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  • Hypothalamus  (19)
  • Dopamine  (7)
  • Striatum  (3)
  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 276 (1973), S. 103-118 
    ISSN: 1432-1912
    Keywords: Hypothalamus ; Noradrenaline ; Gamma-Aminobutyric Acid ; Electrical Stimulation ; Push-Pull Cannula ; Blood Pressure
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The third ventricle and the aqueduct of anaesthetized cats were cannulated and the posterior area of the hypothalamus was stimulated with a monopolar electrode. Electrical stimulation of the posterior area evoked a rise of the arterial blood pressure which was inhibited by the injection of 0.2 ml of gammaaminobutyric acid (GABA, 2M) into the third ventricle. The impairment of the pressor response to electrical stimulation was accompanied by a fall of the “resting” blood pressure and depression of the respiration, presumably by action of GABA on brain areas in the vicinity of the fourth ventricle. In another series of experiments the posterior area was labelled with (±)-3H-noradrenaline and 2 h later superfused with a push-pull cannula and stimulated with the tip of the cannula. Superfusion with GABA (0.1 or 1 M) evoked a dose-dependent increase of release of catecholamines and enhanced the pressor response to electrical stimulation. 1×10−3 M of GABA enhanced the pressor response without increasing the spontaneous release of catecholamines but potentiated the output of radioactivity during electrical stimulation. Superfusion with sucrose (1 M) did not influence either pressor response or release of radioactive compounds. Superfusion with GABA increased slightly but significantly the relative concentration of catechols in the effluents and reduced that of normetanephrine. Pretreatment of animals with pargyline and tropolone evoked a pronounced increase of the relative concentrations of catechols in the effluent, while those of 3-methoxy-4-hydroxyphenylglycol and 3-methoxy-4-hydroxymandelic acid were strongly reduced. It is concluded that superfusion with high concentrations of GABA enhances the pressor response by increasing the release of catecholamines, while the effect of low GABA concentrations is due to facilitation of release of catecholamines from the adrenergic nerve endings during electrical stimulation.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 287 (1975), S. 181-190 
    ISSN: 1432-1912
    Keywords: Caudate Nucleus ; Dopamine ; Ouabain ; Reserpine ; Prenylamine ; Uptake
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Homogenates of the caudate nucleus of the pig were submitted to differential centrifugation. The 20 000 g and 80 000 g fractions were isolated and a part of them was osmotically shocked. The highest dopamine content per mg protein was found in the intact 80 000 g fraction. Incubation experiments with the intact and the osmotically shocked fractions at 25°C revealed that the particles of the intact 20 000 g fraction took up dopamine; the influx of the amine was not enhanced by addition of ATP and magnesium to the incubation medium. On the other hand after osmotic shock the uptake of dopamine into the particles of this fraction was greatly enhanced by addition of ATP and magnesium. The uptake of dopamine into the particles of both intact and osmotically shocked 80 000 g fractions was likewise enhanced by ATP and magnesium. The uptake in all fractions was not influenced by ouabain. The influx of dopamine into the particles of the intact 80 000 g fraction was competitively inhibited by reserpine (K i 0.96×10−8 M) and prenylamine (K i 1.74×10−8 M). It is concluded that the intact 20,000 g fraction contains intact synaptosomes; the uptake of dopamine is independent of the presence of ATP and magnesium. The shocked 20 000 g fraction and the 80 000 g fractions contain synaptic vesicles; the uptake of dopamine into these vesicles is enhanced by ATP and magnesium.
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 347 (1993), S. 301-305 
    ISSN: 1432-1912
    Keywords: Modulation of histamine release ; Dopamine D1-, D2-, D3-receptors ; Hypothalamus ; Push-pull cannula
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The involvement of dopaminergic neurons of the hypothalamus in the modulation of histamine release was studied by the push-pull technique. The posterior hypothalamus of the conscious, freely moving rat was superfused with artificial cerebrospinal fluid (CSF) and the release of histamine was determined radioenzymatically in the superfusate. Agonists and antagonists of dopamine D1-, D2- and D3-receptors were dissolved in CSF and applied to the hypothalamus through the push-pull cannula. Hypothalamic superfusion with the D1-, D2- and D3-receptor agonists dopamine or R(−)-apomorphine enhanced the release rate of histamine. (±) Apomorphine also enhanced the release of histamine, but to a lesser extent than did equimolar concentration of R(−)apomorphine. The D3-agonist quinpirole inhibited the release of histamine, while the D1-receptor agonist SKF 82958 [(±)-6-chloro-7,8-dihydroxy-3-allyl-l-phenyl-2,3,4,5-tetrahydro-1H-3-benzazepine] did not virtually influence the release of the neurotransmitter. On the other hand, [−]-sulpiride which predominantly blocks D2-receptors, decreased histamine release. Hypothalamic superfusion with SKF 83566 [(±)-7-bromo-8-hydroxy-3-methyl-l-phenyl-2,3,4,5-tetrahydro-1H-3-benzazepine], which seems to be a selective antagonist of D1-receptors, enhanced the release rate of histamine. These findings suggest that dopaminergic neurons of the hypothalamus influence the release of histamine from its neurons in a dual way. D2-heteroreceptors stimulate the release of histamine, while D3-heteroreceptors seem to inhibit the release of this neurotransmitter. Both types of dopamine receptors might be located presynaptically on histaminergic neurons. Alternatively, D3- and D2-receptors might be located on histaminergic and non-histaminergic neurons, respectively.
