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PubMed1997

Diversity of connections of the temporal neocortex with amygdaloid nuclei in the dog (Canis familiaris).

Reciprocal connections of amygdaloid nuclei with the temporal neocortex in the dog were investigated. Injections of fluorescent tracers and BDA into particular temporal areas were made in eleven dogs. The topographical arrangement of connections and variations in their density differentiate the temporal neocortex in the dog into a few regions. Among them, the cortex involving the anterior part of the ectosylvian gyrus did not send any amygdalopetal projection. The middle ectosylvian, dorsal zone of the posterior ectosylvian and the anterior part of the Sylvian gyrus were weakly connected with the amygdala. The cortical region involving the ventral zone of the posterior ectosylvian and composite posterior areas, as well as posterior Sylvian gyrus, was characterized by profuse connections with the amygdaloid complex. Cortico-amygdaloid connections originate in the wide cortical area of the auditory cortex of the middle and dorsal part of the posterior ectosylvian gyrus as well as in the auditory association cortex located in the ventral ectosylvian, composite posterior and posterior Sylvian gyri. The connections showed a dorso-ventral gradient of increasing density, in the direction of association fields. The most substantial projection taking rise from the ectosylvian posterior and posterior composite gyri terminated preferentially in the pericapsular sector of the lateral amygdaloid nucleus and, to a lesser degree, in its medial sector. Terminals of connections originating in the Sylvian gyrus occupied preferentially the intermediate part of the lateral nucleus, slightly more medially than that from the ectosylvian and posterior composite areas. Additionally, axonal terminals derived from the composite posterior and Sylvian posterior areas were observed in the basal parvocellular and magnocellular nuclei. Neocortical projections were reciprocated by amygdalofugal connections with two exceptions: the basal magnocellular nucleus was distinguished by a substantial amygdalofugal projection to the temporal neocortex focused on the dorsal Sylvian gyrus, and the central nucleus of the amygdala, in contrast, received an exclusively corticofugal projection.

Amygdala↗

PubMed1999

Graded and areal expression patterns of regulatory genes and cadherins in embryonic neocortex independent of thalamocortical input.

The differentiation of areas of the mammalian neocortex has been hypothesized to be controlled by intrinsic genetic programs and extrinsic influences such as those mediated by thalamocortical afferents (TCAs). To address the interplay between these intrinsic and extrinsic mechanisms in the process of arealization, we have analyzed the requirement of TCAs in establishing or maintaining graded or areal patterns of gene expression in the developing mouse neocortex. We describe the differential expression of Lhx2, SCIP, and Emx1, representatives of three different classes of transcription factors, and the type II classical cadherins Cad6, Cad8, and Cad11, which are expressed in graded or areal patterns, as well as layer-specific patterns, in the cortical plate. The differential expression of Lhx2, SCIP, Emx1, and Cad8 in the cortical plate is not evident until after TCAs reach the cortex, whereas Cad6 and Cad11 show subtle graded patterns of expression before the arrival of TCAs, which later become stronger. We find that these genes exhibit normal-appearing graded or areal expression patterns in Mash-1 mutant mice that fail to develop a TCA projection. These findings show that TCAs are not required for the establishment or maintenance of the graded and areal expression patterns of these genes and strongly suggest that their regulation is intrinsic to the developing neocortex.

Animals↗

PubMed2000

Acute 4-aminopyridine seizures increase the regional cerebral blood flow in the thalamus and neocortex, but not in the entire allocortex of the mouse brain.

Systemic injections of 4-aminopyridine precipitate epileptiform generalized seizures characterized mainly by shivering of the body, tail movements and tonic-clonic convulsions in rats and mice. However, only few details are known as concerns which brain regions are possibly affected and stimulated by the compound. The aim of the present study was to investigate the changes in regional cerebral blood flow in mice by using the lipophilic compound technetium-99m-hexamethyl-propyleneamineoxime (99mTc-HMPAO). Whilst the uptake of 99mTc-HMPAO was increased significantly in the neocortex and thalamus following the induction of acute 4-aminopyridine seizures, no such changes were observed in the allocortex of the mice. The increases in uptake in the neocortex and thalamus were completely prevented by carbamazepine (which abolished the symptoms of the seizure, too). The primary involvement of the neocortex and thalamus points to the importance of thalamocortical circuits in the precipitation and maintenance of experimental 4-aminopyridine convulsions.

