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  • 1
    ISSN: 1432-1106
    Keywords: Key words Fimbria-fornix lesion ; Hippocampus ; Muscarine receptors ; Nicotine receptors ; Noradrenaline release ; Sympathetic sprouting
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  Lesions of the septohippocampal pathways elicit sprouting of sympathetic fibers from the superior cervical ganglion, a phenomenon which, within a few months, raises the hippocampal noradrenaline (NA) content above normal. In peripheral sympathetic fibers, the release of NA is modulated via presynaptic muscarinic receptors. Such receptors have not been detected so far on terminals of noradrenergic neurons originating in the locus coeruleus. Whether the release of NA could become sensitive to muscarinic modulation in the hippocampus following sympathetic fiber ingrowth was the major question in this experiment. The contribution of presynaptic nicotinic receptors was also studied. Slices from the ventral hippocampus (only dentate gyrus+CA3 region) of sham-operated (SHAM) and fimbria-fornix lesioned (LES) Long-Evans rats (8–10 months after surgery) were preincubated with [3H]NA and stimulated either once (S1) with 100 µM nicotine or (in parallel experiments) twice electrically (S1, S2), using conditions (six pulses 100 Hz, 2 ms, 28 mA, 4 V/chamber) that precluded autoinhibition. In experiments using electrical stimulation, the superfusion medium contained desipramine (1 µM). In LES rats, the tissue NA content had almost doubled (171% of SHAM levels), but the amount of [3H]NA taken up by the slices was unchanged, and the overflow evoked at S1 by both nicotinic and electrical stimulation was significantly reduced in comparison with SHAM rats. In both groups, the addition of oxotremorine or oxotremorine+atropine (1 µM, each) before S2 failed to affect the electrically evoked overflow of 3H. Nicotine-induced NA release was inhibited by hexamethonium (100 µM) in both groups, although significantly less potently in LES rats. Tissue activity of choline acetyltransferase was reduced in LES rats to 15% of SHAM levels and the 5-hydroxytryptamine content was also strongly diminished (38% of SHAM values). It is concluded that lesion-induced sprouting of sympathetic fibers into the hippocampus is not accompanied by the emergence of a muscarinic modulation of NA release in this tissue, and that the sensitivity of the presynaptic stimulatory effect of nicotine was modified by the lesion.
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  • 2
    ISSN: 1432-1106
    Keywords: Key words Human neocortex ; Rat neocortex ; Acetylcholine release ; Autoinhibition ; Alzheimer’s disease
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  In order to assess the autoinhibitory control of endogenous acetylcholine (ACh) in rat and human neocortex, slices of these tissues were prelabelled with [3H]choline, superfused continuously and stimulated electrically using various frequencies in the presence or absence of drugs. The autoinhibitory feedback control of [3H]ACh release was operative – despite the absence of blockers of ACh esterase – at stimulation frequencies ≥3 Hz in rat and ≥6 Hz in human neocortex tissue. At these frequencies the muscarinic antagonist atropine (0.1 µM) disinhibited the release of [3H]ACh in both species. Estimation of the biophase concentration of ACh near the autoreceptor in the rat neocortex from concentration-response curves of the muscarinic agonist oxotremorine revealed that at 3 Hz about 25% of the autoreceptors were activated by endogenously released ACh. This estimation is consistent with an increase in [3H]ACh release to about 120% of control values by complete blockade of autoreceptors with atropine. The observation that in human neocortical tissue presynaptic autoinhibition of [3H]ACh release is operative at stimulation frequencies ≥6 Hz suggests that selective blockade of autoinhibition may also increase ACh release in the cortex of Alzheimer’s disease patients, without additional blockade of the enzyme acetylcholinesterase.
