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At least 217 records · Page 12Linked to original sources
PubMed1985

Serotonin-stimulated phosphoinositide turnover: mediation by the S2 binding site in rat cerebral cortex but not in subcortical regions.

In rat cerebral cortex, serotonin (5-HT) stimulates phosphoinositide turnover with an EC50 of 1 microM in the presence of pargyline. The EC50 is 16-fold higher in the absence of pargyline. Selective S2 antagonists inhibit 5-HT-stimulated phosphoinositide turnover. Schild analysis of the blockade by ketanserin of the 5-HT effect gives an estimated Kd of ketanserin for the phosphoinositide-linked receptor of 11.7 nM, which agrees with the Kd (3.5 nM) of [3H]ketanserin for the S2 site. Furthermore, MK-212, 5-HT and 5-fluorotryptamine stimulate phosphoinositide turnover with potencies that resemble their potencies at the S2 but not the S1 binding site. Of 11 agonists tested, the tryptamine derivatives tend to be more efficacious than the piperazine derivatives. The selective S1 agonist 8-hydroxy-2-(di-N-propylamino)tetralin is inactive at stimulating phosphoinositide turnover. No significant relationship exists between the regional distributions of 5-HT-stimulated phosphoinositide turnover and S2 binding sites. Furthermore, the S2 antagonist ketanserin is less potent and less efficacious in hippocampus and limbic forebrain than in cerebral cortex. These data suggest that 5-HT-stimulated phosphoinositide turnover is linked to the S2 binding site in rat cerebral cortex. However, 5-HT increases phosphoinositide turnover in subcortical regions by mechanisms other than stimulation of the S2 receptor.

Animals↗
PubMedDate not supplied

Age-related changes in sulfide-silver stainable fibres in the rat cerebral cortex.

The present study was designed to assess the age-dependent changes in sulfide-silver stainable fibres in frontal, parietal and occipital cortex areas of the rat cerebral cortex. Male Sprague-Dawley rats of 2 months (young), 12 months (adult) and 24 months (aged) were used. Sulfide-silver stainable fibres, which represent predominantly zinc-containing associational fibres arising from local cortical interneurons, were visualized using the neo-Timm histochemical technique. The density of sulfide-silver stainable fibres within the neuropil of laminae I-III (upper zone) and of lamina V (lower zone) of the different cerebral cortex areas was assessed microdensitometrically. In the frontal and parietal cortices the density of sulfide-silver stainable fibres was higher in adult and in aged than in young rats both in the upper and in the lower zones. No significant differences were noticeable in the density of sulfide-silver stainable fibres between adult and old rats. In the occipital cortex the density of sulfide-silver stainable fibres was similar in young or adult rats. but was remarkably increased in old animals. The possibility that the increase in the density of sulfide-silver stainable fibres represents a compensatory mechanism in the cerebral cortex area showing the most consistent nerve cell loss is discussed.

Journal Article↗
PubMed2006

Effect of 7-nitroindazole sodium on the cellular distribution of neuronal nitric oxide synthase in the cerebral cortex of hypoxic newborn piglets.

Cerebral hypoxia results in generation of nitric oxide (NO) free radicals by Ca(++)-dependent activation of neuronal nitric oxide synthase (nNOS). The present study tests the hypothesis that the hypoxia-induced increased expression of nNOS in cortical neurons is mediated by NO. To test this hypothesis the cellular distribution of nNOS was determined immunohistochemically in the cerebral cortex of hypoxic newborn piglets with and without prior exposure to the selective nNOS inhibitor 7-nitroindazole sodium (7-NINA). Studies were conducted in newborn piglets, divided into normoxic (n = 6), normoxic treated with 7-NINA (n = 6), hypoxic (n = 6) and hypoxic pretreated with 7-NINA (n = 6). Hypoxia was induced by lowering the FiO(2) to 0.05-0.07 for 1 h. Cerebral tissue hypoxia was documented by decrease of ATP and phosphocreatine levels in both the hypoxic and 7-NINA pretreated hypoxic groups (P < 0.01). An increase in the number of nNOS immunoreactive neurons was observed in the frontal and parietal cortex of the hypoxic as compared to the normoxic groups (P < 0.05) which was attenuated by pretreatment with 7-NINA (P < 0.05 versus hypoxic). 7-NINA affected neither the cerebral energy metabolism nor the cellular distribution of nNOS in the cerebral cortex of normoxic animals. We conclude that nNOS expression in cortical neurons of hypoxic newborn piglets is NO-mediated. We speculate that nNOS inhibition by 7-NINA will protect against hypoxia-induced NO-mediated neuronal death.

