The evolution of ideas concerning the function of the neocortex.
Explore the source record for details and available documents.
Animals↗
SEARCH · Search PubMed
Results for “Neocortex”
Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Patterns of connectivity in the neocortex of the echidna (Tachyglossus aculeatus).
Patchy connections were traced in the visual and auditory cortex of the echidna (Tachyglossus aculeatus). Labeled neurons and clusters of axon collaterals were distributed in regular arrays after the application of a small crystal (approximately 100-300 microns diameter) of the carbocyanine dye Dil (1,1'-dioctadecyl-3,3,3',3'-tetramethylindocarbocyanine perchlorate) into the upper cortical layers. In general, the anterograde and retrograde labels were in register, but whereas the anterograde label was distributed throughout all six layers, the retrogradely filled neurons were absent from layer 1 and the highest density of labeled cells was in layers 5 and 6. The cells contained within the patches were all pyramidal or pyramid-like and contained long spines on their dendrites. Therefore, despite their unusual location within the lateral posterior cortex, the internal structure of the echidna visual and auditory cortices resembled that of eutherian mammals in containing a regular columnar array of connections that may represent the corticocortical projections.
Animals↗
Connections from the neocortex to the vestibular brain stem nuclei in the common marmoset.
Monosynaptic projections from the cerebral cortex to the vestibular nuclei were studied in the common marmoset monkey (Callithrix jacchus) by injecting fluorescent dextrans into the brain stem vestibular nuclei. The injection sites were determined by single unit vestibular responses identified later histologically. During the recordings sinewave rotation in pitch, roll or yaw or steady tilt was applied. The most notable loci of labelling were found inside the primary sensory cortex, the cortex deep down along the posterior lateral sulcus, the premotor region and the anterior cingulate cortex. From studies in other primates these cortical areas are known to process vestibular information. Their connections with the vestibular nuclei may serve as an internal feedback modulating the vestibular brain stem activity.
Animals↗
Do foetal neural grafts induce repair by the injured juvenile neocortex?
Repair of mechanically injured primary somatosensory cortex in 3 week old mice was studied by placing small, solid foetal neurotransplants into large cortical cavities. After transplantation, the graft and host tissues were distinguished immunocytochemically owing to their expression of two different Thy-1 antigens. Cell proliferation was monitored by 3H-thymidine autoradiography. The following observations were made two months after operation: (i) In 8 out of 11 grafted animals new cortical tissue had taken the place of the cavity. (ii) Five of these 8 animals contained only host tissue; the remainder presented a small piece of grafted tissue. (iii) In the restored cortical area, newly generated cells were predominantly of host origin. These data suggest that the restorative capacity of the already post-mitotic cerebral cortex is not lost and may be reactivated. The presence of a foetal neural graft seems to favour this process.
Age Factors↗
Real time laser-Doppler perfusion imaging of cortical spreading depression in rat neocortex.
Laser-Doppler perfusion imaging (LDPI) is a new technique which provides recordings of blood flow in rapid sequence. In this study we applied LDPI to the brain for the first time to demonstrate propagating waves of cortical spreading depression (CSD) elicited by a needle stab in the frontal cortex of barbiturate-anesthetized rats. Under resting conditions, LDPI recordings of the superficial cortex showed a heterogeneous pattern, partly due to the high flow rate in pial arteries compared with cortical tissue. Within 1 min after elicitation of the CSD a zone of increased signal intensity (96 +/- 5%) up to 6 mm across appeared in the exposed cortex. The rate of propagation away from the site of elicitation for 16 such waves was 2.8 +/- 0.1 mm min-1. The increased signal intensity was partly due to dilatation of pial arterioles and veins, partly to increased blood flow in the microvascular bed. The data are consistent with previous studies of CSD using other techniques for measurement of cortical blood flow. LDPI gives real time images of cerebral blood flow, and may be applied to demonstrate CSD or CSD-like phenomena during neurosurgical operations in man.
Animals↗
Calretinin-positive Cajal-Retzius cells persist in the adult human neocortex.
The occurrence of Cajal-Retzius (CjRe) cells was studied in four cortical areas of five normal adult humans using antibodies against calretinin. Calretinin immunofluorescence and autofluorescence of lipofusin granules in CjRe cells were visualized by dual channel confocal laser scanning microscopy. Three types of CjRe cells existed in the adult human cortex: horizontal, triangular and multipolar, and their number did not decrease with ageing. Horizontal CjRe cells were found in all cortical areas; they contained no lipofusin or less than other cells. Triangular CjRe cells with descending dendrites were less numerous. Multipolar CjRe cells were rare and contained more lipofuscin. We conclude that calretinin-immunoreactivity can be used to study CjRe cell morphology in normal and diseased adult human brain.
Adult↗
Glutathione-induced sodium currents in neocortex.