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  • 3
    ISSN: 1432-1106
    Keywords: Acetylcholine release ; Cholinergic neurons ; Dopamine release ; Dopaminergic transplants ; In vitro release ; Neuronal transplantation ; Nigrostriatal system
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The aim of the study was to examine the influence of intrastriatal dopaminergic grafts on the functioning of striatal cholinergic neurons using an in vitro superfusion method. Rats bearing unilateral 6-hydroxydopamine lesion of the nigrostriatal dopaminergic system received a cell suspension obtained from ED 14 rat embryonic mesencephali which was injected into the denervated striatum. Lesioned animals displayed an ipsilateral rotation in response to amphetamine (5 mg/kg i.p.). This rotational response disappeared following grafting and there was even a significant contralateral rotation in response to the drug. Apomorphine (0.1 mg/kg s.c.) induced a contralateral rotation following the lesion. This latter response was attenuated in the grafted group. Three months after grafting 350 μm thick slices were prepared from striata from the control and experimental sides of lesioned and graft-bearing animals. The slices were preincubated either with 3H-dopamine (10-7 M) or 3H-choline (10-7 M) and then superfused with an oxygenated Krebs-Ringer solution. Stimulation with electrical pulses following preincubation with 3H-dopamine elicited a marked increase of tritium outflow from control slices. Stimulation-evoked overflow was of similar magnitude from slices from striata containing the graft, while it was much reduced in slices from lesioned striata. Amphetamine markedly potentiated the effect of electrical stimulation in slices obtained from control and graft-containing striata. Nomifensine (a dopamine uptake blocker) led to a significant decrease of the overflow of 3H-acetylcholine evoked by electrical stimulation from control striatal slices. This inhibition was antagonized by domperidone, a D2 dopamine receptor blocker, a finding which indicates that the action of nomifensine was indeed due to a potentiation of the action of endogenous dopamine released by the electrical stimulation. A similar, although somewhat attenuated, action of nomifensine and domperidone was observed for striatal slices containing the graft. Amphetamine inhibited the stimulation evoked overflow of 3H-acetylcholine in a dose-dependent manner from striatal slices obtained both from the intact and experimental sides of graft-bearing animals, while it had no action on slices from denervated striata. Finally, the dose-response curve for the inhibition of 3H-acetylcholine release by apomorphine was significantly shifted to the left for slices from the lesioned striata as compared with control slices. This leftward shift was totally abolished in the slices from the graft-containing striatum. These results indicate that the dopaminergic inhibition of the striatal cholinergic interneurons, abolished by the lesion, is restored by intrastriatal dopaminergic grafts both in vitro and in vivo. On the other hand the lack of correlation between the in vivo and the in vitro effects (rotational response vs. inhibition of 3H-acetylcholine release) suggest that the effect of such grafts on rotational behavior cannot be explained solely by their action on the striatal cholinergic neurons.
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  • 4
    ISSN: 1432-1106
    Keywords: Fimbria-fornix lesion ; Hippocampus ; Radial-arm maze ; Spatial memory ; Sympathetic sprouting ; Rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract This longitudinal study, extending over 12 months, assessed the behavioural and biochemical effects of hippocampal sympathetic ingrowth (HSI) into the partially denervated hippocampus. Male Long-Evans rats received fimbria-fornix lesions (FIFO) or sham operations at 90 days of age. At the same time half of the rats from each group sustained bilateral ablation of the superior cervical ganglia (SCGX). A battery of behavioural tests, measuring spontaneous alternation, activity in the open field and home cage, and radial-maze performance, were employed, starting after one very short (16 days) and one extended (216 days) postoperative delay. Neurochemical analyses measuring choline acetyltransferase (ChAT) activity, high-affinity choline (HACU) and noradrenaline uptake by hippocampal synaptosomes (HANU), hippocampal noradrenaline ([NA]), serotonin ([5-HT]) and 5-hydroxyindoleacetic acid ([5-HIAA]) concentrations were carried out in a dorsal, a “middle” and a ventral region of the hippocampus. Lesion of the FIFO induced a significant and enduring deficit in radial-maze performance, in addition to a persistent locomotor hyperactivity. ChAT and HACU were significantly depleted in all three regions of the hippocampus at 12 months, and these deficits were negatively correlated with maze performance. SCGX in the presence of the FIFO lesion significantly reduced [NA] in the middle region of the hippocampus, as compared to SCGX rats, and contributed to a restoration of lesion-induced depletions in [5-HT] and [5-HIAA] in the middle and ventral hippocampal regions, whilst failing to elicit any behavioural changes at either time point. It is concluded that if lesion-induced HSI indeed occurred, as is suggested by neurochemical evidence, it had no effect upon the observed behavioural deficits elicited by transection of the FIFO in the rat.
