape. Dendrites were smooth or sparsely spiny, and the dendritic trees were mainly restricted to layer I, covering an area with a diameter of about 200 microns. Axon collaterals of these cells formed elaborate arbors with diameters of around 700 microns in layer I and extending, in many cases, to layer II/III and even layer IV. This extensive axonal plexus provides a rich anatomical base on which layer I neurons, functioning as local circuit elements, may interact with each other and with neurons in other layers.

Animals↗
PubMed1995

The roles of growth factors and neural activity in the development of the neocortex.

Previous research on primarily the peripheral nervous system has shown that soluble growth factors help control key developmental events by contributing to dynamic autocrine and paracrine signalling systems. Much less is known about the roles of these substances in neocortical development. Using cell and tissue culture paradigms, we have demonstrated that soluble growth factors are produced by the neocortex and its subcortical targets, and that these tissues can respond to them. There are several possible functions for these factors in neocortical development in vivo: they may initiate axonal growth from neocortical neurons and/or their afferents; accelerate or guide that growth; and/or play a role in the later refinement of connections. Although none of these possibilities can be excluded, the existing evidence strengthens the hypothesis that soluble growth factors are important for the early postnatal growth and refinement of neocortical connections, when their levels of release may be regulated by neocortical activity. At present we do not know which growth factors are involved in these processes, but the results of preliminary experiments indicate that neurotrophins and fibroblast growth factor are prime candidates.

Animals↗
PubMed1983

Studies of human and monkey "epileptic" neocortex in the in vitro slice preparation.

The in vitro slice technique was used to study neuronal activity in human cortical tissue removed during neurosurgical procedures for intractable epilepsy and in monkey neocortex rendered epileptogenic by injection of alumina gel. In both cases, biopsies were guided by electrocorticographic signs of epileptiform activity. Intracellular recordings were made from 167 neurons in human tissue and from 73 neurons in monkey tissue samples. There was little spontaneous activity in these biopsies and no indication of spontaneous cellular bursting. Stimulation at the pial surface or in white matter evoked synaptically driven activity that was primarily excitatory. Graded bursts of activity could be elicited from some cells, but no all-or-none paroxysmal depolarization shifts were recorded. Inhibitory postsynaptic potentials were relatively rare. Intracellular injections of dye in a small number of neurons revealed no obvious differences between bursting and nonbursting neurons. These in vitro studies of chronic epileptic cortex have thus far provided few clear insights into the basic mechanisms of epilepsy.

Action Potentials↗
PubMed1988

Acetylcholinesterase-rich pyramidal neurons in the human neocortex and hippocampus: absence at birth, development during the life span, and dissolution in Alzheimer's disease.

Acetylcholinesterase-rich pyramidal neurons in the human association neocortex and hippocampal formation are virtually absent early in life, become established by adolescence, and appear to increase in density during adulthood and perhaps even senescence. Analogous neurons are not detectable in the adult monkey brain. This novel class of neurons may represent a uniquely human adaptation in primate evolution and may provide a neuroanatomical substrate for the mental development that occurs during the adult stages of life. These phylogenetically and ontogenetically progressive neurons are also markedly vulnerable to degeneration in Alzheimer's disease.

Acetylcholinesterase↗
PubMed2003

EphA family gene expression in the developing mouse neocortex: regional patterns reveal intrinsic programs and extrinsic influence.

Parcellation of the mammalian cerebral cortex into distinct areas is essential for proper cortical function; however, the developmental program that results in the genesis of distinct areas is not fully understood. We examined the expression of members of the EphA family-the EphA receptor tyrosine kinases and the ephrin-A ligands-within the developing mouse cerebral cortex, with the aim of characterizing this component of the molecular landscape during cortical parcellation. We found that specific embryonic zones, such as the ventricular, subventricular, intermediate, subplate, and marginal zones, as well as the cortical plate, were positive for particular EphA genes early in corticogenesis (E12-E15). Along with this zone-selective expression, several genes (EphA3, EphA4, EphA5) were evenly expressed along the axes of the developing cortex, whereas one family member (EphA7) was expressed in a distinct anteroposterior pattern. Later in corticogenesis (E16-E18), other EphA family members became selectively expressed, but only within the cortical plate: EphA6 was present posteriorly, and ephrin-A5 was expressed within a middle region. At birth, patterning of EphA gene expression was striking. Thus, we found that the expression of a single EphA gene or a combination of family members can define distinct embryonic zones and anteroposterior regions of the neocortex during development. To examine whether cellular context affects the patterning of EphA expression, we examined gene expression in embryonic cortical cells grown in vitro, such that all cellular contacts are lacking, and in Mash-1 mutant mice, in which thalamocortical connections do not form. We found that the expression patterns of most EphA family members remained stable in these scenarios, whereas the pattern of ephrin-A5 was altered. Taken together, this work provides a comprehensive picture of EphA family expression during mouse corticogenesis and demonstrates that most EphA expression profiles are cell intrinsically based, whereas ephrin-A5 is plastically regulated.

Afferent Pathways↗