α2-Adrenergic receptors mediate inhibition of cyclic AMP production in neurons in primary culture

Weiss, Samuel; Kemp, Dorothy E.; Lenox, Robert H.; Ellis, John E.

doi:10.1016/0006-8993(87)90022-9

Cited by 22 publications

(9 citation statements)

References 11 publications

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“…Pargyline (10 tM) and ascorbic acid (1%) were added to the external solutions in order to prevent oxidative degradation of At the concentrations used, neither IBMX nor forskolin nor the antioxidative agents, applied alone or together, modified the studied K+ current, in the absence of agonist. These observations corroborate our previous studies showing that 0.1 uM forskolin, in the presence of 1 mM IBMX, does not modify basal cyclic AMP concentrations but increases neurotransmitter efficacy in cyclic AMP production, whereas potency remains unaffected (see Figure 1 in article by Weiss et al, 1985).…”

Section: Methodssupporting

confidence: 92%

The 5‐HT₄ receptor subtype inhibits K⁺ current in colliculi neurones via activation of a cyclic AMP‐dependent protein kinase

Fagni¹,

Dumuis²,

Sebben³

et al. 1992

British J Pharmacology

103

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1 The aim of the present study was to examine the effect of 5-hydroxytryptamine (5-HT) on K+ current in primary culture of mouse colliculi neurones and to identify the 5-HT receptor subtype that could be involved in this effect. 2 The voltage-activated K+ current of the neurones was partially blocked by 8-bromo adenosine 3':5'-cyclic monophosphate (8-bromo-cyclic AMP). This effect was mimicked by 5-HT and the action of 5-HT could be antagonized by H7, a non specific protein kinase inhibitor, and by PKI, the specific cyclic AMP-dependent protein kinase blocker. 3 A similar cyclic AMP-dependent blockade of the K+ current was found with renzapride (BRL 24924) and other 5-HT4 receptor agonists such as cisapride, BIMU 8, zacopride and 5-methoxytryptamine (5-MeOT). ICS 205 930, the classical 5-HT4 receptor blocker, could not be used in this study because it inhibited the studied K+ current by itself. However, the novel 5-HT4 receptor antagonist, DAU 6285 blocked the effects of 5-HT and renzapride on the K+ current.4 The current was insensitive to the 5-HTI and 5-HT3 receptor agonists (8-hydroxy-2-(di-n-propylamino) tetralin, RU 24969, carboxamidotryptamine, 2-CH3-5-HT) as well as to 5-HT,, 5-HT2 and 5-HT3 antagonists (methiothepin, ketanserin, ondansetron [GR 38 032]). Moreover, these antagonists did not affect the actions of the tested 5-HT4 receptor agonists. 5 The present results show that part of the voltage-activated K+ current in mouse colliculi neurones is cyclic AMP-sensitive and the blockade of the current by 5-HT involves the 5-HT4 receptor subtype. The putative implication of 5-HT4 receptors in neuronal plasticity, via a blockade of K+ channels, is discussed.

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Section: Methodssupporting

confidence: 92%

The 5‐HT₄ receptor subtype inhibits K⁺ current in colliculi neurones via activation of a cyclic AMP‐dependent protein kinase

Fagni¹,

Dumuis²,

Sebben³

et al. 1992

British J Pharmacology

103

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“…Indeed, the amplitude of the inhibitory effects of DAGO or DTLET was increased in the presence of DA. These results can also be discussed in light of those of Weiss et al (1985) who reported that the inhibitory effects of opiate and dopaminergic D2 agonists on CAMP production in intact striatal neurons in primary culture were nonadditive. Such a nonadditivity favors colocalization of dopaminergic D2 and opiate receptors on neuronal subpopulations.…”

Section: Discussionmentioning

confidence: 72%

Mu and delta opiate receptors coupled negatively to adenylate cyclase on embryonic neurons from the mouse striatum in primary cultures

1988

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Primary cultures of pure populations of neuronal or glial cells from the striatum, the cerebral cortex, and the mesencephalon of the mouse embryo were used to look for the presence of opiate receptors coupled to adenylate cyclase. Leu-enkephalin inhibited cAMP production in membranes of embryonic striatal neurons but not in those of other cell types examined. Mu and delta opiate receptors seemed to be coupled negatively to adenylate cyclase in embryonic striatal neurons. It was found that DTLET (a selective delta agonist), as well as DAGO (a selective mu agonist), inhibited cAMP production on these cells. DTLET but not, however, DAGO produced a similar effect on homogenates from the adult rat striatum and on membranes from the neuroblastoma x glioma hybrid cell line NG 108–15, two preparations known to possess only delta receptors negatively coupled to adenylate cyclase. The selective kappa agonist U 50.488 was ineffective on all types of membrane preparations used. The inhibitory effects of both DTLET and DAGO on basal adenylate cyclase activity in striatal neurons were reversed by naloxone with a similar efficacy. Two other selective mu agonists, trimu 5 and morphiceptin, inhibited cAMP production in membranes of striatal neurons as well. The nonadditivity of the inhibitory effects of DTLET and DAGO on basal or forskolin-induced activation of adenylate cyclase suggested that mu and delta receptors were colocalized on a similar subpopulation of striatal cells in primary culture. These cells possess dopaminergic receptors of the D1 subtype as well since the amplitude of the inhibitory effects of DTLET and DAGO on cAMP production was increased in the presence of dopamine.(ABSTRACT TRUNCATED AT 250 WORDS)

