Host defense response to cytomegalovirus in the central nervous system. Predominance of the monocyte.

Cytomegalovirus (CMV) infection of the brain is common in AIDS; however, little is known of the host defense response to CMV in the central nervous system (CNS). A guinea pig model was developed to study this problem. In the present studies the percentages of T cells and monocytes invading the leptomeninges during the course of acute CMV infection were compared. In addition, qualitative observations on parenchymal infiltrates were made. Such studies have not been performed previously in CMV infection of the CNS. Monocytes, defined cytochemically, predominated in the leptomeninges and in parenchymal foci. In contrast, T cells, defined immunohistologically, were found in a low percentage in the leptomeningeal reaction and only rarely in the parenchyma. These novel results differ significantly from other viral infections in which the T cell predominates in the leptomeningeal response and plays a major role in the parenchyma.     

Macrophages in the central nervous system of the rat

In an immunohistochemical study using monoclonal antibodies, which exclusively recognize cells of the monocyte-macrophage lineage, and monoclonal antibodies against the Ia-antigen, we describe the occurrence of macrophages in the developing and adult central nervous system (CNS). In normal adult brain, no macrophages could be detected in the CNS parenchyma; only in the meninges and the choroid plexes were a few macrophages found. During ontogeny, numerous phagocytic cells infiltrated the CNS parenchyma; these cells which did not express Ia are blood-borne. About three weeks after birth, all macrophages had disappeared from the CNS. As microglia in adult and developing brain do not stain with the anti-macrophage antibodies, we suggest that microglial cells are not related to the mononuclear phagocyte system and do not have a hematogenous origin.     

Effects of stress on opioid receptor binding in the rat central nervous system.

The endogenous opioid peptides are known to play a significant role in the modulation and/or mediation of numerous environmental or experimental stressors. However, the specific opioid peptide(s) and receptor type(s) involved, under what physiologic conditions they are engaged and within which regions of the CNS is not well understood. We therefore examined the effects of both a chronic and an acute stressor-90-h water deprivation and a single 20-min foot shock on opioid receptor binding in 17 specific rat brain nuclei. [3H]DSTLE (Tyr-D-Ser-Gly-Phe-Leu-Thr) and [3H]DAGO(Tyr-D-Gly-Phe-NMe-Phe-Gly-ol) were used to label delta and mu receptors, respectively. Foot shock induced profound antinociception as measured by tail-flick latency which outlasted the stressor by several minutes. However, only the septum responded with a decrease in [3H]DAGO binding to this type of stress-induced analgesia. No other alterations in either [3H]DAGO or [3H]DSTLE binding were seen in response to foot shock. In contrast, water deprivation induced increases in [3H-DAGO] binding in the septum as well as increases in [3H]DSTLE binding in the caudate and accumbens nuclei. Moreover, the presumptive mild stress of handling in the foot shock control group was sufficient to decrease mu or delta receptor binding in seven out of 17 brain regions investigated (including the frontal cortex and olfactory tubercle where both mu and delta binding were increased) when compared to unhandled deprivation control animals. These changes in opioid receptor binding may have been the result of alterations in treatment-induced peptide release, receptor regulation, or interactions with other released neurotransmitter ligand/receptor complexes.(ABSTRACT TRUNCATED AT 250 WORDS)     

Dynorphin-immunoreactive neurons in the central nervous system of the rat

An antiserum specific for the C-terminal region of dynorphin_1–17 (DYN) was used to examine the distribution of this endogenous opioid peptide in the rat brain with the indirect immunofluorescence technique. DYN-positive nerve cell bodies and fibers were found in many nuclei in the spinal cord, medulla, mesencephalon, hypothalamus and forebrain. These findings indicate that a widespread system of DYN neurons is present in the brain distinct from the previously described enkephalin and endorphin systems.     

Cation-dependent structures associated with membranes in the rat central nervous system.

As observed by high magnification electron microscopy, potassium ions induce osmiophilia at the extracellular side of triple layered plasma membranes in the central nervous system of the rat. In contrast, sodium ions induce a widening of the intracellular lamina of these membranes, and do not result in observable extracellular deposits. The observations suggest the existence of potassium and sodium ion-selective structures associated with opposite surfaces of the neuron membrane. Use of the fixative vehicle as a cytochemical reagent is proposed.     