Animals↗
PubMed1980

Ontogeny of beta 1- and beta 2-adrenergic receptors in rat cerebellum and cerebral cortex.

The development of beta 1- and beta 2-adrenergic receptors was studied in rat cerebral cortex and cerebellum. In the cerebral cortex, which contains mostly beta 1-adrenergic receptors, total beta-adrenergic receptor density increased sharply between postnatal days 10 and 21. The density of receptors remained fairly constant through 6 weeks of age and then subsequently declined. The proportion of beta 1 and beta 2 receptors was relatively constant throughout the development of the cerebral cortex. The development of the two receptor subtypes thus paralleled the development of total beta-adrenergic receptors in the cerebral cortex. The ontogeny of beta-adrenergic receptors in the cerebellum, which contains mainly beta 2 receptors, was strikingly different from that observed in the cortex. Total cerebellar beta receptor density exhibited a slow but steady increase from postnatal day 5 through day 42. The density of receptors then plateaued and remained constant until the animals were approximately 6 months of age. Unlike the results obtained in the cortex, the relative proportions of beta 1 and beta 2 receptors in the cerebellum changed markedly during development. Between postnatal days 8 and 13 approximately 18% of the receptors were of the beta 1 subtype. This proportion steadily decreased with age, and in 3- and 6-month-old animals only approximately 2% of the receptors were of the beta 1 subtype. The results demonstrate that the two subtypes of beta-adrenergic receptors can have different developmental patterns in the same brain area, and that a single receptor subtype can follow different developmental patterns in different brain regions. Possible correlations between the ontogeny of beta 1 and beta 2 receptors and various developmental events are discussed.

Aging↗
PubMed2003

Ethanol-induced neuronal death in organotypic cultures of rat cerebral cortex.

Ethanol can affect normal development of the cerebral cortex, e.g., it can disrupt cell migration and exacerbate cell death. In vitro studies using primary cultures or cell lines provide further evidence that cell migration and death are altered by ethanol exposure. Organotypic cultures are more complex than primary cell cultures, and maintain some normal connectivity, thus providing a "more in vivo-like" model of brain development. We predict that exposing organotypic cultures of fetal rat cerebral cortex to ethanol results in changes similar to those described in vivo. Organotypic cultures of brains from 16-day-old fetuses were exposed to ethanol (0, 200, 400 or 800 mg/dl) for 72 h. Stereological methods were used to assess the frequency of viable and dying cells. Dying cells were identified as having DNA with polyadenylated tails or as having condensed chromatin. A small amount of cell death was evident in the marginal zone (MZ) and cortical plate (CP) of control cultures. The MZ, normally a cell body-poor layer, was enriched with somata following exposure to 400 mg/dl ethanol. Ethanol-induced cell death in the MZ; the amount of cell death was doubled following exposure to 800 mg/dl ethanol. The CP was more sensitive than the MZ; cell death increased following treatment with 400 mg/dl ethanol. Thus, organotypic cultures show that ethanol disrupts neuronal migration and increases cell death in the developing cerebral cortex. The effects of ethanol were site-specific and concentration-dependent. These changes are similar to those described in vivo.

Animals↗
PubMed2001

Chronic exposure to aluminium decreases NADPH-diaphorase positive neurons in the rat cerebral cortex.

