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  • 1
    Electronic Resource
    Electronic Resource
    Quantitative cellular changes during postnatal development of the rat dorsal lateral geniculate nucleus (1986)
    Springer
    Anatomy and embryology 174 (1986), S. 321-327 
    Details
    ISSN: 1432-0568
    Keywords: Dorsal lateral geniculate nucleus ; Glial cell number ; Neuron number ; Postnatal development ; Rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Quantitative changes in cell number during development of the dorsal lateral geniculate nucleus were determined using semithin serial sections of tissue obtained from 28 rats on postnatal day 0, 5, 8, 10, 20, 30, 90 or 165. Our results show three phases of postnatal development in the rat dorsal lateral geniculate nucleus: phase 1 from birth until eye opening, which occurs around the 12th day in these litters; phase 2 from eye opening through stabilization of neuron number on the 30th postnatal day, and phase 3 from that event until adulthood. During the first period increases in neuron number and in glial cell number are found accompanying a nearly seven-fold increase in dorsal lateral geniculate nucleus volume. Phase 2 includes a high incidence of neuronal cell death and a continuous increase in the number of glial cells. The third phase is characterized by a stabilization in the number of neurons, although the glial cell number continues to increase. Neuronal density decreases exponentially throughout the postnatal life of the rat, while the density of glial cells remains relatively stable over the period of study. The postnatal phenomenon of an initial increase in neuron number followed by a period of neuron death may be related to modulating and plastic functions which occur in the rat dorsal lateral geniculate nucleus before a stable neuronal population is achieved on the 30th postnatal day.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00698782
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  • 2
    Electronic Resource
    Electronic Resource
    Changes in the Turnover of Monoamines in Prefrontal Cortex of Rats Fed on Vitamin E-Deficient Diet (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 58 (1992), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Turnover of noradrenaline (NA), dopamine (DA), serotonin (5-HT), and their metabolites has been measured after a 15-day vitamin E-deficient diet in adult rat prefrontal cortex. Turnover rates of 3,4-dihydroxyphenylacetic acid, homovanillic acid, and 5-hydroxy-3-indoleacetic acid have been assayed from the disappearance rates after blocking by pargyline inhibition of monoamine oxidase. NA, DA, and 5-HT turnover rates have been measured as accumulation rates of NA, DA, and 5-HT after pargyline inhibition of monoamine oxidase. No change was found in the turnover rate of NA between control and experimental animals. In contrast, turnover rates of DA and homovanillic acid significantly increased in the animals fed on a low-vitamin E diet. However, the most striking results were found on the serotoninergic system. Levels of 5-HT and its main metabolite, 5-hydroxy-3-indoleacetic acid, and their respective turnover rates were lower in the vitamin E-deficient diet. These results could indicate that vitamin E is necessary for the normal functioning of the serotoninergic neurons in the rat prefrontal cortex. The involvement of vitamin E in preventing the formation of free radicals is well known. Therefore, this lack of protective effect after a 15-day vitamin E-deficient diet could be responsible for the neuronal damage to the serotoninergic system. The opposing results found in DA (increase) and 5-HT (decrease) turnover could provide further evidence for an inhibitory control of the serotoninergic ascending pathways to the dopaminergic system in the prefrontal cortex.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1992.tb10066.x
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  • 3
    Electronic Resource
    Electronic Resource