Localization of aggrecan and versican in the developing rat central nervous system.

The localization of aggrecan and mRNA splice variants of versican in the developing rat central nervous system has been examined by using specific polyclonal antibodies to the nonhomologous glycosaminoglycan attachment regions of these hyaluronan-binding chondroitin sulfate proteoglycans. At embryonic day 16 (E16), aggrecan and versican splice variants containing either or both the alpha-and beta-domains are present in the marginal zone and subplate of the cerebral cortex and in the amygdala, internal capsule, and the optic and lateral olfactory tracts. There is strong staining of versican but not of aggrecan in the hippocampus and dentate gyrus by E19, whereas both aggrecan and alpha-versican are present in the fimbria. At E19, aggrecan is seen throughout the cerebral cortex, whereas the distribution of versican is considerably more limited, being confined essentially to the marginal zone and subplate. At 1 week postnatal, both aggrecan and versican are present in the prospective white matter and in the molecular and granule cell layers of the cerebellum, but neither proteoglycan is seen in the external granule cell layer. alpha- but not beta-versican staining is seen in Purkinje cells, and aggrecan staining of Purkinje cells is also rather minimal. In the spinal cord at E13, aggrecan is present in the dorsal root entry zone, ventral funiculus, mantle layer, and floor plate, as well as in the dorsal root ganglia and ventral roots. However, alpha-versican is confined to the dorsal root entry zone and the ependyma surrounding the spinal canal, and beta-versican is not present in spinal cord parenchyma at this developmental stage, being limited to the surrounding connective tissue. By E19, there are significant amounts of all three proteoglycans in the spinal cord. Aggrecan staining is most intense in the lateral funiculus and the fasciculi gracilis and cuneatus, where alpha-versican staining is also strong. In contrast, beta-versican is seen predominantly in the motor columns. Differences in the localization and temporal expression patterns of these chondroitin sulfate proteoglycans suggest that, like neurocan and phosphacan, they have partially complementary roles during central nervous system development.     

静脉普鲁卡因麻醉作用的中枢神经电生理研究

目的：为进一步阐明静脉普鲁卡因到底有无麻醉作用。方法：２０例患者随机分成普鲁卡因组和普鲁卡因加芬太尼组,观察脑电功率谱相对功率、９０％谱边界频率（ＳＥＦ）、中位频率（ＭＰＦ）和中潜伏期听觉诱发电位（ＭＬＡＥＰ）的变化。结果：ＳＥＦ、ＭＰＦ不随剂量的逐级递增而进一步改变,呈快波β节律活动显著增加的脑干兴奋的去同步化ＥＥＧ表现。但达２ｍｇ／ｋｇ·ｍｉｎ时,ＳＥＦ、ＭＰＦ和β相对功率出现骤降（Ｐ＜００１）,呈δ波占绝对优势（５０６０％）的ＥＥＧ表现。ＭＬＡＥＰＰａ、Ｎｂ波潜伏期于１ｍｇ／ｋｇ·ｍｉｎ即已明显延长,振幅降低更为显著,其变化与普鲁卡因剂量呈线性关系。加用芬太尼组的改变与普鲁卡因组在２ｍｇ时几乎一致。结论：普鲁卡因的麻醉作用是肯定的,但仅能达到相当于Ⅱ期的麻醉深度;加用芬太尼完全可以使静脉普鲁卡因麻醉的较浅状态得以加深,达到类似强效麻醉药的麻醉深度。推测其中枢作用部位可能在皮层下和中脑与原始听皮层水平     

Oral motor deficits following lesions of the central nervous system in the rat.

The effects of lesions of the zona incerta (ZI), globus pallidus (GP), midlateral and far lateral hypothalamus (MLH and FLH), and the central amygdaloid complex (CAC) on oral motor deficits were investigated. Lesions of the ZI, GP, and CAC resulted in a significant reduction in tongue extension and lap volume. MLH lesions significantly reduced tongue extension whereas FLH lesions significantly reduced both tongue extension and lap volume. Injections of 6-hydroxydopamine into the GP, MLH, and CAC also significantly reduced tongue extension and lap volume. Water and/or food intakes were reduced in some of the lesioned groups but the oral motor deficits were observed both in the presence and in the absence of reduced water and food intakes. The possibility that oral motor deficits are associated with damage to striatal and non-striatal dopamine neurons needs further investigation.     

