Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    ISSN: 1432-0738
    Keywords: Manganese toxicity ; Dopamine ; Serotonin ; Neurotensin ; Macaca fascicularis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Four monkeys were exposed to a total of 8 g each of manganese as oxide by repetitive subcutaneous injections during 5 months, after which they were left for 1 week to 6 months before they were sacrificed. All animals developed hyperactive behaviour after about 2 months. About 5 months after the start of the exposure the animals became hypoactive with an unsteady gait, and subsequently an action tremor appeared in some of the animals. The animals lost power in both upper and lower limbs and the movements of the hands and feet were very clumsy. The serum content of manganese rose 10–40 times during the exposure time and the content in brain was generally increased more than 10 times, with the highest content found in globus pallidus and putamen. The observed neurochemical effects were also largest in globus pallidus and putamen. In these regions there was a considerable depletion of dopamine and 3,4-dihydroxyphenylacetic acid, while the homovanillic acid content remained almost unchanged. A severe neuronal cell loss was observed in globus pallidus but not in other regions. This is in accordance with results from the most recent neuropathological study of a human suffering from chronic manganese poisoning [Yamada et al. (1986) Acta Neuropathol 70: 273–278] where globus pallidus was devoid of neuronal cells while the content of pigmented cells in substantia nigra was normal. Our data suggest a reduction in number of dopaminergic nerve terminals, as the activity of the dopamine synthesizing enzyme DOPA-decarboxylase was also lowered. In addition to the effects on the dopaminergic system, a reduced content of 5-hydroxyindole acetic acid was observed in the putamen and globus pallidus. Moreover neurotensin, a neuropeptide with functional connection to the dopaminergic system, was found to be reduced in the putamen. It was remarkable that all the neurochemical effects seen in the putamen were more or less absent from the caudate nucleus. These observations are discussed in relation to what has been found in Parkinsonian and MPTP-lesioned brains.
    Type of Medium: Electronic Resource
    Signatur Availability
    BibTip Others were also interested in ...
  • 2
    ISSN: 1432-0738
    Keywords: Key words L-2-Chloropropionic acid ; Cerebellar granule cell toxicity-Excitotoxicity ; Free radical species
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract L-2-Chloropropionic acid (L-CPA), when administered orally to rats, produces selective necrosis to the granule cell layer of the rat cerebellum which is delayed in onset, not appearing until 36 – 48 h after exposure. The present study was conducted to characterise the toxic effect of L-CPA in primary cell cultures of rat cerebellar granule cells in vitro. Exposure to L-CPA produced a time and concentration dependent loss in cerebellar granule cell viability. Mean 50% effective concentration (EC50) values for L-CPA toxicity were 18.3 ± 0.3, 7.4 ± 0.1, and 3.5 ± 0.1 mM for 24, 48 and 72 h exposure respectively. Exposure for 24 h followed by a return to L-CPA free medium for 24 h was more toxic than exposure for 24 h alone. Cells maintained in culture for a longer duration were more susceptible to L-CPA-induced toxicity. The toxic effects of L-CPA could be partially or fully prevented by concomitant exposure of the cells to putative neuroprotective compounds. The N-methyl-D-aspartate (NMDA) receptor antagonist, MK-801 (3 μM), afforded partial protection against L-CPA induced toxicity, whilst other glutamate receptor antagonists including, D(-)-2-amino-5-phosphopentanoic acid (D-AP5; 300 μM), D(-)-3-(2-carboxypiperazine-4-yl)-propyl-1-phosphonic acid (D-CPP; 300 μM), 5,7-dichlorokynurenic acid (10 μM) and 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX; 1 μM) were ineffective. The antioxidant, vitamin E (10 μM), afforded significant but incomplete protection from L-CPA toxicity. However when both MK-801 (3 μM) and vitamin E (10 μM) were present during L-CPA exposure, a greater degree of protection was observed than with either compound alone, although the combination failed to provide complete protection. Cyclosporin A, an inhibitor of the mitochondrial transition pore, also provided partial protection. By contrast, the free radical trapping agent, N-tert-butyl-α-(2-sulfophenyl)-nitrone (S-PBN) provided concentration (1–10 mM) dependent protection against the L-CPA-induced toxicity, which was complete at 10 mM. Our findings suggest that free radical production may be involved in the mechanism of L-CPA-induced toxicity.
    Type of Medium: Electronic Resource
    Signatur Availability
    BibTip Others were also interested in ...
