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  • 1
    Electronic Resource
    Electronic Resource
    Coordinate Expression of the Vesicular Acetylcholine Transporter and Choline Acetyltransferase Following Septohippocampal Pathway Lesions (1998)
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 71 (1998), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The gene for the vesicular acetylcholine transporter (VAChT) was recently cloned and found to be located within a 5′ noncoding intron of the gene for choline acetyltransferase (ChAT). There appear to be several shared and unique promoters for each gene, suggesting that control of expression of these two genes can be either coordinated or independent. Two lesions, axotomy and immunotoxin, directed at the well defined septohippocampal cholinergic pathway were used to determine VAChT and ChAT protein expression in the degenerating terminal fields in the hippocampus and the cell bodies of the medial septum nucleus after injury. Two weeks after lesioning, decreases of up to 90% in VAChT were found in the affected hippocampus by immunoblotting and immunocytochemistry, similar to ChAT activity. The number of VAChT- and ChAT-immunopositive neurons in the medial septum decreased by up to 95%. Eight weeks following axotomy, the number of VAChT- and ChAT-immunopositive neurons had increased to almost 50% in fimbria-fornix-lesioned animals, indicating coordinate reexpression of both cholinergic markers in recovered neurons. There was no recovery of either VAChT or ChAT immunoreactivity after the irreversible immunotoxin lesions. Thus, with use of immunological techniques, there appears to be coordinate expression of VAChT and ChAT in the septohippocampal pathway following either unilateral fimbria-fornix or bilateral immunotoxin lesion.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1471-4159.1998.71062411.x
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  • 2
    Electronic Resource
    Electronic Resource
    Lesion-induced transneuronal plasticity of the cholinergic innervation in the adult rat entorhinal cortex (1998)
    Oxford, UK : Blackwell Science Ltd
    European journal of neuroscience 10 (1998), S. 0 
    Details
    ISSN: 1460-9568
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The present experiments were designed to determine the effect that lesions of the basal forebrain cholinergic system exert on cholinergic interneurons within the entorhinal cortex (EC) in the rat. Unilateral infusion of 192 IgG-saporin into the nucleus of the horizontal diagonal band of Broca (HDB) decreased the number of ipsilateral choline acetyltransferase immunoreactive (ChAT-ir) neurons by 54%. Two–four weeks after the lesion, the ipsilateral EC exhibited a moderate but significant loss of ChAT-ir fibres and interneurons. Adjacent sections revealed a parallel loss of vasoactive intestinal polypeptide (VIP) immunoreactivity. Cell counts in the cingulate cortex were unaffected, suggesting that this effect was indeed specific to the main target area for HDB neurons. Ibotenic acid lesions also induced a significant 36% decrease in the number of cholinergic neurons in the ipsilateral HDB, and disappearance of ChAT terminals in the EC, whereas the number of ChAT-ir neurons in the EC was unchanged. Since ibotenic acid affects all cells and not only cholinergic ones, our results suggest that the specific degeneration of cholinergic neurons in the HDB after 192 IgG-saporin treatment could be inducing transsynaptic effects on their targets. Injections of 192 IgG-saporin directly into the EC also lesioned the cholinergic projection from the HDB, but had no effect on the intrinsic population.Eight weeks after immunolesion, the number of interneurons immunoreactive for ChAT and VIP in the EC had returned to normal values, and persisted for as long as 6 months after the lesion. By contrast, ChAT-ir neurons in the HDB were permanently lost.Our results suggest that the transient down-regulation of the cholinergic phenotype in entorhinal cortex interneurons could be a manifestation of activity-dependent plasticity, and that the loss of cholinergic innervation from the basal forebrain could be responsible for these effects through an imbalance of inputs. We hypothesize that the recovery of the phenotypic expression of entorhinal interneurons could be due to a recovery in their innervation, perhaps from sprouting axons in the same fields, belonging to surviving cholinergic neurons in the basal forebrain.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1460-9568.1998.00116.x
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  • 3
    Electronic Resource
    Electronic Resource
    Functionally and Anatomically Distinct Populations of Vasopressinergic Magnocellular Neurons in the Female Golden Hamster (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neuroendocrinology 4 (1992), S. 0 
    Details
    ISSN: 1365-2826
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The present study was done to determine whether the vasopressinergic neurons in the hypothalamus controlling flank marking behavior are distinct from the magnocellular neurons comprising the hypothalamo-neurohypophysial system. Animals were either hypophysectomized or injected with a suicide transport lectin, volkensin, into the neurohypophysis. Both procedures resulted in a pronounced loss of vasopressin-immunoreactive perikarya throughout the hypothalamus concomitant with increases in water intake and urine output and decreases in circulating levels of vasopressin. The loss of the hypothalamo-neurohypophysial system was most pronounced in volkensin-treated animals that presented with frank diabetes insipidus and exceedingly low levels of plasma vasopressin. However, the vasopressinergic fibers and magnocellular neurons in and around the anterior hypothalamus implicated in the control of flank marking survived the volkensin treatment. Volkensin-treated animals exhibited levels of flank marking typical of untreated animals. These data suggest the presence of anatomically and functionally distinct populations of vasopressinergic magnocellular neurons in the hypothalamus of the golden hamster.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-2826.1992.tb00159.x