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“…This prelabeling technique, onginally described by Shimizu et al (1 969), has afforded results completely consonant with those based on measurement of endogenous levels of CAMP (Daly, 1977) and has been used in various subsequent studies with cell cultures (see Weiss et al, 1987, and references quoted therein).…”

Section: Determination Of Adenylate Cyclase Activitymentioning

confidence: 86%

μ‐Opioid Receptors Mediate the Inhibitory Effect of Opioids on Dopamine‐Sensitive Adenylate Cyclase in Primary Cultures of Rat Neostriatal Neurons

Vliet

Mulder

Schoffelmeer

1990

Journal of Neurochemistry

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The receptors mediating the inhibition of D1 dopamine receptor-stimulated adenylate cyclase by opioids were examined in primary cultures of rat neostriatal neurons. Adenylate cyclase activity was dose-dependently increased by the selective D1 dopamine receptor agonist SKF 38393 (EC50 = 0.05 microM). This stimulation was fully antagonized by the selective D1 dopamine receptor antagonist SCH 23390 (1 microM). SKF 38393 (1 microM)-stimulated adenylate cyclase activity was strongly reduced (by almost 60%) by the highly selective mu-agonist [D-Ala2, MePhe4, Gly-ol5]-enkephalin (DAGO; EC50 = 0.006 microM) and high concentrations of the selective delta-agonist [D-Ser2(O-tert-butyl), Leu5]-enkephalyl-Thr6 (DSTBU-LET; EC50 = 0.13 microM) but not by the selective delta-agonist [D-penicillamine2, D-penicillamine5]enkephalin (DPDPE). D1 dopamine receptor-stimulated adenylate cyclase activity was also slightly reduced (by approximately 20%) by high concentrations of the kappa-agonist U50,488 (EC50 = 0.63 microM). The inhibitory effects of submaximally effective concentrations of DAGO, DSTBULET, and U50,488 were equally well antagonized by the mu-opioid receptor-selective antagonist naloxone (EC50 of approximately 0.1 microM). Neither the irreversible delta-ligand fentanyl isothiocyanate (1 microM) nor the reversible delta-antagonist ICI 174864 (1 microM) reversed the inhibitory effects of DSTBULET. The inhibitory effects of DAGO and U50,488 were equally well reversed by high concentrations (greater than 0.1 microM) of the kappa-opioid receptor-selective antagonist norbinaltorphimine. The effect of DAGO (1 microM) was already detectable after 1 day in culture, whereas DPDPE (1 microM) had no effect even after 28 days in culture. These data indicate that an homogeneous population of mu-opioid receptors coupled as inhibitors to D1 dopamine receptor-stimulated adenylate cyclase is expressed in rat neostriatal neurons in primary culture.

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α2-Adrenergic receptors mediate inhibition of cyclic AMP production in neurons in primary culture

Cited by 22 publications

References 11 publications

The 5‐HT₄ receptor subtype inhibits K⁺ current in colliculi neurones via activation of a cyclic AMP‐dependent protein kinase

The 5‐HT₄ receptor subtype inhibits K⁺ current in colliculi neurones via activation of a cyclic AMP‐dependent protein kinase

Mu and delta opiate receptors coupled negatively to adenylate cyclase on embryonic neurons from the mouse striatum in primary cultures

μ‐Opioid Receptors Mediate the Inhibitory Effect of Opioids on Dopamine‐Sensitive Adenylate Cyclase in Primary Cultures of Rat Neostriatal Neurons

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α2-Adrenergic receptors mediate inhibition of cyclic AMP production in neurons in primary culture

Cited by 22 publications

References 11 publications

The 5‐HT4 receptor subtype inhibits K+ current in colliculi neurones via activation of a cyclic AMP‐dependent protein kinase

The 5‐HT4 receptor subtype inhibits K+ current in colliculi neurones via activation of a cyclic AMP‐dependent protein kinase

Mu and delta opiate receptors coupled negatively to adenylate cyclase on embryonic neurons from the mouse striatum in primary cultures

μ‐Opioid Receptors Mediate the Inhibitory Effect of Opioids on Dopamine‐Sensitive Adenylate Cyclase in Primary Cultures of Rat Neostriatal Neurons

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The 5‐HT₄ receptor subtype inhibits K⁺ current in colliculi neurones via activation of a cyclic AMP‐dependent protein kinase

The 5‐HT₄ receptor subtype inhibits K⁺ current in colliculi neurones via activation of a cyclic AMP‐dependent protein kinase