4-Aminopyridine↗

PubMed2002

Distinct actions of Emx1, Emx2, and Pax6 in regulating the specification of areas in the developing neocortex.

The mammalian neocortex is organized into subdivisions referred to as areas that are distinguished from one another by differences in architecture, axonal connections, and function. The transcription factors EMX1, EMX2, and PAX6 have been proposed to regulate arealization. Emx1 and Emx2 are expressed by progenitor cells in a low rostrolateral to high caudomedial gradient across the embryonic neocortex, and Pax6 is expressed in a high rostrolateral to low caudomedial gradient. Recent evidence has suggested that EMX2 and PAX6 have a role in the genetic regulation of arealization. Here we use a panel of seven genes (Cad6, Cad8, Id2, RZRbeta, p75, EphA7, and ephrin-A5) representative of a broad range of proteins as complementary markers of positional identity to obtain a more thorough assessment of the suggested roles for EMX2 and PAX6 in arealization, and in addition to assess the proposed but untested role for EMX1 in arealization. Orderly changes in the size and positioning of domains of marker expression in Emx2 and Pax6 mutants strongly imply that rostrolateral areas (motor and somatosensory) are expanded, whereas caudomedial areas (visual) are reduced in Emx2 mutants and that opposite effects occur in Pax6 mutants, consistent with their opposing gradients of expression. In contrast, patterns of marker expression, as well as the distribution of area-specific thalamocortical projections, appear normal in Emx1 mutants, indicating that they do not exhibit changes in arealization. This lack of a defined role for EMX1 in arealization is supported by our finding of similar shifts in patterns of marker expression in Emx1; Emx2 double mutants as in Emx2 mutants. Thus, our findings indicate that EMX2 and PAX6 regulate, in opposing manners, arealization of the neocortex and impart positional identity to cortical cells, whereas EMX1 appears not to have a role in this process.

Adaptor Proteins, Signal Transducing↗

PubMed2002

Role of thalamocortical sensory suppression during arousal: focusing sensory inputs in neocortex.

The thalamus serves as a gate that regulates the flow of sensory inputs to the neocortex, and this gate is controlled by neuromodulators from the brainstem reticular formation that are released during arousal. We found recently that sensory-evoked responses are suppressed in the neocortex during arousal. This sensory suppression results from the activity-dependent depression of the thalamocortical connection caused by increased tonic firing of thalamocortical cells during arousal. In the present study, the functional consequences of thalamocortical suppression during arousal were investigated using the vibrissae system of rodents. The results show that thalamocortical suppression is associated with a strong reduction in the spread of sensory inputs through the cortex, thus reducing the size of sensory representations. In addition, when the responses of single cells to principal and adjacent whiskers are compared, the response to the adjacent whiskers was found to be strongly suppressed, much more so than that of principal whiskers. Consequently, the receptive fields of cortical neurons become more focused to the principal whisker. The results indicate that thalamocortical suppression during arousal serves to focus sensory inputs to their appropriate representations in neocortex, which may be computationally helpful for the spatial processing of sensory information.

Animals↗

PubMed2002

[Layer I neurons and their significance in the neocortex embryogenesis].

The literature data and the results of authors own investigations are presented on microarchitectonics and development of molecular layer (layer I) of mammalian neocortex. It originates from the marginal zone of primordial plexiform layer, common with primitive neopallial primordium of reptiles and amphibia, which maintains its initial organization during phylo- and ontogenesis of vertebrates. During initial stages of corticogenesis all migrating neurons establish contacts with Cajal-Retzius cells which coordinate location and exact spatial stratification of neuroblasts in growing cortical plate. The detailed analysis of fundamental mechanisms controlling embryogenesis of neocortex is presented including a) histogenesis of pyramidal and non-pyramidal neurons; b) unifying theory of cytoarchitectonic differentiation of neocortex proposed by M. Marin-Padilla; c) factors of cytoarchitectonic differentiation of cortical areas and specialization of brain hemispheres in mammalian ontogenesis and evolution. The thesis, according to which morphofunctional maturation of both pyramidal and non-pyramidal neurons begins as a result of their contacts with a system of thalamocortical afferent fibers, is substantiated. They grow from the subcortical white matter, initiate layer-by-layer ascending cortical maturation and, ultimately, divide it into descrete functional territories.

