Library

X
feed icon rss

Your email was sent successfully. Check your inbox.

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

Proceed reservation?

Export
  • 1
    Electronic Resource
    Electronic Resource
    THE ROLE OF INTRANEURONAL 5-HT AND OF TRYPTOPHAN HYDROXYLASE ACTIVATION IN THE CONTROL OF 5-HT SYNTHESIS IN RAT BRAIN SLICES INCUBATED IN K+-ENRICHED MEDIUM (1979)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 33 (1979), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract— The incubation of brain stem slices from adult rats in a K+-enriched medium containing a 5-HT uptake inhibitor (fluoxetine) significantly increased their capacity to synthesize 5-HT from tryptophan. The K+-induced stimulation of 5-HT synthesis was at least partly dependent on the depletion of the indoleamine in tissues since: (1) a good correlation was found between the respective changes in 5-HT release and synthesis evoked by high K+ concentrations in the presence of various 5-HT uptake inhibitors; (2) the modifications in endogenous 5-HT levels produced by in vim treatments with drugs (reserpine, pargyline) or by incubating slices with 5-HT altered the stimulating effect of high K+ concentrations and fluoxetine on 5-HT synthesis; (3) the replacement of Ca2+ by Co2+ (4 mM) or EGTA (0.1 mM) in the incubating medium completely prevented the increased 5-HT release and synthesis evoked by high K+ concentrations and fluoxetine.The extraction of tryptophan hydroxylase from incubated tissues revealed that the increased 5-HT synthesis occurring in K+-enriched medium was associated with an activation of this enzyme. Kinetic analyses indicated that this activation resulted from an increase in the Vmax of tryptophan hydroxylase, its apparent affinities for both tryptophan and 6-MPH4 being not significantly affected. In contrast to the tryptophan hydroxylase from tissues incubated in normal physiological medium, the activated enzyme from tissues depolarized by K+ was hardly stimulated by Ca2+-mediated phosphorylating conditions. This led to the proposition of a hypothetical model by which the Ca2+ influx produced by the neuronal depolarization would trigger the activity of a Ca2+-dependent protein kinase capable of activating tryptophan hydroxylase. Although this sequence is still largely speculative it must be emphasized that, as expected from such a model, the regional differences in the K+-evoked activation of tryptophan hydroxylase in slices (cerebral cortex 〉 brain stem 〉 spinal cord) were parallel to those of the Ca2+-dependent protein phosphorylation (r= 0.92) and those of the activating effect of phosphorylating conditions on soluble tryptophan hydroxylase (r= 0.96).
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1979.tb05239.x
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 2
    Electronic Resource
    Electronic Resource
    5-HYDROXYTRYPTAMINE CATABOLISM IN THE RAT BRAIN DURING ONTOGENESIS (1977)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 28 (1977), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Although the serotoninergic innervation is immature in the brains of young rats, the 5-HIAA content is similar to that found in adults. As indicated by the ratio of 5-HIAA to 5-HT levels in the brain stem and the forebrain, the catabolism of the indolamine was more rapid during the first 3 postnatal weeks than in adults. This was contirmed by measuring the total formation of [3H]5-HIAA from [3H]5-HT newly synthesized from L-[3H]tryptophan in brain stem slices of young and adult rats.Electrolytic lesions of midbrain raphe nuclei (B7 and B8) performed on the 5th postnatal day resulted in parallel decreases in brain 5-HT and 5-HIAA levels; this ruled out the possibility that 5-HIAA might be formed from 5-HT synthesized outside serotoninergic neurons, using peripheral 5-hydroxytryptophan. Inhibition of 5-HT storage by reserpine pretreatment did not alter the higher capacity of newborn tissues to catabolize exogenous [3H]5-HT. Therefore, possible differences in 5-HT binding in serotoninergic neurons between newborn and adult rats were not likely to account for the differences in 5-HT catabolism. Estimation of the rate of 5-HIAA efflux from the brain after MAO inhibition did not reveal marked changes with age.The activity of MAO type A, the enzyme involved in 5-HT catabolism, was higher during early life than later on. This could be shown by using 5-HT as substrate and clorgyline as a selective inhibitor. An opposite pattern of development was seen for MAO B, measured with benzylamine as substrate and deprenyl as selective inhibitor.These results suggest that the high 5-HIAA levels found in the brains of young rats can be attributed mainly to the presence of high MAO A activity during early life.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1977.tb07763.x
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 3
    Electronic Resource
    Electronic Resource
