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  • Articles: DFG German National Licenses  (30)
  • Push-pull cannula  (20)
  • Electrical stimulation  (8)
  • Striatum  (3)
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  • Articles: DFG German National Licenses  (30)
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  • 1
    Electronic Resource
    Electronic Resource
    In vivo release patterns and cardiovascular properties of inhibitory and excitatory amino acids in the hypothalamus (1995)
    Springer
    Amino acids 8 (1995), S. 47-58 
    Details
    ISSN: 1438-2199
    Keywords: Amino acids ; Taurine ; GABA ; Glutamate ; Arginine ; Blood pressure ; Push-pull cannula
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The posterior hypothalamus of conscious, freely moving rats was superfused with artificial cerebrospinal fluid through a push-pull cannula and the release of amino acids was determined in the superfusate. Under basal conditions, the release rates of taurine, GABA and glutamate fluctuated according to ultradian rhythms with different frequencies. Hypothalamic superfusion with veratridine or high concentrations of potassium choride enhanced the release rates of taurine, GABA and glutamate in a concentration-dependent way. Tetrodotoxin decreased the basal release rates of the three amino acids. The release of arginine was not influenced significantly by these compounds. A fall of blood pressure elicited by intravenous infusion of nitroprusside decreased the release rates of GABA and taurine and enhanced the release of glutamate. Infusion of noradrenaline increased blood pressure and release rates of GABA and taurine, while the release of glutamate was not influenced. Neither the pressor, nor the depressor responses to drugs influenced the release of arginine in the hypothalamus. It is concluded that the inhibitory amino acids taurine and GABA released from hypothalamic neurons possess a tonic hypotensive function. The excitatory amino acid glutamate, released from glutamatergic neurons of the hypothalamus, seems to possess a hypertensive function in counteracting a fall of blood pressure.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00806543
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Modulation by dopamine receptors of the histamine release in the rat hypothalamus (1993)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 347 (1993), S. 301-305 
    Details
    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.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00167449
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Nitric oxide modulates the release of acetylcholine in the ventral striatum of the freely moving rat (1995)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 352 (1995), S. 67-73 
    Details
    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.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00169191
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    Paper (German National Licenses)
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  • 4
    Electronic Resource
    Electronic Resource
    Nitric oxide modulates the release of acetylcholine in the ventral striatum of the freely moving rat (1995)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 352 (1995), S. 67-73 
    Details
    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.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00169191
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    Paper (German National Licenses)
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  • 5
    Electronic Resource
    Electronic Resource
    Ionic and haemodynamic changes influence the release of the excitatory amino acid glutamate in the posterior hypothalamus (1995)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 352 (1995), S. 620-625 
    Details
    ISSN: 1432-1912
    Keywords: Key words Glutamate release ; Central blood pressure regulation ; Haemorrhage ; Chlorisondamine ; Aortic depressor nerve ; Push-pull cannula
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  The push-pull technique was used to investigate the release of the excitatory amino acid glutamate in the posterior hypothalamic area of the conscious rat. The hypothalamus was superfused through the push-pull cannula with artificial cerebrospinal fluid (CSF), and the superfusate was collected in time periods of 10 min when ionic conditions in the CSF were changed, or in short periods of 3 min when blood pressure changes were evoked. The mean glutamate release rate was 2.8±0.7 pmol/min. Depolarization by hypothalamic superfusion with CSF containing 50 mM K+ enhanced the release of glutamate in the presence of Ca2+. The K+-induced release was attenuated by 40% when the hypothalamus was superfused with Ca2+-free CSF. Replacement of Ca2+ by Mg2+ abolished the K+-induced release of glutamate. Hypovolaemia elicited by haemorrhage enhanced the release rate of glutamate. Similarly, a hypotension elicited by i.v. injection of chlorisondamine (3 mg/kg) led to a pronounced and permanent enhancement in glutamate release. The effects of hypovolaemia and chlorisondamine on glutamate release were abolished in aortic denervated rats, indicating that this response is due to a decrease of impulse generation in baroreceptors. A hypervolaemia elicited by blood infusion did not affect the release of glutamate. Similarly, a pronounced pressor response to phenylephrine (15 μg/kg per minute) infused intravenously for 9 min was ineffective. The results show that the K+-induced release of glutamate in the hypothalamus is dependent on the presence of Ca2+. The increase in glutamate release rate by hypovolaemia or chlorisondamine suggests that the glutamatergic neurons in the posterior hypothalamic area respond to unloading of aortic baroreceptors and possess a counteracting, hypertensive function.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00171320
