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Temporal Neocortex

Textbooks on neuroscience often describe the location and function of hundreds of individual brain regions (see references above). However, for current purposes these will be kept to a minimum (Figure 2.1). Anatomically, the brain can be subdivided into the forebrain containing the telencephalon and diencephalon, the midbrain or mesencephalon and the hindbrain (metencephalon and myelencephalon). The telencephalon includes the left and right cerebral hemispheres encompassed by the cerebral cortex (neocortex). Cortex is a translation of the word bark and is so-called because its surface, made up of numerous sulci (grooves or invaginations) and gyri (raised areas), is on the outer surface of the brain like the bark of a tree. Each hemisphere is divided into four lobes, named from the front (rostral) to back (caudal) of the brain frontal, temporal, parietal and occipital. [Pg.13]

LTP has been shown in many parts of the brain but it has been most extensively studied in the hippocampus, a phy-logenetically old part of the cerebral cortex that in humans is embedded in the temporal horn and in rats and rabbits lies beneath the parietal and temporal neocortex (Fig. 15-3A). The hippocampus is essential for (declarative) memory formation in rats the role of hippocampus in acquisition of spatial information has been studied in... [Pg.272]

Patients with ALS/PDC also show a moderate loss of choline acetyl transferase activity in the midfrontal and inferior parietal cortex and a severe loss in the superior temporal cortex (Masliah et al., 2001). This deficit is similar to that seen in Alzheimer disease and less severe than in Lewy body disease. Thus, cholinergic deficits in the neocortex may contribute to some of the cognitive alterations in ALS/PDC. [Pg.182]

Two major subdivisions of the temporal lobe were investigated PHR and the temporal neocortex (including IT and STG). [Pg.47]

Two main subdivisions of the temporal neocortex were investigated—the visual area IT and the auditory area STG. We did not observe important differences between IT and STG with regard to the distribution and phenotype of BrdU+ cells, and therefore these regions are presented in a common section. [Pg.49]

Fig. 35A-C Double-staining for BrdU and NeuN in temporal neocortex. Digital reconstructions of the cells in the x and y axes were generated to confirm colocalization of signals. A Double-labeled cell in postischemic day-15 IT. B Double-labeled cell in postischemic day-44 STG. Note the complete colocalization of the BrdU signals within the NeuN channels. C The BrdU+ cell appears to be double-labeled when observed in the z axis. However, reconstructions in x and y axes revealed that the BrdU signal (arrowheads) is cytoplasmic, and this cell was not considered double-labeled. Scale bar = 5 pm... Fig. 35A-C Double-staining for BrdU and NeuN in temporal neocortex. Digital reconstructions of the cells in the x and y axes were generated to confirm colocalization of signals. A Double-labeled cell in postischemic day-15 IT. B Double-labeled cell in postischemic day-44 STG. Note the complete colocalization of the BrdU signals within the NeuN channels. C The BrdU+ cell appears to be double-labeled when observed in the z axis. However, reconstructions in x and y axes revealed that the BrdU signal (arrowheads) is cytoplasmic, and this cell was not considered double-labeled. Scale bar = 5 pm...
Fig. 36A-C Glial proliferation in temporal neocortex after ischemia. A Triple-staining for Ibal, NeuN, and BrdU in postischemic day-15 STG. Note Ibal/BrdU double-labeled clusters (arrows) or single cells in the vicinity of NeuN+ neurons (arrowheads). B Double-staining for SI00/3 and BrdU in postischemic day-23 IT. Note an S100/ +/BrdU+ doublet. C A CNP+ oligodendrocyte colabeled for BrdU in the postischemic day-79 IT. Scale bars = 20 pm (A) 10 pm (B) 5 pm (C)... Fig. 36A-C Glial proliferation in temporal neocortex after ischemia. A Triple-staining for Ibal, NeuN, and BrdU in postischemic day-15 STG. Note Ibal/BrdU double-labeled clusters (arrows) or single cells in the vicinity of NeuN+ neurons (arrowheads). B Double-staining for SI00/3 and BrdU in postischemic day-23 IT. Note an S100/ +/BrdU+ doublet. C A CNP+ oligodendrocyte colabeled for BrdU in the postischemic day-79 IT. Scale bars = 20 pm (A) 10 pm (B) 5 pm (C)...
Table 8 Percentages of colabeling of BrdU with glial markers in temporal neocortex. BrdU+ cells were sampled for colabeling with Ibal, SI00/1, or CNP as described in the text... Table 8 Percentages of colabeling of BrdU with glial markers in temporal neocortex. BrdU+ cells were sampled for colabeling with Ibal, SI00/1, or CNP as described in the text...
In in vivo and in vitro studies, Al can potentiate the oxidative stress produced by Fe [41, 42], Transcription factor, nuclear factor (NF)-fcB is activated by oxidative stress. The relevance of NF- cB to neurodegeneration is suggested by a correlation between the amount of activated transcription factor NF-/cB and a key inflammatory enzyme, COX-2, in both aging and AD temporal lobe neocortex [43],... [Pg.71]