Aluminium (Al) exposure is neurotoxic and is considered a possible etiological factor for many neurodegenerative disorders. Since it is known that Al impairs the glutamate-nitric oxide-cGMP pathway in neurons, this study was carried out to monitor the expression of NADPH-d in some central nervous system areas of rats after chronic administration of Al in drinking water. We tested three different nervous areas known to contain NADPH-diaphorase positive neurons: two cortical area (somatosensory cerebral cortex and cerebral cortex), a deep brain area (dorsolateral periaqueductal gray matter) and a spinal area (lumbar enlargement of the spinal cord). Our data showed that Al significantly decreased NADPH-d positive neurons in the cerebral cortex and the NADPH-d staining of many granular neurons in the cerebellum. We also found that Al did not cause neuron loss or apoptosis in the cerebral cortex. These findings suggest that the cortical nitroxidergic neurons and granule cells were a specific target of Al neurotoxicity.

Aluminum↗
PubMed1984

Origins of histamine-containing fibers in the cerebral cortex of rats studied by immunohistochemistry with histidine decarboxylase as a marker and transection.

The origins of histamine-containing fibers in the cerebral cortex were examined by means of the retrograde tracer technique of horseradish peroxidase (HRP)-immunohistochemistry with histidine decarboxylase (HDC) as a marker for the histamine neuron system. Total transection of the brain rostral to the posterior hypothalamus resulted in disappearance of HDC-like immunoreactive (HDCI) fibers in the cerebral cortex, but total transection caudal to the posterior hypothalamus did not decrease the number of HDCI fibers in the cortex, suggesting that HDCI fibers in the cerebral cortex originate in the posterior hypothalamus. The projection of HDCI neurons from the posterior hypothalamus to the cerebral cortex seemed to be bilateral because hemi-transection of the brain rostral to the posterior hypothalamus resulted in a bilateral decrease of HDCI fibers in the cerebral cortex with ipsilateral predominance. After injection of HRP into the cerebral cortex, numerous cells containing both HRP granules and HDCI structures were found bilaterally in the tuberal, caudal and postmamillary magnocellular nuclei, with ipsilateral predominance. These findings indicate that HDCI cells in the above nuclei give rise to axons extending bilaterally to the cerebral cortex.

Animals↗
PubMed2003

Subpial demyelination in the cerebral cortex of multiple sclerosis patients.

The extent and pattern of demyelination in the cerebral cortex was determined in 78 tissue blocks from the brains of 20 multiple sclerosis (MS) patients and 28 tissue blocks from 7 patients without neurological disease. Tissue blocks from 4 predetermined areas (cingulate gyrus, frontal, parietal, and temporal lobe) were studied, irrespective of macroscopically evident MS plaques. All tissue blocks contained cerebral cortex and periventricular and/or subcortical white matter. One hundred and nine demyelinating lesions were detected in the cerebral cortex, of which 92 (84.4%) were purely intracortical and 17 (15.6%) were lesions extending through both white and gray matter areas. In 5 of the 20 MS brains, subpial demyelination was extensive in the 4 widely spaced cortical areas studied, thus considered to represent a general cortical subpial demyelination. The percentage of demyelinated area was significantly higher in the cerebral cortex (mean 26.5%, median 14.1%) than in white matter (mean 6.5%, median 0%) (p = 0.001). Both gray and white matter demyelination was more prominent in the cingulate gyrus than in the other areas examined (p < 0.05). These results indicate that the cerebral cortex is likely to be a predilection site for MS lesions and identify general cortical subpial demyelination as a distinct pattern occurring in a significant subpopulation of MS patients.

Adult↗
PubMed1991

Postmortem cerebral cortex Gs alpha-subunit levels are elevated in bipolar affective disorder.