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 352 (1995), S. 67-73 
    ISSN: 1432-1912
    Keywords: Key words Acetylcholine release ; Striatum ; Nitric oxide ; Push-pull technique
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  The influence of nitric oxide on acetylcholine release in the ventral striatum was investigated by the push-pull superfusion technique in the conscious, freely moving rat. Superfusion with the nitric oxide donors S-nitroso-N-acetylpenicillamine or with 3-morpholino-sydnonimine caused a pronounced increase in striatal acetylcholine release. This effect was prevented by superfusion with tetrodotoxin. Pre-superfusion with the guanylyl cyclase inhibitor methylene blue abolished the effect of 3-morpholino-sydnonimine. Superfusion of the ventral striatum with the guanylyl cyclase inhibitor LY83583 decreased acetylcholine release by 60% of basal release, whereas the less specific guanylyl cyclase inhibitor methylene blue was ineffective in this respect. Superfusion of the ventral striatum with inhibitors of nitric oxide synthase also led to different effects on basal acetylcholine release. Superfusion with L-NG-methylarginine did not influence basal acetylcholine release, whereas superfusion with L-NG-nitroarginine or with L-NG-nitroarginine methyl ester led to a substantial decrease in acetylcholine output, the latter compound being more effective. The effect of L-NG-nitroarginine was abolished by simultaneous superfusion with L-arginine. The effects of NO donors and of LY83583 suggest that NO increases acetylcholine release, probably by a cGMP-dependent mechanism. The effectiveness of nitric oxide synthase inhibitors shows that the activity of striatal neurons is under the permanent influence of nitric oxide, that leads, via a direct or indirect mechanism, to continuous enhancement of acetylcholine release. In conclusion, our findings suggest that NO synthesized in the ventral striatum acts as an intercellular messenger which modulates acetylcholine release.
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  • 5
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 352 (1995), S. 67-73 
    ISSN: 1432-1912
    Keywords: Acetylcholine release ; Striatum ; Nitric oxide ; Push-pull technique
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The influence of nitric oxide on acetylcholine release in the ventral striatum was investigated by the push-pull superfusion technique in the conscious, freely moving rat. Superfusion with the nitric oxide donors S-nitroso-N-acetylpenicillamine or with 3-morpholino-sydnonimine caused a pronounced increase in striatal acetylcholine release. This effect was prevented by superfusion with tetrodotoxin. Pre-superfusion with the guanylyl cyclase inhibitor methylene blue abolished the effect of 3-morpholino-sydnonimine. Superfusion of the ventral striatum with the guanylyl cyclase inhibitor LY83583 decreased acetylcholine release by 60% of basal release, whereas the less specific guanylyl cyclase inhibitor methylene blue was ineffective in this respect. Superfusion of the ventral striatum with inhibitors of nitric oxide synthase also led to different effects on basal acetylcholine release. Superfusion with L-NG-methylarginine did not influence basal acetylcholine release, whereas superfusion with L-NG-nitroarginine or with L-NG-nitroarginine methyl ester led to a substantial decrease in acetylcholine output, the latter compound being more effective. The effect of L-NG-nitroarginine was abolished by simultaneous superfusion with L-arginine. The effects of NO donors and of LY83583 suggest that NO increases acetylcholine release, probably by a cGMP-dependent mechanism. The effectiveness of nitric oxide synthase inhibitors shows that the activity of striatal neurons is under the permanent influence of nitric oxide, that leads, via a direct or indirect mechanism, to continuous enhancement of acetylcholine release. In conclusion, our findings suggest that NO synthesized in the ventral striatum acts as an intercellular messenger which modulates acetylcholine release.
