Disease relevance of Neocortex

• Abeta 1-40-related reduction in functional hyperemia in mouse neocortex during somatosensory activation [1].
• The basal forebrain cholinergic cell groups, which innervate widespread areas of the neocortex, undergo degeneration in Alzheimer disease and also in parkinsonism associated with dementia [2].
• In the majority of the CNS regions examined (neocortex, hippocampus, thalamus, extrapyramidal and motor areas), hemorrhagic hypotension was without significant effect upon local cerebral glucose utilization [3].
• In addition, repeated ECS treatment caused progressively shorter motor seizures (tolerance) in both rats and wild-type mice, as well as reduced NMDA-induced inward currents in pyramidal neurons from superficial layers of the neocortex of wild-type mice [4].
• We have analyzed clonal cell proliferation in the ventricular zone (VZ) of the early developing mouse neocortex with a replication-incompetent retrovirus encoding human placental alkaline phosphatase (AP) [5].

Psychiatry related information on Neocortex

• The aetiology and pathogenesis of this progressive dementia is poorly understood, but symptomatic disease is associated histopathologically with amyloid plaques, neurofibrillary tangles and neuronal loss primarily in the temporal lobe and neocortex of the brain [6].
• Malformations of the human neocortex are commonly associated with developmental delays, mental retardation, and epilepsy [7].
• Based on studies of the effects of neurotoxic lesions in baboons, we previously concluded that damage to the cholinergic structures plays, at best, a marginal role in the association neocortex hypometabolism of Alzheimer's disease [8].
• In this 'Selfish Brain Theory', the neocortex and limbic system play a central role in the pathogenesis of diseases such as anorexia nervosa and obesity [9].
• CONCLUSIONS: These results suggest that generalized epilepsy in early life and functional deficits in the temporal neocortices may be associated with communication delays, and that functional imbalance in subcortical circuits may be associated with stereotypical behaviors and impaired social interaction in children with TSC [10].

High impact information on Neocortex

• X-SCLH/LIS syndrome is a neuronal migration disorder with disruption of the six-layered neocortex [11].
• Clark et al. conclude from their analysis of volumetric brain proportions ("cerebro-types") that cerebellum size is invariant across mammalian taxonomic groups, the neocortex and cerebellum do not co-vary in size (in contradiction to ref. 1), and cerebrotype-based measures identify directional changes in brain architecture [12].
• Signals from the same receptor are targeted to multiple olfactory cortical areas, permitting the parallel, and perhaps differential, processing of inputs from a single receptor before delivery to the neocortex and limbic system [13].
• Acetylcholine is thus not only necessary for learning and memory, as previously argued, but its presence within the neocortex is also sufficient to ameliorate learning deficits and restore memory following damage to the nucleus basalis [14].
• By co-immunoprecipitation with subunit-specific antibodies, we present here direct evidence that NMDA receptors exist in rat neocortex as heteromeric complexes of considerable heterogeneity, some containing both NR2A and NR2B subunits [15].

Chemical compound and disease context of Neocortex

• We therefore examined, using isozyme-specific antibodies and immunohistochemistry, the localization of copper, zinc-superoxide dismutase and manganese-superoxide dismutase in the frontal and temporal neocortices and hippocampi of aged controls and individuals with Alzheimer's disease or Down's syndrome [16].
• Abeta binds Zn(2+), Cu(2+), and Fe(3+) in vitro, and these metals are markedly elevated in the neocortex and especially enriched in amyloid plaque deposits of individuals with Alzheimer's disease (AD) [17].
• Redistribution of glutamate and glutamine in slices of human neocortex exposed to combined hypoxia and glucose deprivation in vitro [18].
• Post hoc felbamate (300 mg/kg) reduced the volume of infarction from 67% +/- 7% of neocortex in unmedicated rats to 32% +/- 8%, 51% +/- 12%, 38% +/- 19%, and 53% +/- 10% when given 0, 1, 2, and 4 hours after hypoxic exposure, respectively [19].
• Markers of serotonin synapses in entire temporal lobe and frontal and temporal neocortex were examined for changes in Alzheimer's disease by use of both neurosurgical and autopsy samples [20].

