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• W2904151552 abstract "Key points Concurrent 5‐HT 2A (Q pathway) and 5‐HT 7 (S pathway) serotonin receptor activation cancels phrenic motor facilitation due to mutual cross‐talk inhibition. Spinal protein kinase Cδ (PKCδ) or protein kinase A inhibition restores phrenic motor facilitation with concurrent Q and S pathway activation, demonstrating a key role for these kinases in cross‐talk inhibition. Spinal PKCδ inhibition enhances adenosine‐dependent severe acute intermittent hypoxia‐induced phrenic long‐term facilitation (S pathway), consistent with relief of cross‐talk inhibition. Abstract Intermittent spinal serotonin receptor activation elicits long‐lasting phrenic motor facilitation (pMF), a form of respiratory motor plasticity. When activated alone, spinal Gq protein‐coupled serotonin 2A receptors (5‐HT 2A ) initiate pMF by a mechanism that requires ERK‐MAP kinase signalling and new BDNF protein synthesis (Q pathway). Spinal Gs protein‐coupled serotonin 7 (5‐HT 7 ) and adenosine 2A (A 2A ) receptor activation also elicits pMF, but via distinct mechanisms (S pathway) that require Akt signalling and new TrkB protein synthesis. Although studies have shown inhibitory cross‐talk interactions between these competing pathways, the underlying cellular mechanisms are unknown. We propose the following hypotheses: (1) concurrent 5‐HT 2A and 5‐HT 7 activation undermines pMF; (2) protein kinase A (PKA) and (3) NADPH oxidase mediate inhibitory interactions between Q (5‐HT 2A ) and S (5‐HT 7 ) pathways. Selective 5‐HT 2A (DOI hydrochloride) and 5HT 7 (AS‐19) agonists were administered intrathecally at C4 (three injections, 5‐min intervals) in anaesthetized, vagotomized and ventilated male rats. With either spinal 5‐HT 2A or 5‐HT 7 activation alone, phrenic amplitude progressively increased (pMF). In contrast, concurrent 5‐HT 2A and 5‐HT 7 activation failed to elicit pMF. The 5‐HT 2A ‐induced Q pathway was restored by inhibiting PKA activity (Rp‐8‐Br‐cAMPS). NADPH oxidase inhibition did not prevent cross‐talk inhibition. Therefore, we investigated alternative mechanisms to explain Q to S pathway inhibition. Spinal protein kinase C (PKC) inhibition with Gö6983 or PKCδ peptide inhibitor restored the 5‐HT 7 ‐induced S pathway to pMF, revealing PKCδ as the relevant isoform. Spinal PKCδ inhibition enhanced the S pathway‐dependent form of pMF elicited by severe acute intermittent hypoxia. We suggest that powerful constraints between 5‐HT 2A and 5‐HT 7 or A 2A receptor‐induced pMF are mediated by PKCδ and PKA, respectively." @default.
• W2904151552 created "2018-12-22" @default.
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• W2904151552 date "2018-12-02" @default.
• W2904151552 modified "2023-10-16" @default.
• W2904151552 title "Protein kinase Cδ constrains the S‐pathway to phrenic motor facilitation elicited by spinal 5‐HT₇receptors or severe acute intermittent hypoxia" @default.
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• W2904151552 doi "https://doi.org/10.1113/jp276731" @default.
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