We examined the relative abundance of G-protein subunits in postmortem brain obtained from 7 patients with bipolar affective disorder (BAD) compared with 7 age- and sex-matched controls. G-protein subunit immunoreactivities were determined in membranes prepared from postmortem prefrontal cortex using SDS-PAGE and immunoblotting with specific polyclonal antisera against selected G-protein subunits: Gsa, Gi(1&2) alpha, Go alpha and G beta(1&2). Of these G-protein subunits, only Gs alpha immunoreactivity was found to be significantly elevated in frontal (+ 34%), and occipital (+ 80%) cortex (P less than 0.05) in BAD compared with control subjects. Smaller increments (+ 22%) in cerebellar Gs alpha immunoreactivity were also found but were not statistically significant. On the basis that increased Gs alpha immunoreactivity may reflect enhanced functional responsiveness of the receptor-effector units to which this coupling protein is integral, the present findings suggest that disturbances in Gs-mediated signal transduction may be involved in the pathophysiology of BAD.

Bipolar Disorder↗
PubMed1980

Distribution of peripherally stained neurons by the colloidal iron histochemical method in albino rat cerebral cortex. A quantitative study.

A few stained neurons were demonstrated in several cortical areas by the Colloidal Iron method. The intense positive histochemical reaction was located surrounding the perikaryon and some neuronal branches. A quantitative study demonstrated that the largest percentage of stained neurons was found in III, IV and V layers of the visual and auditory cortex. The number of stained neurons in the auditory cortex was greater than in the visual cortex. Statistically significant differences (Student's t-test) were obtained between layers I, II, III and VI of both cortical areas. In other cortical areas studied there were no stained neurons (area insularis ventralis, area entorhinalis and area piriformis).

Animals↗
PubMed1997

Immunohistochemical detection of nitrotyrosine in postischemic cerebral cortex in gerbil.

We examined whether or not nitration of tyrosine residues takes place in the ischemic and postischemic reperfused brain. The nitration of tyrosine residues to produce nitrotyrosine is a sensitive marker elicited by peroxynitrite, a powerful oxidant formed by the reaction of nitric oxide (NO) with superoxide. Mongolian gerbils were subjected to 60 min ischemia induced by occlusion of the right common carotid artery (ischemia group), to 30 min recirculation following 60 min ischemia (reperfusion group) or to sham surgery (sham group). Immunohistochemical staining with polyclonal anti-nitrotyrosine antibody revealed the widespread and distinct occurrence of nitrotyrosine in cortical neurons on the reperfused side of the brain in the reperfusion group, while only partial or weak immunoreactivity was noted on the contralateral side. On the other hand, nitrotyrosine was not detected in the brain of the ischemia and sham groups. These findings suggest that nitration of tyrosine residues in various proteins may be closely associated with reperfusion injury of the brain.

Animals↗
PubMed2000

A comparison of visual and auditory motion processing in human cerebral cortex.

Visual and auditory motion information can be used together to provide complementary information about the movement of objects. To investigate the neural substrates of such cross-modal integration, functional magnetic resonance imaging was used to assess brain activation while subjects performed separate visual and auditory motion discrimination tasks. Areas of unimodal activation included the primary and/or early sensory cortex for each modality plus additional sites extending toward parietal cortex. Areas conjointly activated by both tasks included lateral parietal cortex, lateral frontal cortex, anterior midline and anterior insular cortex. The parietal site encompassed distinct, but partially overlapping, zones of activation in or near the intraparietal sulcus (IPS). A subsequent task requiring an explicit cross-modal speed comparison revealed several foci of enhanced activity relative to the unimodal tasks. These included the IPS, anterior midline, and anterior insula but not frontal cortex. During the unimodal auditory motion task, portions of the dorsal visual motion system showed signals depressed below resting baseline. Thus, interactions between the two systems involved either enhancement or suppression depending on the stimuli present and the nature of the perceptual task. Together, these results identify human cortical regions involved in polysensory integration and the attentional selection of cross-modal motion information.

Acoustic Stimulation↗