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Results for “Cerebral Cortex”

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PubMed1998

A light and electron microscopic study of GAT-1-positive cells in the cerebral cortex of man and monkey.

Specimens of human cerebral cortex were obtained during neurosurgical operations and studied by immunocytochemistry and electron microscopy, using antibodies to the GABA transporter GAT-1. Cortical material from macaque monkeys was prepared similarly. Large numbers of GAT-1-positive non-pyramidal neurons were observed in layers I, II, V, and VI of the cortex. Electron microscopy also showed that the GAT-1-positive axon terminals formed symmetrical and not asymmetrical synapses, suggesting that they were the terminals of non-pyramidal neurons. Processes of cells in the walls of blood vessels were also labelled. We conclude that GAT-1 is present in cell bodies and axon terminals of non-pyramidal neurons, and a population of mural cells in blood vessels, in the primate cerebral cortex.

Animals↗

PubMed1998

Regional changes of NADPH-diaphorase and neuropeptide Y neurons in the cerebral cortex of aged Fischer 344 rats.

This study examined the effects of aging on neuropeptide Y (NPY) and NADPH-diaphorase (NADPH-d)-positive neurons of the cerebral cortex in young (3 months) and aged (24 months) Fischer 344 rats by immunohistochemical and histochemical methods. In the aged group, the number of NPY-immunoreactive (IR)/NADPH-d-positive neurons was not significantly changed in all regions of the cerebral cortex compared to the control group. However, the number of NPY-IR/NADPH-d-negative neurons was significantly decreased in frontal association, primary motor, secondary somatosensory, insular, ectorhinal, perirhinal and auditory cortex in the aged group. In the aged rats, about 5-10% of NPY-IR/NADPH-d-positive neurons were dystrophic and scattered within the cerebral cortex. These results suggested that NPY-IR neurons that do not contain NADPH-d are affected by aging and that aging influences NPY-IR/NADPH-d-negative neurons in a region-specific pattern within the cerebral cortex of rats.

Aging↗

PubMed2002

Early expression of thyroid hormone deiodinases and receptors in human fetal cerebral cortex.

Thyroid hormones are known to be important for optimal development of the human central nervous system. Classically, maternal thyroid hormones have not been thought to have a major role in defining central nervous system development. However, recent epidemiological evidence has indicated that subtle deficiencies in circulating maternal thyroid hormones in the first trimester of pregnancy are associated with adverse neurodevelopment. We have used real time PCR to quantitate the expression of mRNAs encoding the thyroid receptor isoforms (TR alpha1, alpha2, beta1 and beta2) and thyronine deiodinase subtypes (5'-DI, 5'-DII and 5-DIII) in human fetal cerebral cortex from the first and second trimesters of pregnancy. Deiodinase subtype activities have also been determined in these tissues and compared to 'normal' adult human cerebral cortex. Iodothyronine deiodinase mRNAs were expressed in human fetal cerebral cortex from 7 to 8 weeks of gestation. The expression of 5'-DI mRNA was variable in fetal life but increased relative to adult cortex (P<0.05), whereas the activity of this enzyme was below the level of assay detection. 5'-DII mRNA and activity in fetal cerebral cortex was detectable from as early as 7-8 weeks but not significantly different from that in adult life except at 15-16 weeks when mRNA expression increased (P<0.05). Fetal cortex 5-DIII mRNA expression was present from the early first trimester but less abundant than in adult tissue (P<0.01) and 5-DIII activity appeared greater in fetal cortex (P<0.01) as compared to adults. Only TR alpha1 mRNA was more abundantly expressed in fetal cortex than adult tissues (P<0.01). In contrast, the TR isoforms (alpha2 and beta1) were expressed significantly less than in adult tissues (P<0.05). Only 26% of fetal cerebral cortex samples expressed TR beta 1. There is evidence that the developing fetal brain, as early as the first trimester, expresses TRs and exhibits the mechanisms of pre-receptor control of thyroid hormone supply.

Adult↗

PubMed1990

Appearance of parvalbumin-specific immunoreactivity in the cerebral cortex and hippocampus of the developing rat and gerbil brain.

Developmental changes in the distribution of parvalbumin-specific immunoreactivity in the brain, in particular in the cerebral cortex and hippocampus, were followed immunohistochemically in two different species, the rat and the Mongolian gerbil (Meriones unguiculatus) using an antibody raised against for rat parvalbumin. The gerbil is known to develop its auditory and visual capacity later than rat. In both the rat and gerbil, parvalbumin-specific immunoreactivity appeared after birth in both the cerebral cortex and hippocampus. The timing of the development of expression of parvalbumin varied among different parts of the cerebral cortex. The parietal cortex showed evidence of the earliest expression of parvalbumin whilst the occipital and temporal cortices expressed parvalbumin at a later stage of a development. This feature was common to both the rat and gerbil but occurred at a relatively later stage in the gerbil. The profile of the distribution of parvalbumin in the brain of the developing and adult gerbil was similar to that of the rat, but there were some differences. The frequency of bead-like structures on the dendrites of the parvalbumin-positive cells in the CA1 region of the hippocampus was markedly lower in the gerbil; instead, straight non-beaded fibers which ran vertically into the pyramidal layer were stained. Parvalbumin-positive fibers were also found in the cerebral cortex of the gerbil.

