Kappa-receptor mechanisms in synaptosomal Ca uptake

Toru, Taro; Konno, Fukio; Takayanagi, Issei; Hirobe, Masaaki

doi:10.1016/0306-3623(89)90025-6

Cited by 7 publications

(2 citation statements)

References 15 publications

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“…In conclusion, this is the first demonstration that in neonatalrat brain cells one of the post-receptor events of CCK-8 is to increase the production of InsP3. The potential importance of InsP3 in mediating the anti-opioid effect of CCK-8 in pain modulation can be derived from the two following established facts (1) that InsP3 accelerated the Ca2+ release from the intracellular Ca2+-storage pool, resulting in an increase in intracellular [Ca2l], and (2) that a cardinal mechanism of the opiate effect was to decrease intracellular [Ca2+] via blockade of Ca2+ influx (MacDonald & Werz, 1986;Tort et al, 1989;Wang et al, 1989). In connection with this, it should be pointed out that a decrease in the InsP3-stimulating effect at higher concentrations of CCK-8 in the experiment in vitro may have some relevance to the finding in vivo, where the anti-opioid effect of CCK-8 tended to diminish and shift to an opio-mimetic effect along with an increase in dosage.…”

Section: Discussionmentioning

confidence: 99%

Influences of cholecystokinin octapeptide on phosphoinositide turnover in neonatal-rat brain cells

Zhang

Han

1992

Biochemical Journal

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Cholecystokinin octapeptide (CCK-8) has been shown to be coupled to phosphoinositide turnover in pancreatic acini as well as in a kind of neuroblastoma cell and a human embryonic cell line. Little is known, however, about its link with phosphatidylinositol breakdown in the brain. The brains (minus cerebella) from 1-2-day-old neonatal rats were enzymically dissociated into single cells. The intact cells were prelabelled by incubation with myo-[3H]inositol for 3 h, and were then stimulated with agonists in the presence of 10 mM-LiCl. Carbachol at 1 mM induced an increase in InsP3 labelling in brain cells (peak at 30 min, and then a gradual decrease), and a static accumulation of InsP with time, whereas the labelling of InsP2 remained essentially unchanged. A very similar time-response curve was obtained for 10 nM-CCK-8 in stimulating phosphoinositide turnover. The dose-response curve for incubated brain cells revealed that the formation of InsP3 increased when the concentration of CCK-8 was increased from 0.1 to 10 nM. A further increase in CCK-8 concentration to 100-1000 nM resulted in a gradual decrease in InsP3 formation. InsP and InsP2 levels stayed relatively stable. The production of InsP3 stimulated by 10 nM-CCK-8 was dose-dependently suppressed by the CCK-A antagonist Devazepide in the concentration range 1-10 nM; the effect declined when the concentration was further increased to 100-1000 nM. In contrast, the CCK-B antagonist L365,260 showed a sustained suppression of InsP3 production at concentrations above 0.1 nM, i.e. in the range 1-1000 nM. The results provide evidence that CCK-8 stimulates the turnover of phosphoinositide and increases InsP3 labelling in dissociated neonatal-rat brain cells, in which both CCK-A and CCK-B receptors seem to be involved.

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Section: Discussionmentioning

confidence: 99%

Influences of cholecystokinin octapeptide on phosphoinositide turnover in neonatal-rat brain cells

Zhang

Han

1992

Biochemical Journal

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“…Και οι τρεις οπιοειδείς υποδοχείς έχει βρεθεί ότι είναι μεμβρανικοί και συνδέονται με κανάλια Ca2 + και Κ + (North 1993). Συγκεκριμένα οι κάππα οπιοειδείς υποδοχείς στον εγκέφαλο συνδέονται με N-τύπου Ca2 + δυναμικά στους νευρώνες και αυτή η αλληλεπίδραση μπορεί να είναι σημαντική για την ικανότητα των κάππα αγωνιστών και της δυνορφίνης Α να εμποδίζουν την απελευθέρωση των νευροδιαβιβαστών προσυναπτικά (Toru et al 1989, North 1993, Gross et al 1987, Weisskopf et al 1993, Reìsine 1995.…”

Section: πρόδρομα μόρια οπιοειδών και το κύριο ενεργό πεπτιδικό προϊόν τουςunclassified

Ο Ρολος Των Νευροπεπτιδιων Στη Φυσιολογια Των Χρωμιοφιλων Κυτταρων Μυελου Επινεφριδιων Και Των Φαιοχρωμοκυττωματων

Βενυχακη¹

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Calcium channel modulation by dihydropyridines modifies sufentanil-induced antinociception in acute and tolerant conditions

Dierssen

Flórez

Hurlé

1990

Naunyn-Schmiedeberg's Arch Pharmacol

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The study was aimed at elucidating the possible participation of L-type Ca2+ channel in the acute analgesic effect of an opiate and the development of tolerance to this action. Sufentanil, a selective mu agonist, and two dihydropyridines, the Ca2+ antagonist nimodipine and the Ca2+ agonist Bay K 8644, were selected. The tailflick test was used to assess the nociceptive threshold. In naive rats, nimodipine (200 micrograms/kg) potentiated the analgesic effect of sufentanil reducing the ED50 from 0.26 to 0.08 microgram/kg. Similar results were observed with its (-)-enantiomer Bay N 5248, while the (+) enantiomer Bay N 5247 was ineffective. Tolerance to the opiate was induced by chronic subcutaneous administration of sufentanil with minipumps (2 micrograms/h, 7 days). In these conditions the dose-response curve to sufentanil was displaced to the right and the ED50 was increased to 1.49 micrograms/kg. In tolerant rats, nimodipine preserved its potentiating ability and prevented the displacement to the right of the sufentanil dose response-curve (ED50 = 0.48 microgram/kg). When nimodipine was pumped (1 microgram/h, 7 days) concurrently with sufentanil, the development of tolerance to the opioid was not disturbed. However, the expression of tolerance was abolished and even the effect of acutely administered sufentanil was markedly potentiated (ED50 = 0.03 microgram/kg). Similar experiments were performed with Bay K 8644. In naive rats, Bay K 8644 at a low dose (20 micrograms/kg) that behaves as a calcium agonist, antagonized the analgesic effect of sufentanil (ED50 = 0.58 microgram/kg), whereas at a high dose (200 micrograms/kg) it potentiated this action (ED50 = 0.15 microgram/kg).(ABSTRACT TRUNCATED AT 250 WORDS)

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Kappa-receptor mechanisms in synaptosomal Ca uptake

Cited by 7 publications

References 15 publications

Influences of cholecystokinin octapeptide on phosphoinositide turnover in neonatal-rat brain cells

Influences of cholecystokinin octapeptide on phosphoinositide turnover in neonatal-rat brain cells

Ο Ρολος Των Νευροπεπτιδιων Στη Φυσιολογια Των Χρωμιοφιλων Κυτταρων Μυελου Επινεφριδιων Και Των Φαιοχρωμοκυττωματων

Calcium channel modulation by dihydropyridines modifies sufentanil-induced antinociception in acute and tolerant conditions

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