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  • 1
    Electronic Resource
    Electronic Resource
    Acute application of NGF increases the firing rate of aged rat basal forebrain neurons (1999)
    Oxford, UK : Blackwell Science Ltd
    European journal of neuroscience 11 (1999), S. 0 
    Details
    ISSN: 1460-9568
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Nerve growth factor (NGF) has been widely used in animal models to ameliorate age-related neurodegeneration, but it cannot cross the blood–brain barrier (BBB). NGF conjugated to an antibody against the transferrin receptor (OX-26) crosses the BBB and affects the biochemistry and morphology of NGF-deprived basal forebrain neurons. The rapid actions of NGF, including electrophysiological effects on these neurons, are not well understood. In the present study, two model systems in which basal forebrain neurons either respond dysfunctionally to NGF (aged rats) or do not have access to target-derived NGF (intraocular transplants of forebrain neurons) were tested. One group of transplanted and one group of aged animals received unconjugated OX-26 and NGF comixture as a control, while other groups received replacement NGF in the form of OX-26–NGF conjugate during the 3 months preceding the electrophysiological recording session. Neurons from animals in both the transplanted and aged control groups showed a significant increase in firing rate in response to acute NGF application, while none of the conjugate-treated groups or young intact rats showed any response. After the recordings, forebrain transplants and aged brains were immunocytochemically stained for the low-affinity NGF receptor. All conjugate treatment groups showed significantly greater staining intensity compared to controls. These data from both transplants and aged rats in situ indicate that NGF-deprived basal forebrain neurons respond to acute NGF with an increased firing rate. This novel finding may have importance even for long-term biological effects of this trophic factor in the basal forebrain.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1460-9568.1999.00644.x
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  • 2
    Electronic Resource
    Electronic Resource
    Candidate neuronal mechanisms for abnormal sensory gating in schizophrenia
    Amsterdam : Elsevier
    Schizophrenia Research 2 (1989), S. 82 
    Details
    ISSN: 0920-9964
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://linkinghub.elsevier.com/retrieve/pii/0920-9964(89)90118-7
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Neuronal development in embryonic brain tissue derived from schizophrenic women and grafted to animal hosts
    Amsterdam : Elsevier
    Schizophrenia Research 13 (1994), S. 259-270 
    Details
    ISSN: 0920-9964
    Keywords: (Schizophrenia) ; Brain derived neurotrophic factor ; Cholinergic receptors ; Growth factors ; Neuronal development
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://linkinghub.elsevier.com/retrieve/pii/0920-9964(94)90051-5
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    Paper (German National Licenses)
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  • 4
    Electronic Resource
    Electronic Resource
    Glial cell line-derived neurotrophic factor improves survival of ventral mesencephalic grafts to the 6-hydroxydopamine lesioned striatum (1997)
    Springer
    Experimental brain research 116 (1997), S. 29-38 
    Details
    ISSN: 1432-1106
    Keywords: Key words Glial cell line-derived neurotrophic factor ; Striatum ; Nigrostriatal dopaminergic pathway ; Transplants ; Neurotrophic factors
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  One approach to replace lost dopaminergic neurons in Parkinson’s disease is to transplant fetal mesencephalic tissue into the striatum. In an attempt to expand the developmental window useful for grafting of mesencephalic tissue and increase the fiber outgrowth from grafted dopaminergic neurons, we have pretreated fetal mesencephalic tissue with the dopaminotrophic factor glial cell line-derived neurotrophic factor (GDNF). Mesencephalic tissue pieces from embryonic day 18–19 Fischer 344 rats were preincubated for 20 min with GDNF (1 μg/μl) or vehicle. Two tissue pieces were then transplanted into the striatum of rats that had been unilaterally lesioned by medial forebrain bundle injections of 6-hydroxydopamine. The animals were tested for apomorphine-induced rotations prior to intracranial grafting. Host rats received intrastriatal injections of 10 μg GDNF or control solution at 10 days and 4 weeks postgrafting. The animals were tested in the rotometer twice monthly following transplantation. Despite the fact that these transplants were from a suboptimal donor stage, the rotations were significantly decreased in both transplanted groups. Immunohistochemical evaluation of the host brains revealed that the overall size of transplanted mesencephalic tissue was significantly increased in the GDNF-treated animals, and that the average size of transplanted tyrosine hydroxylase (TH)-positive neurons was also increased. Furthermore, we found that the innervation density of surrounding host striatal tissue was significantly increased in the GDNF-treated group, as compared with controls. Taken together, these results suggest that treatment of intrastriatal ventral mesencephalon grafts with GDNF can optimize the conditions for intracranial grafting and thus improve the chances for functional recovery following the intrastriatal grafting procedure.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/PL00005741