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  • 6
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 258 (1967), S. 238-250 
    ISSN: 1432-1912
    Keywords: Hypothalamus ; Noradrenaline ; Storage ; Calcium ; Acetylcholine ; Hypothalamus ; Noradrenalin ; Speicherung ; Calcium ; Acetylcholin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Schweine-Hypothalami wurden durch Differentialzentrifugieren fraktioniert und der Noradrenalin- sowie der Eiweiß-Stickstoff-Gehalt der gewonnenen sechs Fraktionen bestimmt. Die Fraktionen III (30 000 g), IV (60 000 g) und V (100 000 g) enthalten den größten Noradrenalin-Gehalt pro mg Eiweiß und stellen somit die spezifischen Fraktionen dar, in denen das Noradrenalin hauptsächlich partikulär gebunden vorliegt. Der molare Quotient Noradrenalin/ATP der Fraktion 30 000–100 000 g beträgt 0,56. Die aminspeichernden Vesikel der Fraktion 30 000–100 000 g wurden 60 min lang bei 37°C inkubiert. Die spontane Noradrenalin-Freisetzung ist mit 31% des Ausgangsgehaltes etwa gleich groß wie die spontane Adrenalin-Freisetzung aus isolierten Nebennierenmark-Granula. Reserpin sowie kleine Prenylamin-Konzentrationen (60 nmol/ml) hemmen die spontane Noradrenalin-Freisetzung, während große Prenylamin-Konzentrationen (1,2 μmol/ml) eine fast vollständige Noradrenalin-Verarmung der Vesikel verursachen. Inkubation mit verschiedenen Calcium-Konzentrationen verursacht eine dosisabhängige Noradrenalin-Freisetzung. Acetylcholin ist ebenfalls in der Lage, die spontane Noradrenalin-Freisetzung zu erhöhen. Bei der gleichzeitigen Inkubation mit Calcium und Acetylcholin konnte keine Addition der Wirkungen der beiden Substanzen festgestellt werden. Reserpin vermag die durch Calcium bedingte Noradrenalin-Freisetzung zu hemmen.
    Notes: Summary In order to study the subcellular distribution of noradrenaline in the hypothalamus this region was removed from pig brains and fractionated by differential centrifugation. From the six obtained fractions fraction III (30,000 g), IV, (60,000 g), and V (100,000 g) contain the highest amounts of noradrenaline per mg protein (69, 60 and 47 ng/mg protein respectively). These fractions represent therefore the main noradrenaline storing fractions of the hypothalamus. The molar ratio noradrenaline/ATP of the vesicles of the fraction 30,000–100,000 g is 0.56. The noradrenaline storing vesicles of the fraction 30,000–100,000 g of the hypothalamus were incubated for 60 min at 37°C. The spontaneous release of noradrenaline amounts to 31% of the original noradrenaline content of the vesicles. It is therefore of the same order of magnitude as the spontaneous release of adrenaline from isolated granules of the suprarenal medulla. Reserpine and prenylamine (60 nmoles/ml) inhibit the spontaneous release of noradrenaline whereas 1.2 μmoles prenylamine/ml deplete the vesicles almost completely. Incubation of the hypothalamus vesicles with calcium chloride (0.31–5.0 μmoles/ml) causes a dose dependent release of noradrenaline. Acetylcholine (55 nmoles/ml) is also able to increase the spontaneous release of noradrenaline. By simultaneous incubation with calcium and acetylcholine no addition of the effects of both substances on the release of noradrenaline could be observed. Reserpine prevents the calcium-induced release of noradrenaline.
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  • 7
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 278 (1973), S. 387-402 
    ISSN: 1432-1912
    Keywords: Catecholamines ; Dopaminergic Vesicles ; Striatum ; Amphetamine ; Amantadine ; Desipramine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Dopamine storing vesicles were isolated from the caudate nucleus of the pig by differential centrifugation and incubated at various temperatures. The spontaneous release of endogenous dopamine was temperature-dependent. Incubation with 14C-dopamine or 14C(±)-noradrenaline revealed that the vesicles were able to take up catecholamines by two different transport mechanisms; one was dependent on ATP, magnesium and temperature, the other one was independent of ATP and magnesium, and partially dependent on temperature. The Km of the ATP-magnesium-dependent uptake was 1.52×10−6 M for dopamine and 3.45×10−6 M for noradrenaline. Incubation with dopamine increased the dopamine content of the vesicles and diminished the endogenous dopamine by approximately 90%. Addition of ATP and magnesium further increased the dopamine content without influencing the per cent exchange between endogenous and exogenous dopamine. The dopamine uptake at 37°C in the presence of ATP and magnesium was of short duration because of the thermo-lability of the vesicles. (+)-amphetamine competitively inhibited the ATP-magnesium-dependent uptake of dopamine and noradrenaline. Amantadine and desipramine influenced neither the ATP-magnesium-dependent nor the ATP-magnesium-independent uptake of the catecholamines.