    Low Selenium Diet Affects Monoamine Turnover Differentially in Substantia Nigra and Striatum (1993)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 61 (1993), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Turnover of dopamine, noradrenaline. serotonin, and their metabolites has been measured in striatum and substantia nigra of adult female rats that were fed control or selenium-deficient diets for 15 days. In addition, the glutathione peroxidase activity has been studied. The most striking result was the increase of dopamine turnover (63%) and 3- methoxytyramine turnover (55%) in substantia nigra between control and experimental animals. On the other hand, no changes were found in the turnover rate of dopamine and its metabolites in the striatum. Likewise, no changes were found in noradrenaline turnover in substantia nigra. In the striatum, there was a significant increase of serotonin turnover versus no change for 5-hydroxy-3-indoleacetic acid. However, in the substantia nigra, serotonin turnover did not show significant changes, whereas 5-hydroxy-3-indoleacetic acid turnover decreased. At the same time, glutathione peroxidase activity significantly decreased in both structures after selenium-deficient diets. These results suggest that a selenium-deficient diet for a short period of time decreases brain protection. principally in the substantia nigra, against oxidative damage.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1993.tb13622.x
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  • 4
    Electronic Resource
    Electronic Resource
    Heterogeneity in the Allosteric Interaction Between the γ-Aminobutyric Acid (GABA) Binding Site and Three Different Benzodiazepine Binding Sites of the GABAA/Benzodiazepine Receptor Complex in the Rat Nervous System (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 58 (1992), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: In the present communication we have investigated the allosteric coupling between the γ-aminobutyric acidA (GABAA) receptor and the pharmacologically different benzodiazepine (BZD) receptor subtypes in membranes from various rat nervous system regions. Two types of BZD receptors (type I and type II) have been classically defined using CL 218.872. However, using zolpidem, three different BZD receptors have been identified by binding displacement experiments in membranes. These BZD receptor subtypes displayed high, low, and very low affinity for zolpidem. The distribution of the high- and low-affinity binding sites for zolpidem was similar to that of type I and type II subtypes in cerebellum, prefrontal cortex, and adult cerebral cortex. On the other hand, the very-low-affinity binding site was localized in relative high proportion in spinal cord, hippocampus, and newborn cerebral cortex and, to a minor extent, in superior colliculus. The allosteric coupling between the GABAA receptor and the BZD receptor subtypes was different. The high- and low-affinity binding sites for zolpidem seemed to have a similar high degree of coupling, except in spinal cord. On the other hand, the very-low-affinity binding site for zolpidem displayed a low degree of coupling with the GABAA receptor. These results seem to indicate that the different efficacy of GABA in enhancing the [3H]flunitrazepam binding could be due to the different BZD receptor subtypes present in the GABAA/BZD receptor complex and, moreover, led us to speculate that the low GABA efficacy found in membranes from spinal cord, hippocampus, and newborn cerebral cortex might be due to the presence in relatively high proportion of the very-low-affinity binding site for zolpidem.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1992.tb09747.x
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  • 5
    Electronic Resource
    Electronic Resource
    Nigral and Striatal Comparative Study of the Neurotoxic Action of 1-Methyl-4-Phenylpyridinium Ion: Involvement of Dopamine Uptake System (1996)
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 66 (1996), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Microdialysis was used in a comparative study of the neurotoxic action of MPP+ in the absence or presence of nomifensine (20 µM) in the striatum and substantia nigra. Three different concentrations of MPP+ (1, 2.5, and 5 mM) were perfused for 15 min at 24 (day 1) and 48 h (day 2) after surgery. The dopamine basal value in the striatum was ∼17 fmol/min. Nomifensine (20 µM) stimulated dopamine release to ∼170 fmol/min. The increase of dopamine extracellular output in the striatum after MPP+ perfusion on day 1 was independent of the concentration of MPP+ perfused and of the absence or presence of nomifensine (20 µM), being ∼2,500 fmol/min. The dopamine basal value in the substantia nigra was below the detection limit of our HPLC equipment. Nomifensine (20 µM) stimulated dopamine release to ∼6.3 fmol/min. The increase of dopamine extracellular output in the substantia nigra was MPP+ dose-dependent (1 mM, 75 fmol/min; 2.5 mM, 150 fmol/min; and 5 mM, 250 