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  • 1
    Electronic Resource
    Electronic Resource
    Amphetamine-Induced Dopamine Release in the Rat Striatum: An In Vivo Microdialysis Study (1988)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 50 (1988), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The effects of a number of biochemical and pharmacological manipulations on amphetamine (AMPH)-induced alterations in dopamine (DA) release and metabolism were examined in the rat striatum using the in vivo brain microdialysis method. Basal striatal dialysate concentrations were: DA, 7 nM; dihydroxyphenylacetic acid (DOPAC), 850 nM; homovanillic acid (HVA), 500 nM; 5-hydroxyindoleacetic acid (5-HIAA), 300 nM; and 3-methoxytyramine (3-MT), 3 nM. Intraperitoneal injection of AMPH (4 mg/kg) induced a substantial increase in DA efflux, which attained its maximum response 20–40 min after drug injection. On the other hand, DOPAC and HVA efflux declined following AMPH. The DA response, but not those of DOPAC and HVA, was dose dependent within the range of AMPH tested (2–16 mg/kg). High doses of AMPH (〉8 mg/kg) also decreased 5-HIAA and increased 3-MT efflux. Depletion of vesicular stores of DA using reserpine did not affect significantly AMPH-induced dopamine efflux. In contrast, prior inhibition of catecholamine synthesis, using α-methyl-p-tyrosine, proved to be an effective inhibitor of AMPH-evoked DA release (〈35% of control). Moreover, the DA releasing action of AMPH was facilitated in pargyline-pretreated animals (220% of control). These data suggest that AMPH releases preferentially a newly synthesised pool of DA. Nomifensine, a DA uptake inhibitor, was an effective inhibitor of AMPH-induced DA efflux (18% of control). On the other hand, this action of AMPH was facilitated by veratrine and ouabain (200–210% of control). These results suggest that the membrane DA carrier may be involved in the actions of AMPH on DA efflux.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1988.tb02919.x
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  • 2
    Electronic Resource
    Electronic Resource
    In Vivo Mechanisms Underlying Dopamine Release from Rat Nigrostriatal Terminals: II. Studies Using Potassium and Tyramine (1990)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 54 (1990), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The brain microdialysis technique has been used to examine the in vivo effects of potassium and tyramine on dopamine (DA) release and metabolism in the striatum of halothane-anaesthetised rats. Increasing the concentration of potassium perfusing the dialysis probe (30–120 mM) induced a dose-related efflux of DA. A dose-related release of DA was also observed following addition of tyramine (1–100 μM) to the perfusing buffer. High concentrations of potassium were found to reduce the dialysate content of the DA metabolites 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid and the serotonin metabolite 5-hydroxyindoleacetic acid. No such effect was observed even when using the highest concentration of tyramine tested. Potassium-evoked DA release was facilitated by pretreatment with the DA uptake inhibitor nomifensine, was inhibited by depletion of extracellular calcium, and was not significantly affected by tetrodotoxin (TTX). The effect of tyramine on DA efflux was inhibited by nomifensine and was insensitive to both TTX and calcium depletion. These data suggest that potassium and tyramine induce release of DA via different mechanisms. Potassium-induced DA release involves a carrier-independent process and may utilise an exocytotic release mechanism. On the other hand, tyramine-induced DA release would appear to involve a carrier-dependent process. Depletion of vesicular stores of DA by pretreatment with reserpine did not significantly affect potassium-induced DA release, whereas a marked inhibition of the effects of tyramine was noted. However, in reserpinised animals the potassium-induced release of DA was inhibited by nomifensine, a result suggesting that a carrier-dependent release mechanism operates in the absence of vesicular DA. Inhibition of DA synthesis by pretreatment with α-methyl-p-tyrosine (α-MPT) reduced potassium-evoked DA release. However, this treatment only impaired the effect of tyramine when α-MPT was given 120 min before tyramine, when vesicular DA stores are also depleted. These data suggest that tyramine induces release of DA from vesicular stores, whereas the effect of potassium involves newly synthesised DA. Because DA metabolite levels are reduced by potassium but not by tyramine, these data suggest that extracellular DOPAC is derived from a newly synthesised pool(s) of DA.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1990.tb04881.x
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  • 3
    Electronic Resource
    Electronic Resource