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  • 5
    ISSN: 1432-1106
    Keywords: Acetylcholine ; Fimbria/fornix ; Hippocampus ; Intracerebral grafts ; Muscarinic receptors ; Noradrenaline ; Phosphoinositides ; Serotonin ; Rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Long Evans female rats sustained aspirative lesions of the septohippocampal pathways; subsequently, they received intrahippocampal suspension grafts of fetal septal-diagonal band or hippocampal tissue. The long term (8–10 months post-surgery) effects of these treatments were examined in the hippocampus for the following variables: concentration of hippocampal acetylcholine (ACh), muscarinic-stimulated (carbachol) formation of inositol monophosphate, accumulation of tritiated choline, noradrenaline (3H-NA) and serotonin (3H-5-HT), electrically evoked release of 3H-acetylcholine (3H-ACh), 3H-NA and 3H-5-HT, and choline acetyltransferase (ChAT) activity. The lesions decreased the levels of endogeneous ACh, the accumulation of 3H-choline and 3H-5-HT and the evoked release of both 3H-ACh and 3H-5-HT as well as the ChAT activity, but they failed to significantly affect the muscarinic-stimulated formation of inositol monophosphate and the accumulation and release of 3H-NA. Grafts of hippocampal cells were found to be ineffective on all lesion-induced effects. In contrast, grafts of septal-diagonal band origin attenuated the deficit of hippocampal concentrations of ACh and accumulation of 3H-choline without, however, improving release of 3H-ACh, accumulation and release of 3H-5-HT, and ChAT activity. These observations suggest that: (i) denervation-induced hippocampal muscarinic supersensitivity might not be long-lasting or the lesions, which in some cases spared the lateral edges of the fimbria, failed to induce any muscarinic supersensitivity, (ii) intrahippocampal grafts rich in cholinergic neurons do not foster recovery from the lesion-induced noncholinergic deficits we assessed, (iii) recovery of function may be expressed by some but not all biochemical or pharmacological cholinergic variables and (iv) graft-derived hippocampal reinnervation may be less efficient than the endogenous innervation of intact rats as indicated by the restoration of only some of the variables related to cholinergic function by intrahippocampal septal-diagonal band grafts.
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  • 6
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: As a first step for experiments investigating the presynaptic characteristics of sympathetic fibers grown into the denervated hippocampus, we studied the time course of changes of neurochemical markers in the rat hippocampus, subsequent to aspiration lesions of the fimbria-fornix and the overlying callosal and cortical structures. At various postsurgical delays (1, 2, 8, 24, and 40 weeks), the activity of choline acetyltransferase, the high-affinity synaptosomal uptake of choline and noradrenaline, and the concentrations of noradrenaline, serotonin, and 5-hydroxyindoleacetic acid were measured in a dorsal, an intermediate, and a ventral part of the hippocampus. Levels of all markers were significantly reduced shortly (1–2 weeks) after the lesions. However, whereas the cholinergic (choline uptake and choline acetyltransferase activity) and the serotonergic (concentrations of serotonin and 5-hydroxyindoleacetic acid) markers remained significantly reduced for up to 40 weeks, both noradrenergic markers recovered to near-normal (noradrenaline uptake) or even supranormal (noradrenaline concentration) levels, although with clear-cut differences in the time course and the regional characteristics. The noradrenaline content reached control levels already 8 weeks after lesion surgery and was about two to three times higher 40 weeks later, with the most dramatic effects in the ventral hippocampus. In contrast, high-affinity noradrenaline uptake reached control values only 24 weeks after lesion and exceeded them only in the ventral hippocampus 40 weeks after surgery. It is concluded (a) that hippocampal noradrenaline concentration is a more sensitive marker for sympathetic sprouting than high-affinity noradrenaline uptake and (b) that functional in vitro studies on hippocampal sympathetic ingrowth appear to fit optimal conditions in the ventral hippocampus at a delay of at least 40 weeks after surgery.