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  • 4
    Electronic Resource
    Electronic Resource
    192 IgG-saporin (1995)
    Springer
    Acta neuropathologica 89 (1995), S. 519-526 
    Details
    ISSN: 1432-0533
    Keywords: Astrocyte ; Cholinergic ; Immunotoxin ; Microglia ; Nerve growth factor receptor
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We have previously shown that an immunotoxin (IT) directed against the p75 component of the nerve growth factor receptor (NGFr) selectively abolished cholinergic neurons in the basal forebrain of the rat following intraventricular administration. We now report the neuropathological responses in the rat brain to the IT, with particular emphasis on the cholinergic basal forebrain (CBF) and other known p75NGFr-positive brain regions. Animals received intraventricular injections of IT and were allowed to survive for various times. Sections through the entire brain were evaluated using (1) hematoxylin and eosin; (2) glial fibrillary acidic protein immunohistochemistry; and (3)Griffonia simplicifolia lectin histochemistry. The only clearly degenerating cells following IT treatment were located in the CBF or in the Purkinje cell layer of the cerebellum. A marked microglial response was demonstrated that was tightly linked both topographically and temporally to the loss of neurons in these areas. The astroglial response was mild in the same regions in which the microglial response was obvious. The other areas of rat brain including the terminal fields of CBF projections showed no consistent reactive cellular responses in IT-treated animals. This study extends and corroborates previous work indicating speciticity of IT, demonstrates active neuronal degeneration by conventional pathological methods for the first time, and illustrates the unexpected and novel finding that the predominant pathological response to the IT-induced loss of neurons is microglial. Both the high degree of specificity and the distinctive glial response distinguish the IT model from other experimental models of CBF neurodegeneration.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00571506
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    Paper (German National Licenses)
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  • 5
    Electronic Resource
    Electronic Resource
    192 IgG-saporin (1995)
    Springer
    Acta neuropathologica 89 (1995), S. 519-526 
    Details
    ISSN: 1432-0533
    Keywords: Key words Astrocyte ; Cholinergic ; Immunotoxin ; Microglia ; Nerve growth factor receptor
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We have previously shown that an immunotoxin (IT) directed against the p75 component of the nerve growth factor receptor (NGFr) selectively abolished cholinergic neurons in the basal forebrain of the rat following intraventricular administration. We now report the neuropathological responses in the rat brain to the IT, with particular emphasis on the cholinergic basal forebrain (CBF) and other known p75NGFr-positive brain regions. Animals received intraventricular injections of IT and were allowed to survive for various times. Sections through the entire brain were evaluated using (1) hematoxylin and eosin; (2) glial fibrillary acidic protein immunohistochemistry; and (3) Griffonia simplicifolia lectin histochemistry. The only clearly degenerating cells following IT treatment were located in the CBF or in the Purkinje cell layer of the cerebellum. A marked microglial response was demonstrated that was tightly linked both topographically and temporally to the loss of neurons in these areas. The astroglial response was mild in the same regions in which the microglial response was obvious. The other areas of rat brain including the terminal fields of CBF projections showed no consistent reactive cellular responses in IT-treated animals. This study extends and corroborates previous work indicating specificity of IT, demonstrates active neuronal degeneration by conventional pathological methods for the first time, and illustrates the unexpected and novel finding that the predominant pathological response to the IT-induced loss of neurons is microglial. Both the high degree of specificity and the distinctive glial response distinguish the IT model from other experimental models of CBF neurodegeneration.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00571506
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    Paper (German National Licenses)
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  • 6
    Electronic Resource
    Electronic Resource
    Leukoencephalopathy complicating intraventricular Catheters: clinical, radiographic and pathologic study of 10 cases (1988)
    Springer
    Journal of neuro-oncology 6 (1988), S. 67-74 
    Details
    ISSN: 1573-7373
    Keywords: methotrexate ; leukoencephalopathy ; intraventricular ; chemotherapy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Ten patients with implanted Ommaya devices developed pericatheter white matter lesions, apparent as focal lucenaries on computed tomographic scan sometimes with contrast enhancement and/or mass effect. Some of the patients had significant neurological signs that related to the lesion. Three of the patients had not received cytotoxic drugs through the reservoir, and two had received neither intrathecal chemotherapy nor cranial radiation therapy. The process appears to be related to back flow of cerebrospinal fluid, with or without contained cytotoxic drugs into the periventricular white matter. Patients with elevated intracranial pressure are at particular risk. Removal of the catheter relieves the condition.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00163543
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