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  • 1
    Electronic Resource
    Electronic Resource
    Involvement of Dihydropyridine-Sensitive Ca2+ Channels in Adenosine-Evoked Inhibition of Acetylcholine Release from Guinea Pig Ileal Preparation (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: The effects of adenosine and nifedipine on endogenous acetylcholine (ACh) release evoked by electrical stimulation from guinea pig ileal longitudinal muscle preparations exposed to physostigmine were evaluated using an HPLC with electrochemical detection (ECD) system. Resting ACh release, which was sensitive to tetrodotoxin (0.3 μM), was enhanced by Bay K. 8644 (0.5 μM; a Ca2+ antagonist) or 4-aminopyridine (30 μM; a K+ channel blocker) but not by theophylline (100 μM; a P1 purinoceptor antagonist) or atropine (0.3 μM). The enhancement of the resting ACh release by Bay K 8644 was virtually unaffected by atropine. Electrically evoked ACh release was enhanced by around two- to fourfold in the presence of theophylline, atropine, Bay K 8644, 4-aminopyridine, or atropine. On the other hand, the evoked ACh release was reduced by adenosine (10–30 μM), nifedipine (0.1–0.3 μM; a dihydropyridine Ca2+ channel antagonist), or bethanechol (1–3 μM) in a concentration-related fashion. The reduction induced by adenosine or nifedipine was almost abolished by either theophylline or Bay K. 8644, whereas that induced by bethanechol was virtually unaffected by these drugs. The inhibition by adenosine of ACh release was not influenced in the presence of 4-aminopyridine or atropine. However, this inhibition by adenosine was considerably enhanced by halving the Ca2+ concentration in the Krebs solution and was diminished by doubling the Ca2+ concentration. These findings suggest that adenosine produces a cholinergic neuromodulation presumably via modifying dihydropyridine-sensitive Ca2+ channel activities in the cholinergic neurons, and thus L-type Ca2+ channels may exist on the nerve terminals. It was also demonstrated that the HPLC-ECD method used for detecting endogenous ACh was suitable for evaluating mechanisms of the neuromodulation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1990.tb04146.x
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  • 2
    Electronic Resource
    Electronic Resource
    POTENTIATION OF DIPSOGENIC ACTIONS BY CENTRALLY ADMINISTERED TYPE-C NATRIURETIC PEPTIDE IN SPONTANEOUSLY HYPERTENSIVE BUT NOT WISTAR-KYOTO RATS (1997)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 24 (1997), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. The effects of type-C natriuretic polypeptides (CNP) on the central dipsogenic and pressor responses to angiotensin II (AngII) were studied by the administration of agents into the lateral cerebral ventricle under conscious and unrestrained conditions in normotensive Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR).2. The fluid intake induced by AngII (25 ng) and water deprivation were potentiated after pretreatment with CNP in SHR but not in WKY rats. However, carbachol-induced water intake was not altered by pretreatment with CNP (2.5 μg) in either WKY rats or SHR.3. In contrast, CNP did not influence the pressor responses to AngII in either WKY rats o. SHR.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1997.tb02721.x
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  • 3
    Electronic Resource
    Electronic Resource
    ATP release by angiotensin II from segments and cultured smooth muscle cells of guinea-pig taenia coli (1996)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 354 (1996), S. 796-799 
    Details
    ISSN: 1432-1912
    Keywords: Key words ATP release ; Angiotensin II ; Losartan ; AT1-receptor ; Cultured smooth muscle cells ; Guinea-pig taenia coli
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Effects of angiotensin II on ATP release were evaluated in segments and cultured smooth muscle cells from the guinea-pig taenia coli. In the segments, angiotensin II (0.3–3 μM) elicited release of ATP which was blocked by losartan and SC-52458, non-peptide angiotensin II type-1 receptor (AT1)-antagonists, but not by PD-123319, an AT2-antagonist. In superfused cultured cells, 10 μM angiotensin II likewise elicited release of ATP. Again the response was blocked by losartan and SC-52458 but not by PD-123319. These findings suggest that angiotensin II releases ATP from the smooth muscles by activation of angiotensin II-, presumably AT1-, receptors.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00166908
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  • 4
    Electronic Resource
    Electronic Resource
    Acute and long-term effects of thyrotropin releasing hormone on behavior mediated by dopaminergic and cholinergic activities in mice (1984)
    Springer
    Psychopharmacology 82 (1984), S. 301-305 
    Details
    ISSN: 1432-2072
    Keywords: Thyrotropin releasing hormone ; Acute effect ; Long-term effect ; Stereotypy ; Tremor ; Mice