The present report demonstrates that glutathione (GSH), a tripeptide composed of glutamate, glycine and cysteine (gamma-L-glutamyl-L-cysteinyl-glycine) and best known as a free radical scavenger, elicits a large fast depolarizing potential when applied to cortical slices. This potential is maximally larger than that produced by either NMDA or AMPA. Like AMPA, the GSH current appears to be carried by sodium ions, but cannot be blocked by the glutamate receptor antagonists AP5 or DNQX. In addition, removal of external calcium or blockade of potassium currents by TEA does not diminish the GSH-induced potential. Together, these results suggest that GSH acts through its own receptor-mediated channels, independently of the known EAA receptors, and that its receptors may be a key, and previously unknown, component of cortical excitatory neurotransmission.
Animals↗
Presynaptic NMDA receptors in the neocortex are both auto- and heteroreceptors.
We used electron microscopic immunocytochemistry with antibodies against NR1 and NR2A and B subunits to study the distribution of N-methyl-D-aspartate (NMDA) receptors in presynaptic axon terminals in the rat cerebral cortex. In all sections examined, NR1 and NR2A/B immunoreactivities were observed in axon terminals: NR1- and NR2A/B-positive axon terminals made both symmetrical and asymmetrical synapses on unlabelled dendritic profiles. Combined pre- and postembedding studies showed that all NR1 and NR2A/B-positive axon terminals making symmetrical synapses were gamma-aminobutyric acid (GABA)-positive. These observations show that both auto- and hetero- NMDA receptors do exist in the cerebral cortex, and indicate that part of the effects of NMDA receptor activation might be determined by modulating glutamate and GABA release.
Animals↗
Memory impairment in humans after bilateral damage to lateral temporal neocortex.
The hippocampus and its adjacent medial temporal regions are crucial for episodic memory. However, it is far less obvious whether other temporal regions beyond the medial part are important for memory processing. The memory performance of a group of patients with bilateral lesions over the lateral temporal lobe sparing the hippocampus was assessed and compared with that of patients with relatively spared cortex and patients with bilateral damage to the lateral temporal lobe and the hippocampus. The results demonstrate that bilateral damage to the lateral temporal lobe results in memory impairment across verbal and visual modalities.
Adult↗
Wide third ventricle correlates with low choline acetyltransferase activity of the neocortex in Alzheimer patients.
We evaluated central, temporal, and cortical atrophy by linear measurements on brain computed tomography (CT) in 17 patients with moderate to severe histologically verified Alzheimer disease (AD) compared with findings in 84 nondemented elderly controls. Measurements were adjusted for age and head size. The AD patients had wider third and lateral ventricles as well as larger temporal horns and Sylvian fissures compared with controls. Cortical atrophy tended also to be more pronounced for AD patients relative to controls. Thus measures of central and temporal atrophy clearly distinguished AD patients from normal aged individuals. In AD patients, the width of the third ventricle was significantly correlated with the choline acetyltransferase (ChAT) activity in the post-mortem frontal cortex (r = 0.65, p = 0.005) and in the temporal cortex (r = 0.59, p = 0.006). CT measures did not correlate significantly with neurofibrillary tangle or senile plaque scores. The result suggests that the width of the third ventricle better reflects the degree of cholinergic deficit than severity of histopathological changes, scores of plaques, and tangles in AD.
Aged↗
Parvalbumin-immunoreactive neurons in the neocortex are resistant to degeneration in Alzheimer's disease.
Recent studies have stressed the fact that specific neuronal subtypes may display a differential sensitivity to degeneration in Alzheimer's disease. For example, large pyramidal neurons have been shown to be vulnerable, whereas smaller neurons are resistant to pathology. Using a monoclonal antibody against the calcium-binding protein parvalbumin, we investigated the possible changes in a subpopulation of interneurons in two cortical areas known to be strongly damaged in Alzheimer's disease. In the prefrontal cortex as well as in the inferior temporal cortex, we observed no differences in parvalbumin-immunoreactive cell counts or cell size in Alzheimer's disease brains as compared to control cases. Moreover, the general cellular morphology of these neurons was preserved in the Alzheimer's disease cases, in that their perikarya and dendritic arborizations were intact. These results suggest that paravalbumin-immunoreactive cells represent a neuronal subset resistant to degeneration, and further support the hypothesis that the pathological process in Alzheimer's disease involves specific neuronal subtypes with particular morphological and molecular characteristics.
Aged↗
Development of the superior temporal neocortex is anomalous in trisomy 21.
Trisomy 21 (Down syndrome) is the most common inherited form of mental retardation in the United States, however, the basis of impaired cognition is unknown. We have used recently developed stereological cell counting techniques to quantitatively examine the pattern of neuronal migration and maturation in one neocortical area during gestation in normal development and in trisomy 21. Normal development of the cerebral cortex occurs in two general sequences: Beginning at approximately 7-8 weeks gestation, migration of cells destined to become neurons results in the accumulation of cells in the cortical mantle. This process is largely complete by 20-21 weeks. Over the next 7-10 weeks an "inside-out" differentiation into lamina of different neuronal densities occurs. Our data suggest that the second phase of cortical development, the emergence of lamination, is both delayed and disorganized in trisomy 21. The observed pattern of cortical maturation may reflect an abnormality in axonal and dendritic arborization that subsequently subserve the connectional and functional units underlying normal cognition.