    In Vivo Mechanisms Underlying Dopamine Release from Rat Nigrostriatal Terminals: I. Studies Using Veratrine and Ouabain (1990)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 54 (1990), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The in vivo mechanisms underlying the dopamine (DA)-releasing actions of veratrine and ouabain in the striatum of halothane-anaesthetised rats have been investigated using brain microdialysis. Relevant catecholamines and indoleamines were separated and quantified using HPLC combined with an electrochemical detection system. Veratrine (10 μg/ml-1 mg/ml) and ouabain (10 μM-1 mM) were added to the medium perfusing the dialysis probes. Both compounds increased dialysate DA content in a dose-related manner. Dialysate levels of the DA metabolites 3,4-dihydroxyphenylacetic acid and homovanillic acid and the serotonin metabolite 5-hydroxyindoleacetic acid were reduced by both veratrine and ouabain. Veratrine-induced DA efflux was maximal in the first 20-min sample collected after drug infusion began, whereas the maximal effect of ouabain was not observed until 20–40 min after administration began. Veratrine-induced DA efflux was unaffected by systemic injection of the DA uptake inhibitor nomifensine but was inhibited by either coperfusion of tetrodotoxin (TTX) or removal of calcium from the perfusing buffer. These data suggest that veratrine induces release of DA via a carrier-independent mechanism, perhaps involving an exocytotic release process. In contrast, ouabain-induced DA release was reduced by nomifensine but was inhibited to a lesser degree by calcium depletion and TTX. Detailed analyses of these data suggest that although ouabain initially induces release of DA via a carrier-dependent mechanism, an exocytotic process may also be involved. The finding that ouabain-induced DA efflux exhibits a degree of TTX and calcium sensitivity suggests that membrane depolarisation caused by Na+,K+-ATPase blockade opens voltage-gated sodium channels and initiates an exocytotic release of DA. The intracellular pools of DA involved in the release of DA induced by veratrine and ouabain were also examined. Depletion of vesicular pools of DA by pretreatment with reserpine reduced the amount of DA release induced by both agents, although this effect was only significant in the case of veratrine. However, in reserpinised animals the residual amount of DA release induced by veratrine was inhibited by nomifensine, a result suggesting that DA may be released via a carrier-dependent process in the absence of vesicular DA. Newly synthesised pools of DA were also depleted by pretreatment with the DA synthesis inhibitor α-methyl-p-tyrosine. Under these conditions, both veratrine- and ouabain-induced DA efflux was reduced. In the case of veratrine, newly synthesised DA is presumably used to replenish the vesicular store released by depolarisation. A similar process may also operate with ouabain, although the newly synthesised pool of DA may also be released directly via the carrier-dependent release process.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1990.tb04880.x
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  • 4
    Electronic Resource
    Electronic Resource
    Effects of Selective Monoamine Oxidase Inhibitors on the In Vivo Release and Metabolism of Dopamine in the Rat Striatum (1990)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 55 (1990), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Brain microdialysis was used to examine the in vivo efflux and metabolism of dopamine (DA) in the rat striatum following monoamine oxidase (MAO) inhibition. Relevant catecholamines and indoleamines were quantified by HPLC coupled with a electrochemical detection system. The MAO-B inhibitor selegiline only affected DA deamination at a dose shown to inhibit partially type A MAO. Alterations in DA and metabolite efflux were not observed when using the MAO-B-selective dose of 1 mg/kg of selegiline. At 10 mg/kg, selegiline reduced the efflux of DA metabolites to ∼70% of basal values without affecting DA efflux. K+-and veratrine-stimulated DA efflux was not affected by selegiline. Experiments using amphetamine and the DA uptake inhibitor nomifensine demonstrated that the effect of selegiline on DA metabolism was unlikely to be mediated either by inhibition of DA uptake or by an indirect effect of its metabolite amphetamine. The possibility that the effect of selegiline is mediated via a nonspecific inhibition of MAO is discussed. In contrast, the MAO-A inhibitor clorgyline inhibited basal DA metabolism and increased basal and de-polarisation-induced DA efflux. A 1 mg/kg dose of clorgyline reduced basal DA metabolite efflux (40–60% of control values) without affecting DA efflux. At 10 mg/kg of clorgyline, DA efflux increased to 253 ± 19% of basal values, whereas efflux of DA metabolites was reduced to between 15 and 26% of control values. The release of DA induced by K+ and vera-trine was not affected by 1 mg/kg of clorgyline but was increased by ∼200% following pretreatment with 10 mg/kg of clorgyline. The nonselective MAO inhibitor pargyline caused similar but more pronounced alterations in these parameters. For example, using a 75 mg/kg dose of pargyline, efflux of DA increased maximally to 310 ± 20% of basal values, and the release of DA induced by K+ and veratrine was increased by ∼300% following pargyline pretreatment. These data suggest that DA metabolism is mediated principally by MAO-A in the rat striatum. However, under conditions of MAO-A inhibition, a component of metabolism mediated by the type B enzyme becomes apparent.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1990.tb04587.x