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Acute and long-term (3 weeks) effects of thyrotropin releasing hormone (TRH) on behavior were investigated in mice. A single injection of TRH produced Straub tail, tremor and salivation, as well as stereotyped responses, such as head bobbing, jaw movement, digging and sniffing. Dose- and time-dependency for the effects of TRH were different depending on each response. A single injection of TRH at a low dose of 2.5 mg/kg SC did not produce stereotypy but this behavior was induced when this dose of TRH was administered in combination with atropine (3 mg/kg IP). In addition, a single low dose of TRH elicited tremor and salivation which were potentiated by physostigmine (0.1 mg/kg IP). A single high dose (20 mg/kg IP) produced marked tremor and salivation which were conversely blocked by atropine. Following daily administration of TRH at a low dose of 2.5 mg/kg SC for 21 days, stereotyped behavior was progressively increased whereas tremor and salivation were decreased. This increase in stereotyped behavior was inhibited by haloperidol (1 mg/kg IP) or physostigmine (0.1 mg/kg IP). When saline was administered instead of TRH for 3 days after long-term administration of TRH, stereotyped behavior was maintained for 2 days but thereafter decreased to some extent. When TRH (1.25 mg/kg SC) was again administered at this stage, there was a marked increase in stereotyped response. These results suggest that TRH induces dopaminergic activation, accompanied by both cholinergic inhibition and cholinergic activation, and that the former is potentiated while the latter is reduced after daily administration of TRH.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00427674
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  • 5
    Electronic Resource
    Electronic Resource
    Direct evidence for involvement of dopaminergic inhibition and cholinergic activation in yawning (1980)
    Springer
    Psychopharmacology 67 (1980), S. 39-43 
    Details
    ISSN: 1432-2072
    Keywords: Yawning ; Apomorphine ; Physostigmine ; Pilocarpine ; Dopaminergic neurons ; Cholinergic neurons
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract A behavioral study was performed in an attempt to understand the neurological mechanism involved in yawning in rats. Intraperitoneal injections of low doses (0.25 mg/kg) of apomorphine, which preferentially activate presynaptic dopamine autoreceptors, elicited yawning. Whereas apomorphine, at a high dose of 2 mg/kg, produces stereotypy which has been thought to be mediated by stimulation of postsynaptic dopamine receptors. The yawning and stereotypy did not occur simultaneously in the rat. The apomorphine-induced yawning was completely inhibited by pretreatment with fluphenazine (9 mg/kg, IM) or scopolamine (0.5 mg/kg IP), but markedly increased by reserpine (5 mg/kg, SC), however it was not affected by methylscopolamine (0.5 mg/kg, IP). Both physostigmine (0.2 mg/kg, IP), an indirect acetylcholine agonist, and pilocarpine (4 mg/kg, IP), a direct acetylcholine agonist, also induced yawning. This was abolished by scopolamine (0.5 mg/kg, IP) and increased by reserpine (5 mg/kg, SC). Fluphenazine (9 mg/kg, IP) did not affect the pilocarpine-induced yawning but increased the physostigmine-induced yawning. The results indicate that apomorphine elicits yawning by stimulating presynaptic dopamine receptors, and that dopaminergic inhibition and cholinergic activation are concomitantly involved in the yawning.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00427593
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  • 6
    Electronic Resource
    Electronic Resource
    The yawning elicited by α-melanocyte-stimulating hormone involves serotonergic-dopaminergic-cholinergic neuron link in rats (1981)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 316 (1981), S. 155-160 
    Details
    ISSN: 1432-1912
    Keywords: Yawning ; ‘Wet-Dog’ body shaking ; α-Melanocyte-stimulating hormone ; Dopaminergic agonists ; Cholinergic agonists
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary A behavioral study was performed in an attempt to understand the neuronal mechanisms involved in yawning and ‘Wet-Dog’ body shaking in rats. 1. Physostigmine (0.2 mg/kg, i. p.) and pilocarpine (4 mg/kg, i. p.) induced yawning. The physostigmine-induced yawning was markedly inhibited by high doses (4, 8 mg/kg, i. p.) of apomorphine which preferentially stimulate postsynaptic dopamine receptors but was not inhibited by methysergide, whereas the pilocarpine-induced yawning was unaffected by either apomorphine or methysergide. 2. Intraperitoneal injections of low doses (5 mg/kg, i. p.) of piribedil, which preferentially activate presynaptic dopamine autoreceptors, also elicited yawning. At a high dose of 80 mg/kg, piribedil produces stereotypy which has been thought to be mediated by stimulation of postsynaptic dopamine receptors. The yawning and stereotypy did not occur simultaneously in the rat. The piribedil-induced yawning was markedly inhibited after treatment with fluphenazine, scopolamine or methysergide. 