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  • 5
    Electronic Resource
    Electronic Resource
    6-Hydroxydopamine induces the loss of the dopaminergic phenotype in substantia nigra neurons of the rat (1996)
    Springer
    Experimental brain research 111 (1996), S. 1-7 
    Details
    ISSN: 1432-1106
    Keywords: Cell death ; Neurotrophins ; Retrograde labeling ; Tyrosine hydroxylase ; Rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Intraparenchymal injections of the neurotoxin 6-hydroxydopamine (6-OHDA) into the medial forebrain bundle in rats destroys the dopaminergic neurons in the pars compacta of the substantia nigra. In other transmitter systems it has been found that axotomy or neurotoxin exposure produces an initial loss of neurotransmitter phenotype, with cell death occurring over a much slower time course. To determine whether this also occurs in dopamine neurons after 6-OHDA, two approaches were utilized. First, the effect of injections of 6-OHDA into the medial forebrain bundle on nigral dopaminergic neurons was studied using combined fluorogold and immunocytochemical labeling. Four weeks after the 6-OHDA injection, there was an 85% reduction in the number of tyrosine hydroxylase (TH)-immunoreactive cells on the lesioned side. In contrast, there was only a 50% reduction in the number of fluorogold-labeled cells on the lesioned side. Second, the time course of the rescue of dopaminergic neurons after 6-OHDA by glial cell line-derived neurotrophic factor (GDNF) was determined using TH immunocytochemistry. Greater numbers of dopamine neurons were rescued 9 weeks after GDNF, compared with counts made 5 weeks after GDNF. Taken together, these results suggest loss of dopaminergic phenotype is greater than cell loss following 6-OHDA injections, and that GDNF restores the phenotype of affected cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00229549
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    Paper (German National Licenses)
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  • 6
    Electronic Resource
    Electronic Resource
    Anatomical distribution of glycoprotein 93 (gp93) on nerve fibers during rat brain development. (1999)
    Springer
    Cell & tissue research 297 (1999), S. 67-79 
    Details
    ISSN: 1432-0878
    Keywords: Key words Growth cones ; Glycoprotein ; gp93 ; Neuronal development ; Transplantation ; Axonal extension ; Rat (Fischer 344)
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract  Recent studies have implicated glycoconjugates on the membrane of growth cones as the necessary markers and intermediaries for axonal recognition, axonal motility, and pathway development. One such glycoconjugate, glycoprotein 93 (gp93), has been characterized, but the relative distribution of gp93 has yet to be described for the embryonic brain. In this study, the anatomical distribution of gp93 has been analyzed at embryonic day 15 (E15) and E18, and on postnatal day 3 in the rat by using a polyclonal gp93 antibody. Furthermore, fetal brain tissue transplanted into the adult rat eye has been tested for gp93 immunoreactivity, since central noradrenergic neurons in brainstem transplants are known to provide a continuous source of growing axons, even in adult tissue. In general, a greater abundance of gp93 immunoreactivity is apparent in the earlier embryonic stages (E15 and E18), whereas less is seen in the postnatal brain. The regions showing unique dispersal patterns of gp93 are the neuroepithelium, cerebral cortex, septo-hippocampal pathways, brainstem, and midbrain. This study has therefore focused on these areas and found implications for gp93 distribution appearing in the early development of specific neuronal pathways. Moreover, axons stain densely for gp93 within brain tissue transplants. The presence of gp93 in areas of extensive axonal outgrowth in the normal brain and in transplants suggests that this antibody is used as an early marker for axonal growth. Furthermore, gp93 might be used to map normal development in order to improve our understanding of diseases arising from developmental abnormalities.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004410051334
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