Lukiw WJ, Bazan NG (1998) Strong nuclear factor-kappaB-DNA binding parallels cyclooxygenase-2 gene transcription in aging and in sporadic Alzheimer s disease superior temporal lobe neocortex. J Neurosci Res 153 583-592... [Pg.76]

Similar to the D5 receptor, the D1B receptor is expressed in the neocortex, with highest expression in frontal, parietal and temporal areas of the rat cortex (Meador-Woodruff et al., 1994b Niznik et al., 2003). Moreover, similarly to Di mRNA, D5 mRNA is most abundant in discrete cortical layers (II, IV, VI) (Beischlag et al., 1995). Di and D5 mRNA are frequently coexpressed in pyramidal neurons, with predominant localization in the dendritic shaft of these cells (Bergson et al., 1995b). [Pg.88]

Gurevich EV, Kordower JH, Joyce JN (2000) Ontogeny of the dopamine D2 receptor mRNA expressing cells in the human hippocampal formation and temporal neocortex. J Chem Neuroanat 20 307-325. [Pg.562]

The typical changes seen in all subtypes of FTD are atrophy of the prefrontal and anterior temporal neocortex. The subtype determines the distribution of the pathology. In FTD there is prominent bilateral and usually symmetrical involvement of the frontal lobes. In PNFA, atrophy is asymmetric, involving chiefly the left frontotemporal lobes, concentrated in Broca s area. In SD, atrophy is typically bilateral and is most marked in the anterior temporal neocortex, with inferior and middle temporal gyri being predominantly affected (Snowden et al., 2002). [Pg.648]

It has been proposed that NFTs are an independent feature accumulating slowly with age within the median temporal lobes. However, under the influence of altered amyloid metabolism, which leads to the formation of Amyloid plaques during the initial stages of the disease, there is an acceleration of NFT formation that spreads further to neocortex (Price and Morris, 2004). However, quantification of Ap in the different brain areas demonstrates that the spreading pathway of tau pathology remains constant, whatever the cortical distribution of A aggregates (Delacourte et al., 2002). In AD brain, tau is abnormally hyperphosphorylated, cleaved, and conformationally changed and is present mostly as PHF (Komori,... [Pg.652]

The presence of Glu has also been examined in the cerebral cortex of humans (Aas et al., 1993). Slices of macroscopically normal parietal or temporal neocortex were obtained... [Pg.29]

Fig. 6. Regional brai n incorporation coefficient A of [ 1 - CJarachidonate, as percent contralateral valne, at 2 wk after a nnilateral ablation of the nucleus basalis in rats, with or without prior administration of arecoline. The gray background identifies regions with decreased acetylcholinesterase (AChE) activity. Lined bar s are means SEM. I, IV, V layers of neocortex Pr-F, prefrontal Fr, frontal Sm, sensorimotor M, motor Par, parietal Occ, occipital. Tern, temporal. (From Nariai et al., 1991b). Fig. 6. Regional brai n incorporation coefficient A of [ 1 - CJarachidonate, as percent contralateral valne, at 2 wk after a nnilateral ablation of the nucleus basalis in rats, with or without prior administration of arecoline. The gray background identifies regions with decreased acetylcholinesterase (AChE) activity. Lined bar s are means SEM. I, IV, V layers of neocortex Pr-F, prefrontal Fr, frontal Sm, sensorimotor M, motor Par, parietal Occ, occipital. Tern, temporal. (From Nariai et al., 1991b).
Hoogland G, van Oort RJ, Proper EA et al (2004) Alternative splicing of glutamate transporter EAAT2 RNA in neocortex and hippocampus of temporal lobe epilepsy patients. Epilepsy Res 59 75-82... [Pg.146]


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See also in sourсe #XX -- [ Pg.47 , Pg.49 , Pg.54 , Pg.55 , Pg.89 ]




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