Animals↗

PubMedDate not supplied

[Thalamocortical dynamics: how do the thalamus and the neocortex communicate during the processing of information?].

INTRODUCTION AND DEVELOPMENT: The thalamus is the gateway to the neocortex. Most of the information that reaches the neocortex is transmitted through thalamocortical fibres. The neocortex, in turn, sends massive feedback to the thalamus through corticothalamic fibres. The sensory input reaches the thalamus by means of the primary sensory fibres. When the properties of these pathways are explored, they are found to present specific response characteristics. These studies have generally been conducted during anaesthesia or other quiescent states. Yet when the properties of these synaptic connections are explored in the active states typical of information processing, their responses are substantially different. CONCLUSION: These changes appear to be necessary to set the pathways of the thalamocortical system in a state of sensory input processing and, therefore, could account for the transformations that take place in order to sustain attentional and perceptive processes.

Action Potentials↗

PubMedDate not supplied

[Structural organization of rabbit neocortex in prenatal ontogenesis].

In the review on the basis of data of different authors, the development dynamics of the rabbit neocortex in prenatal life is presented. The main points of neurons development, interneuronal contacts, layer-by-layer and areal differentiation as well as neocortex afferental and efferental communications, that are elucidated ambiguously by investigators, are discussed. For the purpose of determination of the neocortex maturation to the birth-date the comparative analysis of the reference morphological data and author's own neurophysiological data is accomplished.

Anatomy, Comparative↗

PubMed2004

[Glial fibrillary acidic protein in astrocytes of the human neocortex].

Glial fibrillary acidic protein (GFAP) is a brain astrocyte-expressed protein that is recognized as one of the main immunohistochemical markers of these cells. The aim of the present study was to investigate the structure of GFAP-positive astrocytes of human neocortex. Main types of GFAP-immunoreactive astrocytes in the human neocortex were characterized using immunohistochemistry and confocal laser microscopy. These are astrocytes of the layer I forming the surface border glial membrane, translaminar astrocytes of the layer I with very long processes penetrating several cortical layers, astrocytes of middle layers of the neocortex with a general organization of protoplasmic-type astrocytes which are involved in formation of perivascular border membrane, and typical fibrous astrocytes of the white matter. The data obtained will contribute to unification of evaluation of histopathologic processes observed in various kinds of gliosis in the CNS.

Adolescent↗

PubMed1990

Synaptic transmission in human neocortex removed for treatment of intractable epilepsy in children.

Synaptic transmission to pyramidal cells was studied in slices of neocortex resected from infants and children (n = 10, age 8 months to 13 years) undergoing surgical treatment for intractable epilepsy. Most specimens were from the least abnormal area of the resection. Stable intracellular recordings could be obtained for up to 8 hours. Most of the recorded neurons had electrophysiological characteristics similar to those of regular-firing pyramidal cells and were in layers III to V, which was confirmed by intracellular staining with Lucifer yellow. Local extracellular stimulation evoked a sequence of excitatory and inhibitory postsynaptic potentials. After application of the gamma-aminobutyric acid antagonist, bicuculline (10-30 microM), extracellular stimulation induced large excitatory postsynaptic potentials and epileptiform bursts. Spontaneous bursts occasionally occurred in bicuculline. This effect of bicuculline was observed in all the tissue samples, even those from infant patients (n = 4, age 8-16 months). Kynurenic acid depressed or abolished both spontaneous and stimulation-induced bursts. The competitive antagonist for N-methyl-D-aspartate receptors, DL-2-amino-5-phosphonopentanoic acid decreased the duration of bicuculline-induced bursts. These data provide evidence that, similar to rat and cat neocortex, excitatory and inhibitory amino acids are important transmitters to pyramidal cells in immature human neocortex.

2-Amino-5-phosphonovalerate↗

PubMed1976

Patterns of cell and fiber distribution in the neocortex of the reeler mutant mouse.