fmol/min) and independent of the presence or absence of nomifensine. On day 2, the presence of nomifensine on day 1 produced a total protection against MPP+ (1 mM) perfusion in the striatum, which was not observed against MPP+ (5 mM). MPP+ (1 mM) did not produce any neurotoxic action in the substantia in the absence or presence of nomifensine. The MPP+ (2.5 mM) effect on dopamine extracellular output in the absence of nomifensine (20 µM) in the substantia nigra on day 2 was similar to that of MPP+ (1 mM) in the striatum. The presence of nomifensine (20 µM) partially prevented the neurotoxic effect of MPP+ (2.5 mM) on dopaminergic cell bodies/dendrites in the substantia nigra. The MPP+ (5 mM) effect on dopamine extracellular output was similar in both structures studied in the absence or presence of nomifensine on day 2. These results suggest that terminals in the striatum are more sensitive to the neurotoxicity of MPP+ than cell bodies/dendrites in the substantia nigra.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1471-4159.1996.66031182.x
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  • 6
    Electronic Resource
    Electronic Resource
    In vivo expression of aquaporin-4 by reactive microglia (2004)
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 91 (2004), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Aquaporin-4 (AQP4) is the most abundant aquaporin in the brain and it is widely accepted that this AQP is solely expressed by astrocytes and ependymal cells. AQP4 is particularly enriched in plasma membranes of ependymal cells and astrocyte membrane domains facing blood vessels and pia. AQP4 has gained much attraction due to its involvement in the physiopathology of brain edema, a major cause of death in humans. Consequently, it is of paramount importance to ascertain the phenotypic nature of AQP4 mRNA-expressing cells in the CNS before attempting future clinical studies aimed at minimizing the development of brain edema. We have used intranigral injections of lipopolysaccharide (LPS), a potent immunostimulant that causes disruption of the blood brain barrier, vasogenic edema, loss of reactive astrocytes and activation of microglial cells. These LPS-induced features are ideal for testing the possibility that reactive microglial cells express AQP4 in the adult brain. We have studied AQP4 at the mRNA and protein level. We provide strong evidence that reactive microglial cells highly express AQP4 mRNA and protein in response to LPS injections.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.2004.02759.x
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  • 7
    Electronic Resource
    Electronic Resource
    Expression of BDNF mRNA in substantia nigra is dependent on target integrity and independent of neuronal activation (2003)
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 87 (2003), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: We have analyzed the regulation of brain-derived neurotrophic factor (BDNF) mRNA expression in the nigrostriatal system following neurotoxin ablation of striatal targets by means of kainate (KA) or quinolinic acid (QA) injections. Loss of nigral target cells in the striatum was accompanied by significant induction of BDNF mRNA levels in the ipsilateral substantia nigra (SN) at 12 and 24 h post lesion. Dual tyrosine hydroxylase (TH) and BDNF mRNA in situ hybridization (ISH) confirmed the dopaminergic nature of the BDNF mRNA expressing cells. Analysis of neuronal activity in terms of cFos mRNA expression demonstrated intense induction of this marker in the ipsilateral SN pars reticulata (SNPR), but not in SN pars compacta. Dual glutamic acid decarboxylse (GAD) and cFos mRNA ISH confirmed this view. Colchicine injections into the medial forebrain bundle to specifically disrupt neuronal trafficking between SN and striatum induced BDNF mRNA levels in the ipsilateral SNPC, thus demonstrating that nigral expression of BDNF mRNA is dependent of striatal target tissue. In addition, we found significant elevations of BDNF in the subthalamic nucleus following striatal excitotoxic lesion, which may bring novel roles of BDNF in the basal ganglia complex.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1471-4159.2003.02041.x
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  • 8
    Electronic Resource
    Electronic Resource
    The Endogenous Amine 1-Methyl-1,2,3,4- Tetrahydroisoquinoline Prevents the Inhibition of Complex I of the Respiratory Chain Produced by MPP+ (2000)
    Oxford UK : Blackwell Science Ltd.