Animals↗

PubMed1994

Delayed expression of c-fos protein in rat hippocampus and cerebral cortex following transient in vivo exposure to hypoxia.

The time course of c-fos protein expression after hypoxia was examined in rat hippocampus and cerebral cortex using an immunohistochemical method. The rats were exposed to in vivo hypoxia for 30 min in a chamber containing 5% O2 and 95% N2. Immediately after the treatment, c-fos protein-like immunoreactivity was observed in the granule cell layer of the dentate gyrus. The change was transient, and the density of immunoreactive cells returned quickly to a control level 3 h after the exposure. However, the density of positive cells was again increased 1 day after hypoxia and reached the maximum 7 days after. In the cerebral cortex, on the other hand, no change was detected in the pattern of staining at any time, with an exception on 21 days after hypoxia. At this period, positively stained neurons were significantly increased in both density and intensity throughout the entire extent of the cerebral cortex including the cingulate gyrus. These results clearly indicate that hypoxia induces different patterns of c-fos protein expression among various regions of the brain. The biphasic pattern seen in the dentate gyrus as well as the delayed expression in the cerebral cortex may be related to delayed neuronal damages induced by hypoxia.

Animals↗

PubMed1996

Neurochemical and histochemical evidence for an abnormal catecholamine metabolism in the cerebral cortex of the Long-Evans Cinnamon rat before excessive copper accumulation in the brain.

Distributions of norepinephrine (NE), dopamine (DA) and its metabolites in the cerebral cortex in Long-Evans Cinnamon (LEC) rats, an animal model of Wilson's disease, aged 4, 10 (in the early stage of the disease) and 20 weeks (in the advanced stage of the disease) were determined to elucidate the effect of the abnormal copper (Cu) metabolism observed in the LEC rat on the brain catecholamine metabolism. NE depression as well as excessive accumulations of DA and facilitation of the DA catabolic pathway to its acidic metabolites were observed in the cerebral cortex of the LEC rat at 4 and 10 weeks of age. Furthermore, immunohistochemical analysis of the cuproenzyme dopamine-beta-hydroxylase (DBH) showed lower antigenicity of DBH in the cortical neurons in the cerebral cortex of LEC rats aged 4 weeks than in control rats. These results suggest that neurochemical disturbances involved in an abnormal catecholamine metabolism may occur in the cerebral cortex of the LEC rat before excessive Cu accumulation.

3,4-Dihydroxyphenylacetic Acid↗

PubMed1982

Alpha 1- and alpha 2-adrenoceptors in rat cerebral cortex: effects of neonatal treatment with 6-hydroxydopamine.

Neonatal 6-hydroxydopamine treatment was used to destroy the noradrenergic nerve terminals in rat cerebral cortex and thus give some insight into the in vivo regulation of alpha-adrenoceptor subtypes, which in turn provides information concerning the anatomical localization of alpha 1- and alpha 2-adrenoceptors. Treatment of rats in the neonatal period with 6-OHDA causes an irreversible decrease in noradrenaline levels of the cerebral cortex compared to controls. Differences in [3H]clonidine and [3H]prazosin binding in the cerebral cortex occurred which varied depending upon the time elapsed between denervation and the binding assay. In rats aged 7-14 days there was a 20% decrease in the number of alpha 2-adrenoceptors and a slight increase in alpha 1-adrenoceptors. In older rats (45-50 day old) both types of alpha adrenoceptors were increased. Results of this study indicate that alpha 2-adrenoceptors located on presynaptic noradrenergic terminals represent only a small proportion of the total alpha 2-adrenoceptors in rat cerebral cortex. Increases in the binding capacity after 67-OHDA treatment indicate an up-regulation phenomenon affecting alpha 1-adrenoceptors and alpha 2-adrenoceptors located on structures other than noradrenergic nerve endings.

Animals↗

PubMed1992

Cholinergic hyperinnervation in the cerebral cortex of microencephalic rats does not result in muscarinic receptor down-regulation or in alteration of receptor-stimulated phosphoinositide metabolism.