Ultrastructure of the central nervous system in marek's disease and the effect of route of infection on lesion incidence in the central nervous system

The ultrastructure of the lesions of the central nervous system (CNS) of chickens was examined at intervals after intra-abdominal inoculation of Marek's disease virus (MDV). No transient paralysis occurred. Peri-vascular accumulations of lymphocytes and macrophages (cuffing) were accompanied by invasion of the CNS by these blood-borne leukocytes in the most severe lesions. Only minor damage to axons, myelin or glial cells was detected and no structural evidence for viral replication was observed. Intracerebral inoculation of cell-free MDV induced similar lesions in the CNS and there was no evidence for local exacerbation of their severity, although a few chickens developed transient paralysis. It is concluded that replication of MDV in the CNS is unlikely to be the direct cause of the CNS lesions.     

Oxygen toxicity: augmentation of antioxidant defense mechanisms in rat lung.

In studies directed at determining the activities of selected enzymes in lung tissue after in vivo exposure to hyperoxia, 70-day-old rats were exposed to 85% or 90% O2 for 1-14 days. After 7 days of exposure to 90% O2 (1atm), superoxide dismutase activities in mitochondrial and cytosolic fractions increased, respectively, to 245 and 145% of control; glutathione peroxidase, glutathione reductase, and glucose-6-phosphate dehydrogenase activities increased, respectively, to 317, 175, and 413% of control. The levels of reduced glutathione and total nonprotein sulfhydryl compounds were elevated to 195% and 365% of control. Similar changes were observed in rats exposed to 85% O2 for up to 14 days, but to a lesser degree. The changes are interpreted as a reflection of the overall magnitude of oxidant-induced lung injury-reparative processes. The results suggest that hyperoxia induces an increase in lung "antioxidant" defense capabilities. This apparent adaptive response may be important in decreasing the susceptibility of lung tissue to continued O2 toxicity.     

Caspase-3在大鼠中枢神经系统的表达研究

目的研究caspase-3在大鼠中枢神经系统的表达及其意义。方法用western-blot方法对出生1天和3个月SD大鼠的大脑皮质、中脑和小脑组织的caspase-3进行半定量测定。结果出生1天大鼠脑的caspase-3表达较高,出生3个月大鼠脑的caspase-3表达较低。结论caspase-3在中枢神经系统的发育成熟过程中对神经元的凋亡起着关键性作用。     

Charting of type II glucocorticoid receptor-like immunoreactivity in the rat central nervous system.

The rat brain and spinal cord have been mapped for Type II glucocorticoid receptor-like immunoreactivity in neurons and glia, using a monoclonal antibody, BUGR2, which recognizes an epitope close to the DNA-binding domain of the rat Type II receptor. The study revealed a widespread distribution of Type II-like immunoreactive neurons and glia, and a heterogeneity of densities and intensities of immunoreactive elements. Our results corresponded to a large extent with previous immunocytochemical mapping using Ig2a, a monoclonal antibody against a different epitope in the variable domain, with some notable differences in the hippocampus, hypothalamus and cerebellum. There was also a good correlation between immunocytochemical mapping and binding studies, [3H]steroid autoradiography and mRNA localization of the Type II receptor.     

Glycoproteins and polyanions in the synapses of rat and mouse central nervous system.

In the present work, it is investigated the location and characteristics of receptors for Con A in synapses of rat and mouse central nervous system. Negatives charges of synaptic surface are also studied. It is observed the presence of glycoproteins on synaptosomal plasma membrane. Presence of negatives charges homogenously distributed all over the synaptosome surface is also notice. These negative charges are revealed by Colloidal Iron, FeOH++cation and cationized Ferritin. Enzymatic extraction experiments suggest that presence of sulphated mucopolysaccharides.     