    RAT BRAIN STEM TRYPTOPHAN HYDROXYLASE: MECHANISM OF ACTIVATION BY CALCIUM (1977)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 28 (1977), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract— The activity of soluble tryptophan hydroxylase from rat brain stem was increased in presence of mm concentrations of calcium. Similarly to that observed by treating the enzyme with sodium dodecyl sulphate or trypsin, this activation resulted mainly from an increased affinity of tryptophan hydroxylase for both its substrate, tryptophan, and the cofactor 2-amino-4-hydroxy-6-methyl-5,6,7,8-tetrahydropteridine (6-MPH4). In addition, the optimal pH for the enzymic activity was shifted from 7.6 to 7.9 following activation by calcium, sodium dodecyl sulphate or trypsin.Under the assay conditions used for measuring tryptophan hydroxylase activity, calcium also stimulated a neutral proteinase. This latter enzyme could be eliminated from the solution of tryptophan hydroxylase by filtration through Sephadex G 200. The resulting partially purified tryptophan hydroxylase could be activated by calcium only when the neutral proteinase was included in the assay mixture. In support of this conclusion, the effect of calcium on tryptophan hydroxylase was very small in the new born rat when the activity of the neutral proteinase was low. In addition, the activating effect of Ca2+ could be antagonized not only by a chelating agent like EGTA but also (partially) by specific inhibitors of proteinases such as benzethonium and PMSF.These results strongly suggest that the activation of tryptophan hydroxylase by calcium is the consequence of a partial proteolysis of the enzyme by the calcium-dependent neutral proteinase. Therefore, the physiological significance of this irreversible effect is doubtful.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1977.tb10632.x
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 4
    Electronic Resource
    Electronic Resource
    Cholecystokinin: Corelease with dopamine from nigrostriatal neurons in the cat (1989)
    Oxford, UK : Blackwell Publishing Ltd
    European journal of neuroscience 1 (1989), S. 0 
    Details
    ISSN: 1460-9568
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Halothane-anaesthetized cats were implanted with push-pull cannulae to demonstrate the in vivo release of cholecystokinin-like immunoreactivity (CCK-LI) in the substantia nigra and the ipsilateral caudate nucleus. The spontaneous and the calcium-dependent potassium-evoked release of CCK-LI were observed in both structures. In addition, the local application of tetrodotoxin (10−6 M) reduced the spontaneous release of the peptide. 6-OHDA lesions made in the substantia nigra pars compacta led to a complete destruction of nigrostriatal dopaminergic neurons. CCK-LI levels were not affected in the caudate nucleus but were reduced substantially in the substantia nigra. The activation of dopaminergic cells induced by the nigral application of alpha-methyl-para-tyrosine (10−4 M) stimulated the release of CCK-LI and dopamine in the ipsilateral caudate nucleus, whilst opposite effects were seen in the substantia nigra. Similar results were obtained when dopaminergic transmission was blocked in the caudate nucleus suggesting that the evoked release of CCK-LI by the alpha-methyl-para-tyrosine treatment originates from dopaminergic nerve terminals and not from other CCK-LI containing fibres in response to released dopamine. Dopamine (10−7 M) as well as the D1 agonist SKF 38393 (10−5 M) stimulated CCK-LI release when applied into the caudate nucleus while the D2 agonist, LY 171555 (10−6 M) slightly reduced peptide release. The local application of cholecystokinin-8 sulfate (CCK-8S) (10−8 M, for 30 min) into the substantia nigra pars compacta increased the firing rate of dopaminergic cells and stimulated the release of newly synthesized 3H-dopamine from dendrites and nerve terminals.These results suggest, but do not definitively prove, that, in the cat, CCK-LI and dopamine are coreleased from nigrostriatal mixed dopaminergic/CCK-LI neurons and that CCK-LI released from dendrites is, like dopamine, involved in the regulation of the activity of these cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1460-9568.1989.tb00784.x
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 5
    Electronic Resource
    Electronic Resource
    Contribution of endogenously formed arachidonic acid in the presynaptic facilitatory effects of NMDA and carbachol on dopamine release in the mouse striatum (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: Arachidonic acid stimulated the release of [3H]-dopamine from striatal microdiscs in a concentration-dependent and partially calcium-dependent manner. Inhibitors of cytosolic and membrane-bound phospholipase A2 were used to determine whether endogenously formed arachidonic acid also contributes to the release of [3H]-DA (previously taken up in tissues or endogenously synthesized from [3H]-tyrosine) evoked by N-methyl-d-aspartate (NMDA) and carbachol alone or in combination. In the presence of magnesium, carbachol was found to remove the magnesium block of NMDA receptors and to facilitate the NMDA-evoked release of [3H]-DA from striatal microdiscs and synaptosomes. In addition, in the absence of magnesium, synergistic responses were induced by both agonists on microdiscs but not on synaptosomes. Responses induced by NMDA, carbachol or both agonists on microdiscs were reduced by phospholipase A2 inhibitors, the most striking effects being observed with mepacrine. Mepacrine was also shown to reduce the oxotremorine, but neither the nicotine- nor the potassium-evoked release of [3H]-DA. Tetrodotoxin decreased the release of [3H]-DA evoked by the co-application of NMDA and carbachol on microdiscs, but mepacrine still decreased this tetrodotoxin-resistant response. Similarly, mepacrine still decreased the release of [3H]-DA evoked by NMDA and carbachol on synaptosomes. Altogether, these results indicate that arachidonic acid which is formed in striatal neurons, and to a lesser extent in DA fibres, under stimulation of NMDA and muscarinic receptors, partially contributes to the presynaptic facilitation of DA release evoked by NMDA and carbachol.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1460-9568.1999.00534.x
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 6
    Electronic Resource
    Electronic Resource
