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  • Macaca fascicularis (Primates)  (3)
  • Striatum  (2)
  • 1
    Electronic Resource
    Electronic Resource
    GM1 ganglioside administration partially counteracts the morphological changes associated with haloperidol treatment within the dorsal striatum of the rat (1995)
    Springer
    Psychopharmacology 121 (1995), S. 461-469 
    Details
    ISSN: 1432-2072
    Keywords: GM1 ; Haloperidol ; Glutamate synapses ; Perforated PSD ; Striatum ; Dopamine receptors
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Haloperidol, a typical antipsychotic drug, causes an increase in the mean percentage of synapses within the striatum containing a discontinuous, or perforated, postsynaptic density (PSD) following 1 month of treatment (Meshul et al. 1994). This effect is not observed with the atypical antipsychotic drug, clozapine, following subchronic administration (Meshul et al. 1992a). This morphological change is also associated with an increase in the density of dopamine D2 receptors. The synapses containing the perforated PSD are asymmetrical and the nerve terminals contain the neurotransmitter, glutamate, as demonstrated by immunocytochemistry. We have also shown that subchronic treatment with haloperidol (0.5 mg/kg per day, 30 days) results in a decrease in the density of glutamate immunoreactivity within asymmetric nerve terminals associated with perforated and non-perforated PSDs (Meshul and Tan 1994). This could be due to an increase in glutamate release, perhaps due to activation of corticostriatal synapses. Agnati et al. (1983a) reported that administration of GM1 ganglioside blocks the increase in dopamine D2 receptors following haloperidol treatment. GM1 has also been shown to attenuate the release of glutamate (Nicoletti et al. 1989). In order to determine if similar treatment with ganglioside could block the haloperidol-induced ultrastructural changes noted above, rats were coadministered GM1 (10 mg/kg per day) and haloperidol (0.5 mg/kg per day) for 30 days. We report that GM1 blocked the haloperidol-induced increase in striatal asymmetric synapses containing a perforated PSD, but had no effect on the increase in dopamine D2 receptors or the decrease in nerve terminal glutamate immunoreactivity. GM1, either alone or co-administered with haloperidol, also caused a small, but significant, increase in the density of all asymmetric synapses within the striatum. It is possible that the effect of GM1 in attenuating the haloperidol-induced change in glutamate synapses with perforated PSDs is primarily postsynaptic, since GM1 did not block the change in density of glutamate immunoreactivity within asymmetric nerve terminals.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02246494
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Correlation of vacuous chewing movements with morphological changes in rats following 1-year treatment with haloperidol (1996)
    Springer
    Psychopharmacology 125 (1996), S. 238-247 
    Details
    ISSN: 1432-2072
    Keywords: Haloperidol ; Vacuous chewing movements ; Glutamate synapses ; Perforated postsynaptic density ; Striatum ; Tardive dyskinesia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Long-term treatment with the typical antipsychotic drug, haloperidol, can lead to a sometimes irreversible motor disorder, tardive dyskinesia (TD). It has been hypothesized that increased release of glutamate due to prolonged neuroleptic drug treatment may result in an excitotoxic lesion in specific neuronal populations within the basal ganglia, leading to TD. We reported that treatment with haloperidol for 1 month results in an increase in the mean percentage of striatal asymmetric synapses containing a perforated postsynaptic density (PSD) and that these synapses are glutamatergic. Using quantitative immunocytochemistry, we found that depending on how long the animals had been off haloperidol following subchronic (30d) treatment, there was either a decrease (1 day off) or increase (3–4 days off) in the density of glutamate immunolabeling within the presynaptic terminals of synapses with perforated PSDs. Using a rat model for TD, animals in the current study were treated for 1 year with haloperidol and spontaneous oral dyskinesias (i.e. vacuous chewing movements, VCMs) were recorded. In these long-term treated animals we wanted to determine if there was a correlation between glutamate function, as measured by changes in synapses with perforated PSDs and the density of nerve terminal glutamate immunoreactivity, and VCM behavior. In drug treated rats which demonstrated either a high or low rate of VCMs, there was a significant increase in the mean percentage of asymmetric synapses in the dorsolateral striatum with perforated PSDs in both haloperidol-treated groups compared to vehicle-treated rats. There was a small but significant increase in the density of glutamate immunolabeling within striatal nerve terminals of the high VCM group compared to the low VCM group. There was, however, no difference in the density of glutamate immunolabeling between the high VCM group compared to the vehicle-treated animals. One reason for this lack of difference was partially due to a significant increase in nerve terminal area within the high VCM group compared to either the low VCM- or vehicle-treated groups. The larger nerve terminal size in the high VCM group may be due to a small but sustained increase in glutamate neurotransmitter release with the ability of the terminal to maintain its supply of glutamate, while the terminals in the low VCM group showed evidence of glutamate depletion. This finding would be consistent with the hypothesis that increased glutamatergic activity may be associated with TD.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02247334
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Distribution of laminin, type IV collagen, and fibronectin in the cell columns and trophoblastic shell of early macaque placentas (1992)
    Springer
    Cell & tissue research 270 (1992), S. 241-248 
    Details
    ISSN: 1432-0878
    Keywords: Trophoblast ; Placenta ; Laminin ; Collagen ; Fibronectin ; Extracellular matrix,-structures ; Macaca fascicularis (Primates)