Biological context of Neocortex

• We have examined responses of neurons in slices of adult neocortex to focal applications of excitatory amino acids and glycine and report enhancement by glycine of NMDA receptor-mediated excitatory postsynaptic potentials [21].
• We used electroporation of plasmids encoding short hairpin RNA to create interference (RNAi) of DCX protein in utero, and we show that DCX is required for radial migration in developing rat neocortex [22].
• In this report, we have examined the requirement for the retinoblastoma (Rb) gene family in neuronal determination with a focus on the developing neocortex [23].
• Although high-affinity 3H-PZ, low-affinity 3H-NMS binding (M1 sites) and high-affinity 3H-OXO-M, high-affinity 3H-NMS binding (M2 sites) occurred across all layers of the temporal neocortex, the laminar distribution of M1 and M2 receptor binding sites was different [24].
• Synaptic transmission in human neocortex removed for treatment of intractable epilepsy in children [25].

Anatomical context of Neocortex

• Acidic amino acids, such as glutamate and aspartate, are thought to be excitatory transmitters in the cerebral neocortex and hippocampus [26].
• The number of GABA-expressing cells in neocortical slices is reduced by separating the neocortex from the subcortical telencephalon [27].
• These results provide morphological evidence for a gamma-aminobutyric acid pathway arising in magnocellular neurons of the posterior hypothalamus and innervating the neocortex [28].
• We show that genetic ablation of neurotrophin-3 (NT-3) in the mouse neocortex results in reduction of a set of anatomically distinct axonal bundles projecting from thalamus through cortical white matter [29].
• GABAergic, somatostatin-containing bitufted interneurons in layer 2/3 of rat neocortex are excited via glutamatergic excitatory postsynaptic potentials (EPSPs) by pyramidal neurons located in the same cortical layer [30].

Associations of Neocortex with chemical compounds

• We report here that in the presence of picrotoxin, a gamma-aminobutyric acid (GABA) antagonist, these segments spontaneously generate synchronized rhythmic bursts comparable with the interictal epileptiform discharges observed in the hippocampus and neocortex in the presence of penicillin [31].
• This indicates that in the neocortex the activation threshold of the NMDA-mechanism and consequently the susceptibility to LTP, are strongly influenced by inhibitory processes [32].
• Methylazoxymethanol treatment of fetal rats results in abnormally dense noradrenergic innervation of neocortex [33].
• Cholinergic markers in neocortex were reduced, while catecholamine and indoleamine metabolism was largely unaffected at this time [34].
• Inhibitors and promoters of thalamic neuron adhesion and outgrowth in embryonic neocortex: functional association with chondroitin sulfate [35].

Gene context of Neocortex

• Regulation of area identity in the mammalian neocortex by Emx2 and Pax6 [36].
• Mice deficient in p35--an activator of cyclin-dependent kinase 5 (Cdk5)--are characterized by a neocortex that has inverted layering [37].
• Tbr-1 and Id-2 expression in the neocortex have discontinuities that define molecularly distinct neocortical areas [38].
• EMX2 regulates sizes and positioning of the primary sensory and motor areas in neocortex by direct specification of cortical progenitors [39].
• Moreover, the neocortex of young Fyn mutants exhibited a significant in vivo reduction in these AMPA receptor proteins but not in their mRNA levels [40].

Analytical, diagnostic and therapeutic context of Neocortex

• We used in situ hybridization techniques to map the anatomical distribution of precursor amyloid-beta-protein mRNA in the neocortex of brains from three subjects with no known neurologic disease and from five patients with Alzheimer disease [41].
• The objective of this MRI-guided 2-[(18)F]fluoro-2-deoxy-d-glucose/positron-emission tomography (FDG/PET) study was to examine the hypothesis that among normal elderly subjects, EC METglu reductions predict decline and the involvement of the Hip and neocortex [42].
• Quantitative RT-PCR analyses from the same TLE neocortex specimens revealed that GABA(A)-receptor beta 1, beta 2, beta 3, and gamma 2 subunit mRNAs were significantly overexpressed (8- to 33-fold) compared with control autopsy tissues [43].
• As revealed with 5-HT immunocytochemistry, BDNF infusions into the neocortex of intact (non-PCA-lesioned) rats caused a substantial increase in 5-HT axon density in a 3 mm diameter region surrounding the cannula tip [44].
• Northern blot analysis showed that the MARCKS mRNA level was higher in the association areas than in the primary sensory and motor areas of the cerebral neocortex [45].

References