    Basic and Regulatory Mechanisms of In Vitro Release of Met-Enkephalin from the Dorsal Zone of the Rat Spinal Cord (1984)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 43 (1984), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Under control conditions, superfused slices of the dorsal half of the lumbar enlargement from adult rats released Met-enkephalin-like material (MELM) that behaved as authentic Met-enkephalin under two different chromatographic procedures (Bio-gel filtration, HPLC). MELM release increased markedly on exposure of slices to batrachotoxin (0.5 μM) or to an excess of K+ (28 and 56 mM instead of 5.6 mM). The K + -evoked release was totally dependent on the presence of Ca2+ in the super-fusing fluid whereas the spontaneous efflux of MELM was only partially Ca2+-dependent. Further experiments performed with tissues of polyarthritic rats indicated that the increase in their MELM levels was associated with a lower fractional rate constant of MELM release, therefore suggesting that spinal Met-enkephalin turnover might be reduced in chronically suffering animals. Examination of the possible modulation of MELM release by various neuroactive compounds present within the dorsal horn revealed that cholecystokinin (10 μM), but not its desulphated derivative, substance P-sulphoxide (10 μM), and to a lesser extent substance P, enhanced the K+-evoked MELM release. In contrast, γ-aminobutyric acid (10 μM) and (–)-baclofen (1 μM) partially prevented the stimulatory effect of K+ on MELM release. Other compounds such as serotonin, somatostatin, and neurotensin altered neither the spontaneous nor the K+-evoked release of MELM.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1984.tb12798.x
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 7
    Electronic Resource
    Electronic Resource
    Direct and indirect presynaptic control of dopamine release by excitatory amino acids (1998)
    Springer
    Amino acids 14 (1998), S. 63-68 
    Details
    ISSN: 1438-2199
    Keywords: Excitatory amino acids ; Dopamine release ; Mouse striatal microdiscs ; Presynaptic mechanisms ; Diffusible messengers ; Arachidonic acid
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Dopamine (DA) release from nerve terminals of the nigrostriatal DA neurons not only depends on the activity of nigral DA cells but also on presynaptic regulation. Glutamatergie neurons of cortical origin play a prominent role in these presynaptic regulations. The direct glutamatergic presynaptic control of DA release is mediated by N-methyl-D-aspartate (NMDA) andα-amino-3-hydroxy-5-methyl-4-isoxazole-4-propionate (AMPA) receptors, located on DA nerve terminals. In addition, by acting on striatal target cells, these glutamatergic neurons contribute also to indirect regulations of DA release involving several transmitters such as GABA, acetylcholine and neuropeptides. Diffusible messengers such as nitric oxide (NO) or arachidonic acid (AA) which are particularly formed under the stimulation of NMDA receptors may also participate to the regulation of DA release. In the present study, it will be shown that the co-application of NMDA and carbachol synergistically increases the release of [3H]-DA and that this effect is reduced by mepacrine or 4-bromophenacylbromide (107M), two inhibitors of PLA2. Therefore endogenously released AA induced by the co-stimulation of NMDA and cholinergic receptors seems to be involved, at least partly, in the release of DA.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01345244
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 8
    Electronic Resource
    Electronic Resource
    Paradoxical decrease of brain 5-HT turnover by metergoline, a central 5-HT receptor blocker (1978)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 302 (1978), S. 313-321 
    Details
    ISSN: 1432-1912
    Keywords: Receptors ; Serotonin ; 5-HT-Sensitive adenylate cyclase ; 5-HT High affinity binding ; 5-HT Turnover
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Since metergoline (1-methyl-8-beta-carbobenzyloxy-aminomethyl-10-alpha-ergoline) is a potent 5-HT antagonist in peripheral organs, its possible blocking effects on 5-HT receptors in the rat brain were investigated. In vitro, metergoline inhibited both the specific high affinity binding of 3H-5-HT onto synaptosomal membranes (IC 50=18 nM) and the stimulating effect of 10 μM 5-HT on the adenylate cyclase activity in colliculi homogenates from newborn rats (IC 50=12 μM). In vivo, the administration of metergoline (10 mg/kg i.p., 60 min before death) resulted in a significant decrease in the 3H-5-HT binding capacity of synaptosomal membranes from the forebrain of adult rats. Taken together, these data clearly indicated that metergoline is a potent blocker of some serotoninergic receptors in the rat brain. Surprisingly, the changes in 5-HT turnover occurring in the brainstem and in the forebrain 1 h after metergoline (2–10 mg/kg) treatment were similar to those normally induced by a central 5-HT agonist: both the rate of 5-HT utilisation and that of 5-HT synthesis were significantly decreased. These changes were in contrast to the acceleration of 5-HT turnover induced by the administration of another potent central 5-HT antagonist, methiothepin. These results are discussed in relation to the possible existence of several types of serotoninergic receptors in the rat brain. It is possible that the positive feedback regulation of 5-HT turnover is triggered by the blockade of serotoninergic receptors sensitive to methiothepin, but not to metergoline.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00508301
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...