Cell Movement↗
Developmental neuropathology and impact of perinatal brain damage. II: white matter lesions of the neocortex.
The neuropathology and developmental impact of acute, subacute, and chronic white matter lesions has been studied in infants who survived (days, weeks, months, or years) this type of perinatal brain damage. The study emphasizes the survival of the developing gray matter overlying extensive white matter lesions (multicystic encephalopathy, porencephaly, and hydranencephaly ex-vacuo). Although partially isolated from afferent inputs (corticipetal fiber destruction) and unable to reach other cortical centers (corticofugal fiber destruction), this overlying gray matter is able to survive because neither its independent leptomeningeal blood supply nor its intrinsic anastomotic vasculature are affected by the underlying lesion. Moreover, the postinjury structural and functional development of this partially isolated gray matter is altered. Some of its axotomized pyramidal neurons are transformed into local-circuit interneurons, some of its interneurons are structurally and functionally enlarged (hypertrophy), and its intracortical neuropil (deprived of afferent synaptic terminals) increases by an expansion of intrinsic terminals (hypertrophy). An attempt has been made to correlate these postinjury alterations with the pathogenesis of the ensuing neurologic sequelae (7 infants develop epilepsy). The study proposes that neurological sequelae (e.g. epilepsy and cerebral palsy) following perinatal white matter lesions are a direct consequence of the postinjury gray matter transformations.
Brain Damage, Chronic↗
Attenuation of ischemia-reperfusion injury in the rat neocortex by the hydroxyl radical scavenger nicaraven.
OBJECTIVE: Oxygen free radicals are considered important contributors to cerebral ischemia-reperfusion injury. The purpose of this study was to examine the effects of the hydroxyl radical scavenger, (+/-)-N, N'-propylenedinicotinamide (nicaraven), on cerebral injury after focal ischemia-reperfusion. METHODS: A total of 58 male Sprague-Dawley rats was subjected to transient focal ischemia by occluding both carotid arteries and one middle cerebral artery for 3 hours. Animals received continuous infusions of doses of 20 mg/kg per hour or 60 mg/kg per hour of nicaraven beginning either 10 minutes before (pretreatment) or immediately after (posttreatment) ischemia. Infarction volumes were evaluated by staining coronal brain sections with 2% 2,3,5-triphenyltetrazolium chloride (n = 40). In other animals (n = 18), brain edema was evaluated 1 hour after ischemia. RESULTS: A dose of 20 mg/kg per hour of nicaraven elicited small reductions in infarction volume (14.7 and 12.3% for the pre- and posttreatment groups, respectively). Treatment with a dose of 60 mg/kg per hour of nicaraven provided significant reductions in the volume of infarction (18.6% [P < 0.05] and 20.9% [P < 0.01] reductions for the pre- and posttreatment groups, respectively). The reductions in infarction size did not differ significantly between the pre- and posttreatment groups receiving a dose of 60 mg/kg per hour of nicaraven. Posttreatment with either dose of nicaraven significantly reduced brain edema. CONCLUSIONS: This study demonstrates the neuroprotective effects of a hydroxyl radical scavenger when administered systemically during the reperfusion phase after transient focal ischemia. The results provide, to our knowledge, the first evidence that nicaraven is effective against ischemia-reperfusion injury in the brain and demonstrate that oxygen free radicals generated during reperfusion are important triggers of ischemic brain damage. Furthermore, the findings suggest that nicaraven may be a useful agent in limiting brain injury after ischemic stroke.
Animals↗
A theory for cerebral neocortex.
Explore the source record for details and available documents.
Cerebral Cortex↗
An electron microscopic study of terminal degeneration in the neocortex of the cat.
Explore the source record for details and available documents.
Animals↗
The progression of the pathological changes of Alzheimer's disease in frontal and temporal neocortex examined both at biopsy and at autopsy.
Brains were obtained at autopsy from five patients with Alzheimer's disease, each of whom had undergone diagnostic craniotomy 3-7 years previously. It was possible, therefore, to examine the number (density) and nucleolar volume of pyramidal nerve cells, and the density of senile plaques and neurofibrillary tangles within the cerebral cortex on two occasions during the progression of their illness, and to assess how these measures might have changed during the period between biopsy and death. In all five patients, at biopsy, the density and the nucleolar volume of pyramidal nerve cells was significantly less than controls and, in general, values for both these measures fell significantly further from biopsy to death. By contrast, in none of the five patients did senile plaque density consistently change from biopsy to death; neurofibrillary tangle density either did not change, or indeed sometimes decreased from biopsy to death. These data show that both the clinical and the pathological progression of Alzheimer's disease is marked by a continuing loss of pyramidal cells from frontal and temporal cortex, although the densities of plaques and tangles within the cortex do not, per se, correlate with the stage of the illness. The usefulness of measurement of plaque and tangle densities as pathological criteria by which the clinical and neurochemical deficits of Alzheimer's disease can be compared in different patients is clearly questionable.
Alzheimer Disease↗
The neocortex of the dog. 1. A classical cytoarchitectonic map.
Explore the source record for details and available documents.
Animals↗
Refine your search to explore more results.