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  • 5
    Electronic Resource
    Electronic Resource
    Selective Enhancement of an A Type Potassium Current by Dexamethasone in a Corticotroph Cell Line (1994)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neuroendocrinology 6 (1994), S. 0 
    Details
    ISSN: 1365-2826
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Perforated patch recording was used to examine the effect of the synthetic steroid dexamethasone on the whole cell potassium (K+) current, in the mouse corticotroph tumour cell line AtT20/D16-16. In 15 out of 52 control cells (29%) there was a rapidly-activating, rapidly- inactivating K+ current of the A type, the amplitude of which was strongly dependent on the holding potential in use prior to its activation by depolarising voltage pulses, and which was blocked by 1 mM 4-aminopyridine (4-AP, n = 5). The effect of dexamethasone (100nM, 2h, 37°C) was that the A current increased in prevelance (24 out of 31 cells, 77%), lost its dependence on holding potential (over the range studied), and as a result became significantly larger than in controls, for certain voltage steps (peak A current density was 18.5 +2.4 pA/pF (n = 12) for control cells and 26.3 ± 3.9 pA/pF (n = 18) for dexamethasone treated cells, for a step to +30mV from -60mV, values are mean ± SEM). All cells exhibited a slowly-activating, sustained K+ current, which was unaffected by changes in the holding potential, unaffected by 4-AP and consisted of at least 3 components: one blocked by 30 mM tetraethylammonium(TEA) or 100 nM charybdotoxin (CTX); a second blocked by 100 nM apamin; and a third not blocked by TEA, CTX, apamin, clofilium (100 nM) or niflumic acid (0.1 mM). Dexamethasone produced no change in the slowly-activating, sustained current nor in any of its individual components. The effect of dexamethasone on the A current was completely blocked by 0.1 mM puromycin, a protein synthesis blocker, while puromycin alone did not affect the size or frequency of the A current, nor alter the slowly-activating, sustained current. Secretion studies using 4-AP confirmed that the A current has a role in stimulated adrenocorticotrophic hormone (ACTH) secretion. In summary, AtT20 cells contain at least four types of K+ current: an A current and 3 currents contributing to the slowly-activating current. Selective enhancement of the A current by dexamethasone, shown here to require synthesis of new protein, is one of the mechanisms whereby glucocorticoids exert inhibitory control on ACTH secretion.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-2826.1994.tb00587.x
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  • 6
    Electronic Resource
    Electronic Resource
    Cholecystokinin as a Potent Excitant of Neurons of the Dentate Gyrus of Rats (1985)
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 448 (1985), S. 0 
    Details
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1749-6632.1985.tb29931.x
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  • 7
    Electronic Resource
    Electronic Resource
    Intracellular recorded synaptic antagonism in the rat dentate gyrus (1982)
    [s.l.] : Nature Publishing Group
    Nature 300 (1982), S. 450-452 
    Details
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] It has been proposed that three types of pharmacologically distinct excitatory amino acid receptors can be distinguished in the spinal cord, classified according to their most potent agonists as NMDA, kainate and quisqualate5. Thus APV is the most specific and potent antagonist of NMDA ...
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1038/300450a0
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  • 8
    Electronic Resource
    Electronic Resource
    Peptides in profusion (1979)
    [s.l.] : Nature Publishing Group
    Nature 280 (1979), S. 103-104 
    Details
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] IN the coming year at least nine major international meetings are being devoted to the peptides present within neural tissue. The first * was a massive affair: for three days, an audience of at least 700 from all over Europe and North America listened to 28 invited speakers. Almost half the ...
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1038/280103a0
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  • 9
    Electronic Resource
    Electronic Resource
    Antagonism between Na + and Ca 2+ at the Neuromuscular Junction (1965)
    [s.l.] : Nature Publishing Group
    Nature 205 (1965), S. 296-297 
    Details
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] By methods similar to those described by Fatt and Katz7 intracellular records were made of evoked and spontaneous end-plate potentials from frog sartorii bathed in solutions which contained 0.23 mM Ca2+, 2.0 mM K+ and various concentrations of Na+; tonicity being maintained by the ...
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1038/205296a0
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