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  • 8
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 271 (1971), S. 311-319 
    ISSN: 1432-1912
    Keywords: Hypothalamus ; Noradrenaline ; Electrical Stimulation ; Chemical Sympathectomy ; Blood Pressure
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The third ventricle and the aqueduct of the anaesthetized cat were cannulated and the hypothalamus was superfused with artificial cerebrospinal fluid. Electrical stimulation of the nucleus posterior of the hypothalamus elicited a rise of the blood pressure of 58±3 mm Hg (n=20). Superfusion of the hypothalamus with artificial cerebrospinal fluid containing bretylium (5×10−3 M) caused a gradual and long lasting impairment of the rise of blood pressure due to stimulation of the nucleus posterior. Tetracaine (1×10−3 M) diminished the rise of blood pressure to about the same extent as did 5×10−3M of bretylium; the inhibitory action of tetracaine was completely reversed within 120 min. Pretreatment of cats with 6-hydroxydopamine, which was applied through a Collison cannula implanted into the lateral ventricle, evoked a decrease of the noradrenaline content of the hypothalamus and of the rest of the brain and an impairment of the rise of blood pressure during stimulation of the nucleus posterior (33±3 mm Hg;n=6). The blood pressure of the anaesthetized cats was not affected by pretreatment with 6-hydroxydopamine. Superfusion of the hypothalamus with desipramine (1×10−4M) enhanced the rise of blood pressure elicited by electrical stimulation. The results are compatible with the assumption that the rise of blood pressure during stimulation of the nucleus posterior of the hypothalamus is mediated by adrenergic neurons of the brain.
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  • 9
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 297 (1977), S. 219-225 
    ISSN: 1432-1912
    Keywords: Hypothalamus ; Beta-adrenoreceptor blocking drugs ; Isoproterenol ; Tolazoline ; Pressor response ; Electrical stimulation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The posterior hypothalamus of cats anaesthetized with pentobarbital sodium was superfused and electrically stimulated with a push-pull cannula. Superfusion of the hypothalamus with (±)-, (-)-propranolol, sotalol, practolol or metoprolol caused a concentration-dependent inhibition of the pressor response to hypothalamic stimulation. (+)-Propranolol and a procaine concentration equi-anaesthetic to the concentration of (+)- and (-)-propranolol were ineffective. Lower concentrations of propranolol and metoprolol were needed to inhibit the pressor response than of sotalol or practolol. Superfusion with practolol and tolazoline impaired the pressor response to a greater extent than did superfusion with each of the drugs alone. Hypothalamic superfusion with isoproterenol elicited a concentration-dependent enhancement of the rise of blood pressure during electrical stimulation of the hypothalamus. It is concluded that beta-adrenoreceptors are present in the posterior hypothalamus and that they are involved in the pressor response elicited by electrical stimulation of the hypothalamus. Propranolol and metoprolol seemed to possess a higher affinity to the beta-receptors of the hypothalamus than sotalol or practolol.
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  • 10
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 321 (1982), S. 282-286 
    ISSN: 1432-1912
    Keywords: Release of endogenous histamine ; Hypothalamus ; Cat ; Freely moving rabbit ; Electrical stimulation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The hypothalamus of anaesthetized cats and conscious, freely moving rabbits was superfused with CSF through double-walled, push-pull cannulae and the release of endogenous histamine was determined in the superfusates by a radioenzymatic assay. In the posterior hypothalamic area of the anaesthetized cat, the rate of release of endogenous histamine varied rhythmically; phases of high rate of release appeared at 60 min cycles. The release of histamine was increased by electrical stimulation of the superfused area, as well as by hypothalamic superfusion with potassium-rich CSF. In the conscious rabbit, the anterior hypothalamic area and the posterior hypothalamic nucleus were superfused simultaneously. In both regions, the resting release of histamine varied rhythmically at approximately 70 min cycles. Phases of high or low-rate of release in the anterior hypothalamic area coincided with the corresponding phases in the posterior hypothalamic nucleus. The rhythmic release of endogenous histamine in the hypothalamus, as well as the ability of depolarizing stimuli to enhance the release of the amine support the idea that histamine acts as a neurotransmitter in the central nervous system.
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