  • 3
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: In this study we have described a series of new and potent inhibitors of the vesicular uptake of glutamate. The two most efficient inhibitors were the dyes Evans blue and Chicago Skye Blue 6B, which are structurally related to glutamate and were competitive inhibitors in the nanomolar range. The anion channel blocker 4,4′-diisothiocyanostilbene-2,2′-disulfonic acid (SITS) and the diuretics furosemide and bumetanide are inhibitors of chloride transport in other organs but were competitive inhibitors of glutamate and noncompetitive with respect to chloride ions. Evans blue, Chicago Skye Blue 6B, SITS, furosemide, and bumetanide are all large organic acids with two centers of negative charge and an electron-donating group at close vicinity of the negative charge at physiological pH. The inhibition of the glutamate uptake with these inhibitors was noncompetitive with respect to Cl−. The inhibitors, therefore, probably interact directly with the glutamate carrier. Bafilomycin A1, which is a specific vacuolar ATPase inhibitor, was used as a control and inhibited the vesicular dopamine, glutamate, and GABA uptake to the same extent. None of the inhibitors had any effect on the plasma membrane carrier, which is therefore clearly different from the vesicular carrier.
    Type of Medium: Electronic Resource
    Signatur Availability
    BibTip Others were also interested in ...
  • 4
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Rat brain synaptic vesicles exhibit ATP-dependent uptake of γ-[3H]amino-n-butyric acid ([3H]GABA) and l-[3H]glutamate. After hypotonic shock, the highest specific activities of uptake of both l-glutamate and GABA were recovered in the 0.4 M fraction of a sucrose gradient. The uptakes of l-glutamate and GABA were inhibited by similar, but not identical, concentrations of the mitochondrial uncoupler carbonyl cyanide m-chlorophenylhydrazone and the ionophores nigericin and gramicidin, but they were not inhibited by the K+ carrier valinomycin. N, N′-Dicyclohexyl-carbodiimide and N-ethylmaleimide, Mg2+-ATPase inhibitors, inhibited the GABA and L-glutamate uptakes similarly. Low concentrations of CI− stimulated the vesicular uptake of l-glutamate but not that of GABA. The uptakes of both l-glutamate and GABA were inhibited by high concentrations of CI−. These results indicate that the vesicular GABA and l-glutamate uptakes are driven by an electrochemical proton gradient generated by a similar Mg2+-ATPase. The vesicular uptake mechanisms are discussed in relation to other vesicle uptake systems.
    Type of Medium: Electronic Resource
    Signatur Availability
    BibTip Others were also interested in ...
  • 5
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 50 (1988), S. 0 
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: γ-Aminobutyric acid (GABA) was taken up by a MgATP-dependent mechanism into synaptic vesicles isolated by hypoosmotic shock and density gradient centrifugation. The properties of the vesicular uptake differed clearly from those of synaptosomal and glial uptake, both with respect to Na+, Mg2+, and ATP dependence and with respect to response to general GABA uptake inhibitors such as nipecotic acid, diaminobutyric acid, and β-alanine. The uptake showed a Km of 5.6 mM and a net uptake rate of 1,500 pmol/min/mg of protein. It is suggested that the vesicular uptake of GABA is driven by an electrochemical proton gradient generated by a Mg2+-ATPase.
    Type of Medium: Electronic Resource
    Signatur Availability
    BibTip Others were also interested in ...
  • 6
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The synaptosomal effluxes of d-aspartate and γ-aminobutyric acid (GABA) induced by a substitution of the Cl- ions with propionate in the incubation medium were measured in preparations of hippocampal tissue homogenates. The efflux of aspartate was significantly higher than spontaneous efflux at 125 mM Cl- (normal = 144 mM) and was increased with decreasing Cl- concentration. GABA efflux was much less sensitive to a reduction in Cl concentration than D-aspartate. The efflux was Ca2+-dependent in both cases.
    Type of Medium: Electronic Resource
    Signatur Availability
    BibTip Others were also interested in ...
  • 7
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 35 (1980), S. 0 
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The activities of five enzymes involved in acetyl-CoA synthesis, pyruvate dehydrogenase complex, ATP citrate lyase, carnitine acetyl-transferase, acetyl-CoA synthetase, and citrate synthase, were determined in normal nucleus interpeduncularis and nucleus interpeduncularis in which cholinergic terminals were removed following lesion of the habenulo-interpeduncular tract. The activities of aspartate transaminase, fumarase, and GABA transaminase also were determined to compare the effect of lesion on other mitochondrial enzymes which are not linked to the biosynthesis of ACh. In normal nucleus interpeduncularis the activities of carnitine acetyltransferase and pyruvate dehydrogenase complex were higher than the activity of ChAT (choline acetyltransferase), whereas the activities of acetyl-CoA synthetase and citrate synthase were considerably lower than that of ChAT. The effect of the lesion separated the enzymes into two groups: the activities of pyruvate dehydrogenase complex, carnitine acetyltransferase, fumarase and aspartate transaminase decreased by 30–409%, whereas the activities of the other enzymes decreased 5–15%. ChAT activity was in all cases less than 159% of normal. It could be concluded that none of the acetyl-CoA synthesizing enzymes decreased to the degree that ChAT did. Only pyruvate dehydrogenase complex and carnitine acetyltransferase seem to be localized in cholinergic terminals to a significant degree. ATP citrate lyase as well as acetyl-CoA synthetase seem to have less significance in supporting acetyl-CoA formation in cholinergic nerve terminals.
    Type of Medium: Electronic Resource
    Signatur Availability
    BibTip Others were also interested in ...