Effects of castration and testosterone replacement on the antioxidant defense system in rat left ventricle

There is strong evidence that oxidative stress plays a key role in the pathophysiology of several cardiovascular diseases. On the other hand, the presence of specific receptors for androgens and estrogens in the myocardium implies that sex hormones play a physiological role in cardiac function, myocardial injury, and the regulation of the redox state in the heart. The present study was designed to determine whether castration and androgen replacement result in changes in the capacity of the antioxidant defense system in the left ventricle (LV) of adult male rats. To assess this, the activities of antioxidant enzymes (superoxide dismutase [SOD], glutathione peroxidase [GPX], catalase [CAT], and glutathione reductase [GR]), concentrations of nonenzymatic antioxidants (reduced glutathione [GSH] and alpha- and gamma-tocopherols), and oxidative stress biomarkers (tissue sulfhydryl groups, protein nitrotyrosine levels, and lipid peroxidation) were measured in castrated animals (CAS), castrates replaced with testosterone (CAS+T), and sham-operated controls (Sham). Testosterone was not detectable in serum from gonadectomized rats. The results indicate that castration significantly and negatively affected the antioxidant status of rat LV, as evidenced by a significant decline in activities of all antioxidant enzymes, by a tendency toward lower levels of GSH and protein thiol groups, and by enhanced lipid peroxidation and higher nitrotyrosine concentrations in left ventricular tissue. Increases in LV tissue concentrations of alpha- and gamma-tocopherols seem to be a compensatory response to enhanced oxidative stress induced by gonadectomy. The reestablishment of physiological serum testosterone level by androgen replacement resulted in a tendency toward a further decrease in the antioxidant defense status in the LV tissue.     

Immunocytochemical localization of acyl-CoA oxidase in the rat central nervous system

Peroxisomal -oxidation, consisting of four steps catalysed by an acyl-CoA oxidase, a multifunctional protein and a thiolase, is responsible for the shortening of a variety of lipid compounds. The first reaction of this pathway is catalysed by a FAD-containing acyl-CoA oxidase, three isotypes of which have been so far recognised. Among these, straight-chain acyl-CoA oxidase (ACOX) acts on long and very long chain fatty acids, prostaglandins and some xenobiotics. We investigated ACOX localisation by means of a sensitive, tyramide based, immunocytochemical technique, thus obtaining a complete distribution atlas of the enzyme in adult rat CNS. Granular immunoreaction product was found in the cytoplasm of neuronal and glial cells, both in the perikarya and in the cell processes. ACOX immunoreactive neurons were present to variable extent, in either forebrain or hindbrain areas. Specifically, the strongest signal was detected in the pallidum, septum, red nucleus, reticular formation, nuclei of the cranial nerves, and motoneurons of the spinal cord. We then compared the ACOX immunoreactivity pattern with our previous distribution maps of other peroxisomal enzymes in the adult rat brain. While ACOX appeared to colocalise with catalase in the majority of cerebral regions, some differences with respect to d-amino acid oxidase were noted. These observations support the hypothesis of heterogeneous peroxisomal populations in the nervous tissue. The wide distribution of the enzyme in the brain is consistent with the severe and generalised neurological alterations characterising the peroxisomal disorder caused by ACOX deficiency (pseudo-neonatal adrenoleukodystrophy).     

Ultrastructural observations of astrocyte end-feet in the rat central nervous system

Astrocytic end-feet in the rat CNS were studied by thin-section electron microscopy. Astrocyte processes that enclose neuronal elements extended to blood vessels and the pia mater, where the processes expanded to form end-feet or glial limiting membranes. At the end-feet, cell junctions such as gap junctions and desmosome-like junctions were formed between the astrocyte processes. The end-foot plasma membrane facing the basal lamina was undercoated with electron-dense, layered materials, with an internal substructure of filamentous networks, with which bundles of glial filaments (GFs) appeared to be closely associated via fine filamentous structures, often showing a hemi-desmosome-like appearance. In specimens treated with Triton X-100, the internal substructure of the undercoat was better visualized and the association with GFs was well preserved. At the end-feet, some unique tubular structures were found in spatial relationship to the plasmalemmal undercoat. Plectin visualized by immunofluorescence was localized to astrocytes and their processes, especially at the end-feet facing the pia mater. Immunoelectron microscopy located plectin on fine filamentous structures lying between GFs and the plasmalemmal undercoat. These observations suggest that plasmalemmal undercoats at the astrocyte end-feet may serve as attachment sites of GFs to the plasma membrane and that plectin may be involved in such attachment.