In the neocortex of the reeler mutant mouse, there is inversion in the normal relative positions of polymorphic and pyramidal cells and of large with respect to medium-sized and small pyramidal cells. Granule cells are concentrated at a near-normal mid-cortical level in the mutant. As in the normal animal, and despite cell malposition in reeler, the principal tangential fiber system lies in the zone of polymorphic cells. Large fiber fascicles, known from experimental studies to be principally thalamo-cortical afferents, enter the tangential fiber system in the polymorphic cell zone of both reeler and normal neocortex. In the mutant these fascicles must traverse the full width of the cortex to reach this fiber system in its superficial location. In both normal and mutant animals single fibers, again principally thalamo-cortical afferents, pass from the principal tangertial fiber system to ramify in a fiber feltwork in the zone of granule cells. In the mutant these descend whereas in the normal animal they ascend. Also, as in the normal mouse, single fibers pass radially between all levels of the mutant cortex and the central white matter. Regional variations in the character, the pattern of distribution and the relative prominence of homologous cell and fiber elements are closely parallel in reeler and normal. This suggests that cell differentiation and the tangenital organization of reeler neocortex are normal despite cell malposition in the mutant.

Animals↗

PubMed1989

Corticotropin-releasing factor immunoreactivity in monkey neocortex: an immunohistochemical analysis.

Corticotropin-releasing factor (CRF) has been implicated in the pathophysiology of certain human neuropsychiatric disorders that affect neocortical function. However, the anatomical organization of CRF-containing structures in the expanded and highly differentiated primate neocortex has not been previously described. In this study, the distribution of CRF-immunoreactive neurons and processes was characterized in the neocortex of New World squirrel monkeys (Saimiri sciureus). Substantial regional differences were present in the density, laminar distribution, and morphological appearance of CRF-immunoreactive neurons. The greatest density of labeled neurons was present in anterior cingulate cortex. A wide range of intermediate densities of CRF-immunoreactive neurons was evident in the association regions of the prefrontal, parietal, and temporal cortices. The lowest numbers of CRF-immunoreactive neurons were observed in the primary visual and primary motor cortices. For example, the density of labeled neurons was nearly five times greater in the anterior cingulate cortex than in the precentral cortex. CRF-immunoreactive neurons were also distributed in at least four different laminar patterns. For example, in the agranular anterior cingulate cortex, labeled cell bodies were distributed throughout layers II, III, and V. In other regions, such as the posterior cingulate cortex, labeled neurons were present in layers II, III, and IV. In contrast, labeled neurons were predominantly present in layers II and superficial III of the visual cortex, whereas in the inferior temporal cortex, they were present predominantly in layer IV. Regional and laminar differences were also present in the relative distributions of the two major morphological types (as defined by cell body shape) of CRF-immunoreactive neurons. Vertically oriented oval neurons, which frequently had a single dendritic process arising from each somal pole, were most frequently found in layer III. In contrast, the labeled neurons in layers II and IV tended to have a round- or triangular-shaped soma. In layer IV of some association cortices, these multipolar neurons were associated with a high density of rod-like structures composed of large immunoreactive varicosities clustered together in vertical arrays. These structures were frequently found to be located immediately below the soma of pyramidal neurons. Comparison of these findings with Golgi impregnation studies strongly suggests that CRF is present in the soma and axonal cartridges of a subset of chandelier neurons. The heterogeneous distribution and morphological diversity of CRF-containing neurons suggest that CRF may mediate distinct functions in different regions and layers of monkey neocortex.

Animals↗

PubMed1989

Brain neocortex influence on the mononuclear phagocyte system.

The cerebral neocortex is known to modulate asymmetrically certain components of the immune system. It was previously shown that large ablation of the left cortex reduces B and T cell-mediated responses, whereas symmetrical right lesions enhance these responses. We have studied the immunomodulatory role of the brain cortex on the mononuclear phagocytic system. Resident and BCG-activated macrophages were investigated in female C3H/He mice at 8-10 weeks after right or left cortical ablation. After an intraperitoneal injection of BCG, the number of peritoneal macrophages was found to be lower in both right- and left-lesioned mice, the difference being stronger and more significant in left-lesioned animals than in sham-operated controls. Furthermore, the oxidative metabolism as assessed by chemiluminescence was depressed only in left-lesioned mice. On the other hand, cortical lesions were shown to have no effect on either the number or the endocytic activity of resident peritoneal macrophages. The possible implication of the brain neocortex on infectious diseases was assayed by using the Trypasonoma musculi model, in which macrophages are known to be effective in parasite eradication. Although the number of peritoneal macrophages was significantly depressed after left cortical lesions 11 days after T. musculi inoculation, the course of the infection was not modified significantly. Our results argue in favor of brain neocortex modulation of the mononuclear system.