  • 8
    ISSN: 1432-0738
    Keywords: Trichlorfon ; Teratogenicity ; Brain ; Guinea pig
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The organophosphorus compound trichlorfon, dimethyl (2,2,2-trichloro-1-hydroxyethyl) phosphonate, was administered by stomach tube (100 mg/kg) to pregnant guinea pigs at two different stages of gestation (days 36, 37, 38 and 51, 52, 53). The pups developed locomotory disturbances, and post mortem examination revealed significantly decreased weights of the total brain and the cerebellum, as compared to controls. There was also a significant weight reduction particularly of the medulla oblongata, but also of the hippocampus, the thalamus, and the colliculi. Histological examination of the cerebellum revealed reduction of the external granular layer and the molecular layer, and regional absence of Purkinje cells. The activities of the neurotransmitter enzymes choline acetyltransferase (ChAT), and glutamate decarboxylase (GAD) in cerebellum were reduced as compared to the control values.
    Type of Medium: Electronic Resource
    Signatur Availability
    BibTip Others were also interested in ...
  • 9
    ISSN: 1432-0738
    Keywords: Organophosphorus inhalation ; Tracheal smooth muscle contraction ; Oxime treatment ; Pyridostigmine pretreatment
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The ex vivo contraction response of the rat tracheal smooth muscle was examined after 10 min in vivo inhalation of soman and/or pretreatment with pyridostigmine and/or post-exposure treatment with HI-6 ([[[(4-aminocarbonyl) pyridinio]methoxy]methyl]-2[(hydroxyimino) methyl]pyridinium dichloride) or Toxogonin® (1,1′-[oxybis-(methylene)]bis[4-[(hydroxyimino)methyl]-pyridinium] dichloride). In vivo pretreatment with pyridostigmine was achieved by subcutaneous (s. c.) implantation of an osmotic pump that delivered pyridostigmine continuously (0.01 mg/h) in the neck region of the rat 18 h before soman exposure. The ex vivo cholinergic tracheal smooth muscle response increased during the first 60 min after soman exposure in animals pretreated with pyridostigmine. The amplitude of the contraction response in pyridostigmine pretreated animals was about 60% of control, compared to 15% of control without pyridostigmine pretreatment. Pyridostigmine pretreatment also produced significant recovery of the total cholinesterase (ChE) activity in plasma, but not in trachea and lung. Intraperitoneal (i. p.) injection of HI-6 or Toxogonin® (50 mg/kg), immediately after 10 min inhalation exposure to soman, also significantly improved the ex vivo cholinergic contraction response of the trachea (decapitation 15 min after oxime administration). The recovery of the physiological response with Toxogonin® was, however, not stable. HI-6 was superior to Toxogonin® with respect to the initial airway contraction response, and the response increased up to a stable level not significantly different from control. There was no significant reactivation of the ChE activity after treatment with the oximes. Combination of pyridostigmine pretreatment and oxime treatment enhanced the recovery of the tracheal contraction response and the ChE activity in the trachea compared to treatment with oximes alone. Experiments with in vitro exposure to soman followed by washout and addition of oximes were also performed. The results show that both oximes effectively re-establish the tracheal response when administered 10 min, but not 30 min, after soman. The effect of Toxogonin® was, however, contrary to the effect of HI-6, not stable. These results correspond to the in vivo exposure experiments. The results from this study indicate that HI-6 produces a more potent and stable recovery of an ex vivo peripheral cholinergic response than Toxogonin® after 10 min inhalation exposure to soman.
    Type of Medium: Electronic Resource
    Signatur Availability
    BibTip Others were also interested in ...
  • 10
    ISSN: 1600-051X
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background: Inability to mount a suitable brain-neuroendocrine response to bacterial or other antigenic challenges has been found to play an important rôle in infectious and inflammatory disease susceptibility and progression, including periodontal disease.Objective: The present study was designed to determine the effects of glutamate administration to new-born Wistar rats on the development and progression of naturally occurring and ligature-induced periodontal disease in the rats as adults. Postnatal glutamate administration is known to permanently damage neurones in the hypothalamic arcuate nucleus.Method: New-born rats were treated 1× daily subcutaniously with 2 mg/g of monosodium-L-glutamate (MSG) for 5 days from day 3 to 6. Control animals were injected with similar amounts of saline. Experimental ligature-induced periodontal disease was induced in the rats at the age of 12 weeks at maxillary right 2nd molar teeth. The contralateral maxillary left 2nd molars served as control teeth, and for assessment of naturally occurring periodontal disease. Disease progression was evaluated histometrically.Results: The results revealed that the glutamate-lesioned rats developed significantly more periodontal tissue destruction compared to sham-lesioned control rats in both the ligated and non-ligated teeth.Conclusions: This study supports our resent findings indicating that inappropriate brain-neuroendocrine-immune regulation may play a rôle in periodontal disease susceptibility and progression.
    Type of Medium: Electronic Resource
    Signatur Availability
    BibTip Others were also interested in ...
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...