A1-adenosine acute withdrawal response and cholecystokinin-8 induced contractures are regulated by Ca 2+ - and ATP-activated K + channels

Cascio, Maria Grazia; Valeri, Daniela; Tucker, Steven; Marini, Pietro

doi:10.1016/j.phrs.2015.03.014

Cited by 2 publications

(2 citation statements)

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“…Ion channels involved in CCK-induced responses include L-type voltage-dependent Ca 2+ channels and TRP channels that contribute to the neuronal Ca 2+ influx elicited by CCK (21,(28)(29)(30). ATP-sensitive potassium channel (K ATP ) and A-type K channels may also be involved in responses to CCK (31,32).…”

Section: Introductionmentioning

confidence: 99%

TMEM16B determines cholecystokinin sensitivity of intestinal vagal afferents of nodose neurons

Wang¹,

Lu²,

Cicha³

et al. 2019

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Section: Introductionmentioning

confidence: 99%

TMEM16B determines cholecystokinin sensitivity of intestinal vagal afferents of nodose neurons

Wang¹,

Lu²,

Cicha³

et al. 2019

JCI Insight

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“…The subtypes have been shown to modulate intracellular levels of adenosine 3’,5’-cyclic monophosphate (cAMP) in different ways [ 3 ]. In certain cells, the adenosine receptor (AR) is also coupled to the calcium-mobilizing G protein subunit, G αq [ 4 ]. The adenosine derivative N 6 -(2-hydroxyethyl)-adenosine (HEA) was first isolated from the Cordyceps pruinosa and was identified as a calcium antagonist that inhibits muscle contraction [ 5 ].…”

Section: Introductionmentioning

confidence: 99%

N6-(2-Hydroxyethyl)-Adenosine Exhibits Insecticidal Activity against Plutella xylostella via Adenosine Receptors

et al. 2016

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The diamondback moth, Plutella xylostella, is one of the most important pests of cruciferous crops. We have earlier shown that N6-(2-hydroxyethyl)-adenosine (HEA) exhibits insecticidal activity against P. xylostella. In the present study we investigated the possible mechanism of insecticidal action of HEA on P. xylostella. HEA is a derivative of adenosine, therefore, we speculated whether it acts via P. xylostella adenosine receptor (PxAdoR). We used RNAi approach to silence PxAdoR gene and used antagonist of denosine receptor (AdoR) to study the insecticidal effect of HEA. We cloned the whole sequence of PxAdoR gene. A BLAST search using NCBI protein database showed a 61% identity with the Drosophila adenosine receptor (DmAdoR) and a 32–35% identity with human AdoR. Though the amino acids sequence of PxAdoR was different compared to other adenosine receptors, most of the amino acids that are known to be important for adenosine receptor ligand binding and signaling were present. However, only 30% binding sites key residues was similar between PxAdoR and A1R. HEA, at a dose of 1 mg/mL, was found to be lethal to the second-instar larvae of P. xylostella, and a significant reduction of mortality and growth inhibition ratio were obtained when HEA was administered to the larvae along with PxAdoR-dsRNA or antagonist of AdoR (SCH58261) for 36, 48, or 60 h. Especially at 48 h, the rate of growth inhibition of the PxAdoR knockdown group was 3.5-fold less than that of the HEA group, and the corrected mortality of SCH58261 group was reduced almost 2-fold compared with the HEA group. Our findings show that HEA may exert its insecticidal activity against P. xylostella larvae via acting on PxAdoR.

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A1-adenosine acute withdrawal response and cholecystokinin-8 induced contractures are regulated by Ca 2+ - and ATP-activated K + channels

Cited by 2 publications

References 58 publications

TMEM16B determines cholecystokinin sensitivity of intestinal vagal afferents of nodose neurons

TMEM16B determines cholecystokinin sensitivity of intestinal vagal afferents of nodose neurons

N6-(2-Hydroxyethyl)-Adenosine Exhibits Insecticidal Activity against Plutella xylostella via Adenosine Receptors

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