Animals↗

PubMed1994

Modulation of cellular excitability in neocortex: muscarinic receptor and second messenger-mediated actions of acetylcholine.

Muscarinic-type acetylcholine (ACh) receptor are involved in a variety of cortical functions. ACh "activates" neocortex; simultaneously modifying spontaneous subthreshold activity, intrinsic neuronal oscillations and spike discharge modes, and responsiveness to fast (putative glutamatergic) synaptic inputs. However, beyond the general involvement of muscarinic receptors, a mechanistic understanding of integrated cholinergic actions, and interactions with non-cholinergic transmission, is lacking. We have addressed this problem using intracellular recordings from the in vitro auditory neocortex. First, we investigated cholinergic modification of responses to the excitatory amino acid glutamate. ACh, or the muscarinic agonist methacholine, produced a lasting enhancement of glutamate-mediated membrane depolarizations. Muscarinic receptors of the M1 and/or M3 subtype, rather than M2 or nicotinic receptors, mediated this enhancement. Subsequently, we investigated whether second messenger systems contribute to observed muscarinic actions. Activation of protein kinase C with phorbol 12,13-dibutyrate (4 beta-PDBu), enhanced neuronal responses to glutamate. The effect of 4 beta-PDBu was attenuated by the kinase antagonist H7. Finally, we attempted to identify postsynaptic actions of endogenous ACh. Tetanic stimulation of cholinergic afferents elicited voltage-dependent effects, including reduced spike frequency adaptation and reduced slow afterhyperpolarization (sAHP) elicited by transmembrane depolarizing stimuli. These effects were mimicked by methacholine, enhanced by eserine, and antagonized by muscarinic receptor antagonists. These data suggest that cholinergic modulation in neocortex likely involves the integrated actions of diverse mechanisms, primarily gated by muscarinic receptors, and at least partly involving second messenger systems.

Acetylcholine↗

PubMed1991

A correlation between gene transcriptional activity and cerebral glucose metabolism in Alzheimer's disease-affected neocortex: cause or effect?

Our laboratory has measured mRNA pool sizes in neocortex afflicted with Alzheimer's disease (AD). We have observed a repression of gene expression in the temporal and parietal regions compared to age-matched control neocortex. These changes in messenger RNA pool size closely parallel the observed alterations in local cerebral metabolic rates for glucose (LCMR-g), as detected by positron emission tomography (PET). For example, deficits in both gene transcription and glucose metabolism appear to be the greatest in AD-affected superior temporal neocortex (Brodmann area 22) but are less apparent in the primary visual cortex (Brodmann area 17) or in the cerebellum. The unresolved question is whether changes in gene expression are the cause or effect of altered glucose metabolism. However, the non-random reductions in the pool size for certain neocortical mRNAs argue in favour of altered gene expression as the primary event.

Alzheimer Disease↗

PubMed2002

Gap junctions and their implications for neurogenesis and maturation of synaptic circuitry in the developing neocortex.

More and more data accumulate which provide evidence for an important role of gap junctions for the development and function of the mammalian brain. In the neocortex, gap junctions are already present at very early stages of development and they seem to be involved in neurogenesis and neuronal migration. At postnatal stages of development, gap junctions obviously participate in the differentiation of neurons and formation of synapses. Recently, it has been shown that they are responsible for the synchronization of inhibitory network activity, even within the adult mammalian neocortex. Gap junction-mediated interneuronal communication seems to be complementary to the signal transfer created by chemical synapses and, in some cases, these two systems interact or act synergistically. There are, however, many open questions which need to be answered before we can achieve a comprehensive understanding of the function of gap junctions and electrical synapses for the development and function of the neocortex.

Animals↗

PubMed1990

Differential effects of calcium channel antagonists (omega-conotoxin GVIA, nifedipine, verapamil) on the electrically-evoked release of [3H]acetylcholine from the myenteric plexus, phrenic nerve and neocortex of rats.