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    Paper (German National Licenses)
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  • 6
    Electronic Resource
    Electronic Resource
    Dopamine and noradrenaline transport into subcellular vesicles of the striatum (1973)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 278 (1973), S. 387-402 
    Details
    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.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00501482
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  • 7
    Electronic Resource
    Electronic Resource
    Inhibition by locally applied alpha-adrenoreceptor blocking drugs of the depressor response to stimulation of the anterior hypothalamus (1976)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 295 (1976), S. 1-7 
    Details
    ISSN: 1432-1912
    Keywords: Anterior hypothalamus ; Alpha-adrenoreceptor blocking drugs ; Electrical stimulation ; Arterial blood pressure ; Depressor response ; Phenylephrine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Cats were anaesthetized with pentobarbital sodium and the anterior hypothalamus was superfused with artificial cerebrospinal fluid through a push-pull cannula. Electrical stimulation of the superfused area with the tip of the cannula elicited a fall of the arterial blood pressure which was dependent on frequency and voltage. Maximal depressor response was obtained at 60 Hz with 2–4 V; further increase of the voltage often led to a rise of the arterial blood pressure. Superfusion of the anterior hypothalamus with the alpha-adrenoreceptor blocking drugs tolazoline, piperoxan, yohimbine or phentolamine caused a dose-dependent inhibition of the depressor response to hypothalamic stimulation. Tolazoline was less effective than the other drugs. Superfusion of the anterior hypothalamus with the alpha-sympathomimetic drug phenylephrine prior to and during superfusion with phentolamine abolished the inhibitory action of the latter drug. It is concluded that alpha-adrenoreceptors are present in the anterior hypothalamus and involved in the depressor response to electrical stimulation of this hypothalamic area.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00509764
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    Paper (German National Licenses)
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  • 8
    Electronic Resource
    Electronic Resource
    Presence of Beta-adrenoreceptors in the hypothalamus; their importance for the pressor response to hypothalamic stimulation (1977)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 297 (1977), S. 219-225 
    Details
    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.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00509264
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    Paper (German National Licenses)
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  • 9
    Electronic Resource
    Electronic Resource
    Release of endogenous histamine in the hypothalamus of anaesthetized cats and conscious, freely moving rabbits (1982)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 321 (1982), S. 282-286 
    Details
    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.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00498514
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  • 10
    Electronic Resource
    Electronic Resource
    In vivo release by histamine agonists and antagonists of endogenous catecholamines in the cat hypothalamus (1984)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 326 (1984), S. 116-123 
    Details
    ISSN: 1432-1912
    Keywords: Hypothalamus ; Push-pull cannula ; Catecholamines ; Histamine ; Histamine receptor agonists ; Histamine receptor antagonists
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The posterior hypothalamus of anaesthetized cats was superfused through a push-pull cannula with histamine agonists and antagonists and the release of endogenous catecholamines was determined in the superfusate. Hypothalamic superfusion with histamine, 2-methylhistamine (H1-agonist), dimaprit (H2-agonist) or metiamide (H2-antagonist) enhanced the release of the catecholamines dopamine, noradrenaline and adrenaline. The releasing effects of these substances depended on the presence of calcium ions. Superfusion with 2-pyridylethylamine (H1-agonist) was virtually ineffective, while superfusion with 2-thiazolethylamine (H1-agonist) enhanced the rate of release of noradrenaline and adrenaline without influencing the release of dopamine. Superfusion with mepyramine (H1-antagonist) inhibited the release of noradrenaline and adrenaline without affecting the release of dopamine. Hypothalamic superfusion with a concentration of procaine which was equi-anaesthetic to that of mepyramine was ineffective. Ranitidine (H2-antagonist) did not alter the rates of release of the catecholamines. The releasing effect of histamine was inhibited on hypothalamic superfusion with mepyramine and ranitidine. Ranitidine also inhibited the releasing effects of dimaprit and 2-methylhistamine thus indicating that the releasing action of the latter compound was mainly due to stimulation of H2-receptors. These data suggest that blockade of H1-receptors of the posterior hypothalamus reduces the release of noradrenaline and adrenaline, while stimulation of H1-receptors seems to increase the rates of release of these two catecholamines. Stimulation of H2-receptors enhances the release of all three catecholamines. Thus, dopaminergic neurones of the hypothalamus seem to possess H2-receptors, while noradrenergic and adrenergic neurones possess H1- and H2-receptors.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00517307
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    Paper (German National Licenses)
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