Administration of methylazoxymethanol (MAM; 25 mg/kg) to pregnant rats at gestational day 15 (GD 15) induces a marked reduction of telencephalic areas of the offspring brain. Previous neurochemical studies demonstrated a marked cholinergic hyperinnervation in the cerebral cortex of microencephalic rats. In this study we have evaluated whether this cholinergic hyperinnervation could result in altered functionality of muscarinic receptors. Acetylcholinesterase activity (AChE) was increased by 69% in the cerebral cortex of MAM treated rats, confirming a relative hyperinnervation, whereas in the hippocampus and striatum no significant changes were observed. Despite the marked hyperinnervation, in the cerebral cortex of microencephalic rats neither muscarinic receptor-stimulated phosphoinositide metabolism nor muscarinic receptor density were altered. No differences in receptor density were also observed in the hippocampus and striatum. Chronic diisopropylfluorophosphate (DFP) administration induced a marked decrease of AChE activity and down-regulation of muscarinic receptors whereas atropine administration resulted in receptor up-regulation in cerebral cortex, striatum and hippocampus of both control and MAM rats. The results confirm a relative cholinergic hyperinnervation in the cerebral cortex of microencephalic rats and demonstrate that the regulation of muscarinic receptor-stimulated phosphoinositide metabolism and muscarinic receptor plasticity is not modified in a condition of increased cholinergic presynaptic terminals.

Abnormalities, Drug-Induced↗

PubMed1966

Amino acid incorporation into the protein of mitochondrial preparations from cerebral cortex and spinal cord.

1. Washed guinea-pig cerebral-cortex mitochondria incorporate [(14)C]leucine into their protein at a rate comparable with the rates reported for liver or heart mitochondria only if the mitochondria are separated from myelin and nerve endings by density-gradient centrifugation. 2. The non-mitochondrial components (myelin and nerve endings) of brain mitochondrial preparations incorporated [(14)C]leucine at a negligible rate. 3. The mitochondria do not require an exogenous supply of energy or a full supply of amino acids to support the process. 4. The incorporation rate was linear up to 2hr. aerobic incubation at 30 degrees and was inhibited by chloramphenicol, only slightly by actinomycin D and not by penicillin or pretreatment with ribonuclease. The observed incorporation is considered to be unlikely to be due to contaminating cytoplasmic ribosomes or bacteria. 5. The process was also studied in mitochondrial preparations from rabbit cerebral cortex and spinal cord.

Amino Acids↗

PubMed1995

Participation of tubulin in the stimulatory regulation of adenylyl cyclase in rat cerebral cortex membranes.

This study examined effects of tubulin on the activation of adenylyl cyclase in rat cerebral cortex membranes. Tubulin, prepared from rat brain by polymerization with the hydrolysis-resistant GTP analogue 5'-guanylylimidodiphosphate (GppNHp) caused significant activation of the enzyme by approximately 156% under conditions in which stimulation rather than inhibition of the enzyme was favored. Tubulin-GppNHp activated isoproterenol-sensitive adenylyl cyclase, potentiated forskolin-stimulated activity of the enzyme, and reduced agonist binding affinity for beta-adrenergic receptors. When tubulin, polymerized with the hydrolysis-resistant photoaffinity GTP analogue [32P]P3(4-azidoanilido)-P1-5'-GTP ([32P]AAGTP), was incubated with cerebral cortex membranes, AAGTP was transferred from tubulin to Gs alpha as well as Gi alpha. These results suggest that, in rat cerebral cortex membranes, the tubulin dimer participates in the stimulatory regulation of adenylyl cyclase by transferring guanine nucleotide to Gs alpha, as well as affecting the Gi-mediated inhibitory pathway.

Adenylyl Cyclases↗

PubMed2001

A columnar-supporting mode of astroglial architecture in the cerebral cortex of adult primates?

Neuronal modular (columnar) organisation of the cerebral cortex may represent an evolutionary acquisition that could optimize communication and information processing with the least volume compromise in terms of wiring. Yet, for such columns to be functionally operative adequate isolation from neighbouring units would be required, otherwise their spatial definition could be compromised. Evidence for "cable-like" processes stemming from astroglial cells has been recently presented although their existence has been forgotten for more than a century. These processes tend to form a sort of "palisade" or "brush" whose spatial distribution appears to correlate with the distribution of apical dendrites within the supragranular cortical layers. Patterned neuronal organization in the striate cortex is associated with a patterned distribution of GFAP-IR processes, both at the cellular and cell-aggregate levels. It can be tentatively proposed that evolutionary pressures resulted, in primates, in the progressive appearance of an increased length of astroglial processes in the supragranular region which may be associated with optimization of cerebral cortex modular (columnar) organization. It is interesting that this cortical region has undergone the larger growth among mammalian species during evolution, and would bear a crucial role in corticocortical interactions.

Animals↗

PubMed1966