Electrically-evoked release of [3H]acetylcholine from autonomic neurons (myenteric plexus), motoneurons (phrenic nerve) and the central nervous system (neocortex) was investigated in the presence and absence of the calcium channel antagonists omega-conotoxin GVIA, nifedipine and verapamil, whereby the same species (rat) was used in all experiments. Release of [3H]acetylcholine was measured after incubation of the tissue with [3H]choline. omega-Conotoxin GVIA markedly reduced (70%) the evoked release of [3H]acetylcholine from the myenteric plexus of the small intestine (IC50: 0.7 nmol/l) with a similar potency at 3 and 10 Hz stimulation. An increase in the extracellular calcium concentration attenuated the inhibitory effect of omega-conotoxin GVIA. Release of [3H]acetylcholine from the rat neocortex was also inhibited (90%) by omega-conotoxin GVIA, but the potency was 19-fold lower (IC50: 13 nmol/l). However, the release of [3H]acetylcholine from the phrenic nerve was not reduced by omega-conotoxin GVIA (100 nmol/l) at 1.8 mmol/l calcium (normal concentration), whereas omega-conotoxin GVIA inhibited evoked [3H]acetylcholine release by 47% at 0.9 mmol/l calcium. Neither nifedipine (0.1 and 1 mumol/l) nor verapamil (0.1, 1 and 10 mumol/l) modified the evoked release of [3H]acetylcholine from the myenteric plexus and the phrenic nerve. Acetylcholine release from different neurons appears to be regulated by different types of calcium channels. N-type channels play the dominant role in regulating acetylcholine release from both the myenteric plexus and the neocortex, whereas acetylcholine release from motor nerves is regulated by calcium channel(s) not yet characterized.

Acetylcholine↗

PubMed1992

Projections from fetal neocortical transplants placed in the frontal neocortex of newborn rats. A Phaseolus vulgaris-leucoagglutinin tracing study.

Fetal rat neocortex grafted into lesion cavities made in the newborn rat neocortex can exchange multiple axonal connections with the host brain. Most previous studies demonstrating efferent transplant-to-host brain connections have used fluorescent retrograde tracers injected into the host brain (Castro et al. 1985, 1987; Floeter and Jones 1984; O'Leary and Stanfield 1989). Other studies have used anterograde axonal tracing with either tritium-labelled amino acids impregnating the transplant and its efferents (Floeter and Jones 1985) or horseradish peroxidase injected into the transplants (Chang et al. 1984, 1986). In the present study we used the anterograde axonal tracer Phaseolus vulgaris-leucoagglutinin (PHA-L) to examine in detail the course and termination of the efferent neocortical graft fibers. Twenty-six newborn rats had the right frontal cortex forepaw area removed by vacuum aspiration, while anesthetized by hypothermia. A piece of fetal frontal cortex 14-16 embryonic days old (E14-16) was immediately thereafter placed in the lesion, and the recipient rats allowed to survive for 5-7 months. At this time the rats were reoperated under sodium pentobarbital (Nembutal) anesthesia and the transplants iontophoretically injected with PHA-L. Two weeks later the animals were again anesthetized, perfused, and processed for PHA-L immunocytochemistry and routine histology. Analysis of acetylcholinesterase- (AChE) and Nissl-stained sections showed graft survival in 19 of the 26 animals used in this study. When these 19 brains were processed for PHA-L immunocytochemistry, 5 of them were found with certainty to have the PHA-L injection confined to the transplant. Based on these cases PHA-L-reactive fibers arising from labelled transplant neurons were traced into the ipsilateral host neocortex adjacent to the transplant and found to project through the subcortical white matter to the ipsilateral parietal neocortical area 1, and claustrum. Callosal fibers were traced to the contralateral frontal neocortical forelimb and parietal areas. Transplant fibers were also observed to descend through the caudate putamen in the dispersed fiber bundles of the internal capsule to distribute as terminal branches and varicose fibers within the mesencephalic periaqueductal gray, red nucleus, deep mesencephalic nucleus, and intermediate gray of the superior colliculus, as well as in the pontine gray. Similar fibers and terminations were present in the caudate putamen, the reticular, ventrobasal, centrolateral, posterior, and parafascicular thalamic nuclei.(ABSTRACT TRUNCATED AT 400 WORDS)

Acetylcholinesterase↗