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary The cytotrophoblastic cell columns and trophoblastic shell of macaque placentas accumulate progressively greater amounts of intercellular material during early gestation. We studied the composition of this material in placentas collected from 22–34 days of gestation by using immunoperoxidase techniques directed to the extracellular matrix molecules fibronectin, type IV collagen, and laminin. These antigens co-localized within the intercellular deposits at all stages studied. At day 22 the proximal cell columns were composed of cells with narrow interstices and which lacked immunoreactivity for the 3 antigens. Distally the cells were vacuolated and the intercellular spaces increased in size and contained dense matrix deposits. The trophoblastic shell consisted of closely packed, non-vacuolated cytotrophoblast cells with only a delicate meshwork of matrix. By day 27 the matrix deposits of the distal cell columns increased markedly in size. The trophoblastic shell contained larger numbers of vacuolated cells and was occupied by accumulations of matrix. By 34 days the matrix deposits of the cell columns expanded substantially along the longitudinal axes of the columns. These deposits were often continuous with a matrix-dense, cell-deficient layer in the trophoblastic shell. This matrix-rich zone lay between a cellular layer adjacent to the intervilous space and a similar, but discontinuous, cell layer that formed the junctional zone with the endometrium.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00328009
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    Paper (German National Licenses)
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  • 4
    Electronic Resource
    Electronic Resource
    Trophoblastic invasion and the development of uteroplacental arteries in the macaque: immunohistochemical localization of cytokeratins, desmin, type IV collagen, laminin, and fibronectin (1993)
    Springer
    Cell & tissue research 272 (1993), S. 227-236 
    Details
    ISSN: 1432-0878
    Keywords: Trophoblastic cells ; Spiral artery ; Extracellular matrix ; Uterus ; Macaca fascicularis (Primates) ; Macaca mulatta (Primates)
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract The processes by which trophoblast cells invade and modify the walls of the uteroplacental arteries of macaques during the course of gestation were examined. Antibodies to cytokeratins were employed to identify trophoblast, anti-desmin antibody to identify smooth muscle, and antibodies to type IV collagen, laminin, and fibronectin to examine changes in extracellular matrix distribution in the arterial wall. During early gestation, endovascular trophoblast adhered to the arterial wall, often in an asymmetrical distribution. As trophoblast cells moved outwardly into the tunica media, the basement membrane underlying the endothelium was lost, as indicated by gaps in the layer when stained for type IV collagen and laminin. Trophoblast cells became sequestered in the vessel wall where they hypertrophied and became surrounded by a capsule containing type IV collagen and laminin. As the trophoblast cells became established in the vessel wall, the muscular layer of the artery became discontinuous. Throughout gestation it was common for trophoblast cells to invade the vessel intimal layer and share the lining of the artery with typical endothelial cells. This general disposition of endovascular and intramural trophoblast persisted into late gestation. In addition, and contrary to the results of earlier studies of macaques, we identified trophoblastic invasion and modification of myometrial segments of the uteroplacental arteries in later gestation. We also found evidence of interstitial trophoblast cells among the stromal cells of the endometrium, especially during early gestation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00302728
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    Paper (German National Licenses)
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  • 5
    Electronic Resource
    Electronic Resource
    Trophoblastic invasion and modification of uterine veins during placental development in macaques (1993)
    Springer
    Cell & tissue research 274 (1993), S. 135-144 
    Details
    ISSN: 1432-0878
    Keywords: Trophoblast ; Uterus ; Veins ; Basement membrane ; Placenta ; Macaca fascicularis (Primates) ; Macaca mulatta (Primates)
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Trophoblast cells invade and modify the uterine vasculature to provide circulation of maternal blood through the placenta. Although evidence indicates fundamental differences between trophoblast modification of arteries and veins, interactions between trophoblast cells and uterine veins have not been addressed. In this report we describe the processes by which trophoblast cells invade and restructure uterine veins during placentation in the macaque. Antibodies were used to identify trophoblast, endothelium, and basement membranes. During early gestation, trophoblast migrated from the trophoblastic shell and, by intravasation, replaced portions of the wall and endothelium of veins in the vicinity of the shell; this is in contrast to invasion by extravasation reported for the arteries in this species. These areas had discontinuous endothelial basement membranes and the endothelial cells were variably hypertrophied. Deeper portions of veins were not invaded; this too is in contradistinction to the spiral arteries where trophoblastic modification extends to the myometrial segments. Later in gestation, those portions of veins interacting with trophoblast were contained within the trophoblastic shell or situated such that one side abutted the shell. These regions of the veins were lined by endothelium, but it could not be determined whether this represented re-endothelialization of regions formerly lined by trophoblast or if these endothelial cells were never displaced.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00327994
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    Paper (German National Licenses)
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