    Journal of neurochemistry 75 (2000), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract : The endogenous monoamine 1-methyl-1,2,3,4-tetrahydroisoquinoline has been shown to prevent the neurotoxic effect of MPP+ and other endogenous neurotoxins, which produce a parkinsonian-like syndrome in humans. We have tested its potential protective effect in vivo by measuring the protection of 1-methyl-1,2,3,4-tetrahydroisoquinoline in the neurotoxicity elicited by MPP+ in rat striatum by tyrosine hydroxylase immunocytochemistry. Because we know that cellular damage caused by MPP+ is primarily the result of mitochondrial respiratory inhibition at the complex I level, we have extended the study further to understand this protective mechanism. We found that the inhibitory effect on the mitochondrial respiration rate induced by MPP+ in isolated rat liver mitochondria and striatal synaptosomes was prevented by addition of 1-methyl-1,2,3,4-tetrahydroisoquinoline. This compound has no antioxidant capacity ; therefore, this property is not involved in its protective effect. Thus, we postulate that the preventive effect that 1-methyl-1,2,3,4-tetrahydroisoquinoline has on mitochondrial inhibition for MPP+ could be due to a “shielding effect,” protecting the energetic machinery, thus preventing energetic failure. These results suggest that this endogenous amine may protect against the effect of several parkinsonism-inducing compounds that are associated with progressive impairment of the mitochondrial function.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1471-4159.2000.0750065.x
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  • 9
    Electronic Resource
    Electronic Resource
    Thrombin induces in vivo degeneration of nigral dopaminergic neurones along with the activation of microglia (2003)
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 84 (2003), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Seven days after the injection of different concentrations of thrombin into the nigrostriatal pathway, a strong macrophage/microglial reaction was observed in the substantia nigra (SN), indicated by immunostaining, using OX-42 and OX-6 antibodies, and by the induction of iNOS, IL-1α, Il-1β and TNF-α. Moreover, selective damage to dopaminergic neurones was produced after thrombin injection, evidenced by loss of tyrosine hydroxylase immunostaining and tyrosine hydroxylase mRNA-expressing cell bodies, and the unaltered transcription of glutamic acid decarboxylase mRNA in the SN and striatum. These thrombin effects could be produced by its ability to induce the activation of microglia described in in vitro studies, and are in agreement with the effects described for other proinflammatory compounds. Thrombin effects are produced by its biological activity since they almost disappeared when thrombin was heat-inactivated or injected along with its inhibitor α-NAPAP. Thrombin is a multi-functional serine protease rapidly produced from prothrombin at the sites of tissue injury, and also upon breakdown of the blood–brain barrier, which strongly suggests it could easily enter into the CNS. These results could have special importance in some degenerative processes of the nigrostriatal dopaminergic system.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1471-4159.2003.01634.x
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  • 10
    Electronic Resource
    Electronic Resource
    Group II metabotropic glutamate receptor activation protects striatal dopaminergic nerve terminals against MPP+-induced neurotoxicity along with brain-derived neurotrophic factor induction (2001)
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 76 (2001), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: We have studied the in vivo effect of the selective agonist for group II metabotropic glutamate receptors (2S, 2′R, 3′R)-2-(2′3′-dicarboxycyclopropyl)glycine (DCG-IV) against MPP+-induced toxicity on rat striatal dopaminergic nerve terminals by using both microdialysis and immunohistochemical techniques. Perfusion of 1 mm DCG-IV during 1 h protected dopaminergic nerve terminals against the degeneration induced by a 15-minute perfusion of 1 mm MPP+. In addition, the microglial cell population was markedly activated 24 h after DCG-IV perfusion. The astroglial cell population was only markedly activated around the microdialysis probe. This protective effect seems to be dependent on protein synthesis since 1 mm cycloheximide, an inhibitor of protein synthesis, abolished the neuroprotective effect of 1 mm DCG-IV against MPP+ toxicity. Perfusion of DCG-IV induced an upregulation of striatal brain-derived neurotrophic factor (BDNF) mRNA expressing cells which were confined precisely around the microdialysis probe. Taken together, our results suggest that the induction and release of brain-derived neurotrophic factor (BDNF) by activated glial cells induced by DCG-IV perfusion may account for its protective action against MPP+-induced dopaminergic terminal degeneration.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1471-4159.2001.00056.x
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