Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0043167 (pertussis)
 19,595 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Regulation of dopamine (DA) release from PC12 cells was investigated. Apomorphine and quinpirole, a selective D2 agonist, significantly reduced K(+)-evoked DA release, and this reduction was reversed by haloperidol. Furthermore, spiroperidol, a selective D2 antagonist, and haloperidol, a nonselective DA antagonist, enhanced the K(+)-evoked DA release. Pertussis toxin treatment of the cells abolished the quinpirole-induced reduction of K(+)-evoked DA release. Also, the haloperidol-induced enhancement of K(+)-evoked DA release was not seen in pertussis toxin treated cells. These results, therefore, suggest the presence of D2 receptors on PC12 cells which result in the modulation of K(+)-evoked DA release via a pertussis toxin-sensitive G protein.
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PMID:Dopaminergic regulation of dopamine release from PC12 cells via a pertussis toxin-sensitive G protein. 182 17

To identify the involvement of dopamine receptors in the transmembrane signaling of the adenosine receptor-G protein-adenylate cyclase system in the CNS, we examined the effects of pertussis toxin (islet-activating protein, IAP) and apomorphine on A1 adenosine agonist (-)N6-R-[3H]phenylisopropyladenosine ([3H]PIA) and antagonist [3H]xanthine amine congener ([3H]XAC) binding activity and adenylate cyclase activity in cerebral cortex membranes of the rat brain. Specific binding to a single class of sites for [3H]XAC with a dissociation constant (KD) of 6.0 +/- 1.3 nM was observed. The number of maximal binding sites (Bmax) was 1.21 +/- 0.13 pmol/mg protein. Studies of the inhibition of [3H]XAC binding by PIA revealed the presence of two classes of PIA binding states, a high-affinity state (KD = 2.30 +/- 1.16 nM) and a low-affinity state (KD = 1.220 +/- 230 nM). Guanosine 5'-(3-O-thio)triphosphate or IAP treatment reduced the number of the high-affinity state binding sites without altering the KD for PIA. Apomorphine (100 microM) increased the KD value 10-fold and decreased Bmax by approximately 20% for [3H]PIA. The effect of apomorphine on the KD value increase was irreversible and due to a conversion from high-affinity to low-affinity states for PIA. The effect was dose dependent and was mediated via D2 dopamine receptors, since the D2 antagonist sulpiride blocked the phenomenon. The inhibitory effect of PIA on adenylate cyclase activity was abolished by apomorphine treatment. There was no effect of apomorphine on displacement of [3H]quinuclidinyl benzilate (muscarinic ligand) binding by carbachol. These data suggest that A1 adenosine receptor binding and function are selectively modified by D2 dopaminergic agents.
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PMID:Possible involvement of pertussis toxin-sensitive G proteins and D2 dopamine receptors in the A1 adenosine receptor-adenylate cyclase system in rat cerebral cortex. 214 96

Activation of synthesis-modulating dopamine autoreceptors by dopamine or its agonists has been shown to inhibit dopamine synthesis in the rat striatum. However, systemic administration of the direct-acting dopamine agonist apomorphine failed to inhibit dopamine synthesis in striata from rats that had received local unilateral administration of pertussis toxin. Apomorphine did reduce dopamine synthesis by greater than 50% in sham injected control rats as well as in the striata opposite to the side of pertussis toxin injection. Examination of G proteins in striatal tissue revealed that 61% of the G proteins were ADP-ribosylated in vivo by direct pertussis toxin injection. These data suggest that guanine nucleotide regulatory proteins mediate the effects of activation of striatal synthesis-modulating dopamine autoreceptors.
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PMID:The effects of pertussis toxin on autoreceptor-mediated inhibition of dopamine synthesis in the rat striatum. 297 20