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  • 7
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: In Huntington's disease (HD), neuronal loss is most prominent in the striatum leading to emotional, cognitive and progressive motor dysfunction. The R6/2 mice, transgenic for exon 1 of the HD gene, develop a neurological phenotype with similarities to these features of HD. In striatal tissue, electrically evoked release of tritiated acetylcholine (ACh) and dopamine (DA) were compared in wild-type (WT) and R6/2 mice. In R6/2 mice, the evoked release of ACh, its M2 autoreceptor-mediated maximum inhibition and its dopamine D2 heteroreceptor-mediated maximum inhibition was diminished to 51%, 74% and 87% of controls, respectively. Also, the activities of choline acetyltransferase and of synaptosomal high-affinity choline uptake decreased progressively with age in these mice. In the DA release model, however, electrical stimulation elicited equal amounts of [3H]-DA both in WT and R6/2 mice. Moreover, high-affinity DA uptake into striatal slices was similar in WT and R6/2 mice. In order to confirm these findings in vivo, intrastriatal levels of extracellular DA were measured by intracerebral microdialysis in freely moving mice: striatal DA levels were found to be equal in WT and R6/2 mice. In conclusion, in the transgenic R6/2 mice changes occur mainly in striatal cholinergic neurones and their pre-synaptic modulation, but not in the dopaminergic afferent terminals. Whether similar events also contribute to the pathogenesis of HD in humans has to be established.
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  • 8
    ISSN: 1432-1335
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Die cytostatischen Effekte der Vitamin-A-Säure auf Ehrlich-Ascites-Tumorzellen in-vitro, sowie auf einige zellfreie Enzymsysteme wurden untersucht. Vitamin-A-Säure beeinflußt konzentrationsabhängig, jedoch unspezifisch die Einbauraten von 14C-Thymidin,-Uridin und -Leucin. Teilweise gereinigte Thymidinkinase aus Ascites-Tumorzellen wird ebensowenig durch Vitamin-A-Säure beeinflußt wie die DNA-Polymerase-Aktivität isolierter Zellkerne. Dagegen lassen sich Einflüsse der Vitamin-A-Säure auf zellfreie Proteinbiosynthese-Systeme, sowie auf die RNA-Polymerasen von Tumorzellkernen nachweisen. Es wird diskutiert, daß für die primären, starken Hemmeffekte auf Ehrlich-Ascites-Tumorzellen in-vitro, die schon bekannten lysosomen-labilisierenden Eigenschaften der Vitamin-A-Säure verantwortlich sind.
    Notes: Summary The cytostatic effects of vitamin-A-acid on Ehrlich-ascites tumor cells in-vitro and on some cell-free enzyme systems were investigated. In the presence of various vitamin-A-acid concentrations the rates of 14C-thymidine-, -uridine- and -leucine-incorporation were progressively diminished in an unspecific way. Neither partially purified thymidine kinase nor the DNA polymerase activity of isolated nuclei proved to be affected by vitamin-A-acid. In contrast, some influence on the cell-free systems of protein biosynthesis and on the tumor nuclei RNA polymerases could be shown. It is discussed, that the known lysosome-labilizing properties of vitamin-A-acid are responsible for the primary strong inhibitory effects on Ehrlich ascites tumor cells in-vitro.
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  • 9
    ISSN: 0163-1047
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Psychology
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  • 10
    Electronic Resource
    Electronic Resource
    Springer
    Psychopharmacology 90 (1986), S. 422-422 
    ISSN: 1432-2072
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
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