3. Intraventricular injection of α-melanocyte-stimulating hormone (α-MSH, 10 μg/rat) elicited not only yawningstretching syndrome but also ‘Wet-Dog’ body shaking. Yawning synchronized with stretching in almost all cases. The α-MSH-induced yawning-stretching syndrome was blocked by scopolamine, apomorphine (8 mg/kg×3, i. p.), fluphenazine or methysergide, while body shaking was inhibited by methysergide, apomorphine or fluphenazine but was not inhibited by scopolamine. 4. Body shaking was also produced by 5-hydroxytryptophan (150 mg/kg, s. c.) in combination with a peripheral decarboxylase inhibitor, Ro 4-4602 (50 mg/kg, i. p.), accompanied rarely by yawning and stretching. 5. The present results indicate that a reciprocal balance of serotonergic activation-dopaminergic inhibition-cholinergic activation is involved in the yawning, and that α-MSH also induces body shaking by activating in part the central serotonergic neuron system.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00505310
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  • 7
    Electronic Resource
    Electronic Resource
    Occurrence of yawning and decrease of prolactin levels via stimulation of dopamine D2-receptors after administration of SND 919 in rats (1989)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 340 (1989), S. 21-25 
    Details
    ISSN: 1432-1912
    Keywords: Dopamine D2-receptor agonists ; SND 919 ; Talipexole ; Yawning behavior ; Prolactin secretion
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary SND 919 ((S)-2-amino-4,5,6,7-tetrahydro-6-propylamino-benzothiazole) is expected to have a potent and selective dopamine D2-receptor agonistic activity. From this information, the present study was performed to investigate effects of SND 919 on yawning behavior and prolactin secretion in rats. Subcutaneous injections of SND 919 (25–500 gm/kg, s. c.) elicited yawning responses. Its dose-response curve was bell-shaped with maximal effects at a dose of 100 μg/kg. Yawning behavior was also evoked by the putative dopamine autoreceptor agonists, talipexole (6-allyl2-amino-5,6,7,8-tetrahydro-4H-thiazolo [4,5-d]azepine) (BHT 920) (5–100 μg/kg, s. c.) and (+)-3-PPP ((+)-3-(3-hydroxyphenyl)-N-n-propylpiperidine) (5−15 mg/kg, s. c.). The yawning induced by SND 919 (100 μg/kg, s. c.) as well as talipexole (25 μg/kg, s. c.) was inhibited by pretreatment with dopamine D2-receptor antagonists such as spiperone (0.5 mg/kg, i.p.) and YM-09151-2 (cis-N-(1-benzyl-2methylpyrrolidin-3-yl)-5-chloro-2-methoxy-4-methylaminobenzamide) (0.1 mg/kg, i. p.), or the muscarinic receptor antagonist, scopolamine (0.5 mg/kg, i.p.). However, the yawning was not affected by the dopamine D1-receptor antagonist, SCH 23390 (R(+)-8-chloro-2,3,4,5-tetrahydro-3methyl-5-phenyl-1 H-3-benzazepine-7-ol) (0.5 mg/kg, i. p.). Stereotypy such as licking and biting was not observed following the administration of SND 919, talipexole and (+)-3-PPP. Administration of SND 919, talipexole or (+)-3-PPP in respective yawn-inducing doses caused a reduction in both the basal prolactin levels and the a-methyl-p-tyrosine-induced hyperprolactinemia. The results suggest that SND 919 as well as talipexole exerts selective agonistic activities for specific dopamine D2-receptors, which are not related to the occurrence of stereotypy and have a high affinity for dopamine receptor agonists quite similar to that of the pituitary lactotroph dopamine D2-receptors.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00169201
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  • 8
    Electronic Resource
    Electronic Resource
    Inhibition by ouabain and veratridine of acetylcholine-evoked phasic contraction in the guinea-pig taenia coli (1991)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 343 (1991), S. 574-579 
    Details
    ISSN: 1432-1912
    Keywords: Guinea-pig taenia coli ; Acetylcholine-evoked phasic contraction ; Ouabain ; Veratridine ; Fura-2
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Inhibitory action of ouabain and veratridine on acetylcholine (ACh)-evoked phasic contraction was examined in the guinea-pig taenia coli. ACh (5×10−4 m) produced a biphasic (phasic and tonic) contraction. As the phasic contraction, but not the tonic contraction, was resistant to gallopamil (D600, 2 × 10−7 m), a blocker of voltage-dependent Ca2+ channels, all experiments were carried out in the presence of gallopamil at this concentration. Addition of high Ca2+ (30 mm) to the solution containing ACh induced a sustained contraction, which increased in the presence of ouabain (10−5 m), an inhibitor of the Na+-K+ exchange system. On the other hand, the ACh-evoked phasic contraction was suppressed by ouabain 10−7−(10−5 m) in a time- and dose-dependent manner. The suppression by ouabain (10−6 m) of the phasic contraction was transiently potentiated by the addition of veratridine (10−6 m), an activator of Na+ channel. In contrast, the greater suppression by ouabain (10−5 m) of the contraction was antagonized by amiloride (10−4 m), a blocker of Na+ channel. This antagonism by amiloride was transiently inhibited in the presence of veratridine. In the absence of ouabain, the amplitude of the phasic contraction was transiently reduced by adding veratridine but was increased by amiloride. In addition, the phasic contraction by ACh increased 80 min after exposure to Na+-free isotonic high-K+ solution (K+, 143 mm), which elicited greater depolarization of the cell membrane. In a fluorescence study with Fura-2, an intracellular free-Ca2+ indicator, ACh increased the fluorescence intensity from the tissue by excitative light at 340 nm, which coupled with the phasic contraction. Both the increased fluorescence and tension development were reduced by ouabain. These findings suggest that the ACh-evoked phasic contraction is induced by an increase in intracellular free-Ca2+ levels and seems to be inhibited by an elevation of intracellular free-Na+ levels.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00184287
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  • 9
    Electronic Resource
    Electronic Resource
    Involvement of central β-adrenoceptors in the regulation of yawning responses (1989)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 340 (1989), S. 26-30 
    Details
    ISSN: 1432-1912
    Keywords: Yawning ; Dopamine receptor agonists ; Muscarinic cholinoceptor agonists ; β-Adrenoceptors ; β-Adrenoceptor agonists and antagonists
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary A behavioral study was performed in an attempt to understand the role of central β-adrenoceptors in yawning in rats. Yawning was evoked by apomorphine and piribedil, mixed dopamine D1/D2-receptor agonists, but not by SK&F 38393 [1-phenyl-2,3,4,5-tetrahydro-(1H)-3-benzazepine-7,8diol], a dopamine Dr-receptor angonist. The apomorphine-induced yawning was increased by pindolol, propranolol, indenolol, alprenolol and bukumolol which block the central β-adrenoceptors, but not by the peripheral β-adrenoceptor antagonists, carteolol and atenolol. These β-adrenoceptor antagonists given alone did not elicit yawning. Conversely, the yawning was inhibited by salbutamol, a β-adrenoceptor agonist, without being affected by prazosin, an α-adrenoceptor antagonist. The combined administration of SK&F 38393 and the β-adrenoceptor antagonists did not induce yawning. The yawning elicited by either apomorphine or piribedil in combination with pindolol was suppressed by spiperone and YM-09151-2 [cis-N-(1-benzyl-2-methylpyrrolidin-3-yl)-5-chloro-2-methoxy-4-methylaminobenzamide], dopamine D2-receptor antagonists, and scopolamine, a muscarinic receptor antagonist, but not by SCH 23390 [R(+)-8-chloro-2,3,4,5-tetrahydro-3-methyl-5-phenyl-1H-3-benzazepine-7-ol], a dopamine D1-receptor antagonist. Physostigmine or pilocarpine induced yawning, which was also enhanced by pindolol and propranolol. This enhanced yawning was inhibited by scopolamine, but not by spiperone, YM-09151-2 and SCH 23390. The present results suggest that the \-adrenoceptor blockade facilitates the occurrence of yawning induced by dopaminergic and cholinergic agonists. Therefore, the central adrenergic neuron systems may participate in the regulation of yawning responses.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00169202
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  • 10
    Electronic Resource
    Electronic Resource
    Antagonism by γ-aminobutyric acid of the stimulant effect of angiotensin II on cardiac sympathetic ganglia in spinal dogs (1981)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 317 (1981), S. 149-153 
    Details
    ISSN: 1432-1912
    Keywords: Angiotensin II ; GABA ; Saralasin ; Cardiac sympathetic ganglia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effects of angiotensin II and neuro-aminoacids administered through the right subclavian artery (i. a.) to the cardiac sympathetic ganglia were investigated in spinal dogs. Angiotensin II (1–8 μg) elicited a dose-dependent positive chronotropic effect which was reduced after i. a. injection of saralasin (100μg). The effect of angiotensin II was not reduced after combined treatment with either hexamethonium (10 mg/kg) plus atropine (0.1 mg/kg) or hemicholinium-3 (5 mg/kg) plus preganglionic stimulation. The dosedependent response to angiotensin II of heart rate was inhibited by GABA (50, 500μg), GABOB (500μg) and muscimol (50, 100μg). The inhibition of the response to angiotensin II by a small dose of GABA (50μg), but not by a high one (500μg), was antagonized by i. a. injection of picrotoxin (2 mg). The positive chronotropism induced by bethanechol (25, 50μg) and a small dose of acetylcholine (25μg) were significantly inhibited by a high dose (500μg) but not by a low dose (50μg) of GABA. These results confirm that angiotensin II stimulates cardiac chronotropism by acting on the angiotensin II receptor located at the cardiac ganglia and show that this stimulant effect is antagonized by GABA.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00500071
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