2018
DOI: 10.1016/j.brainresbull.2018.07.013
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Colitis-induced alterations in response properties of visceral nociceptive neurons in the rat caudal medulla oblongata and their modulation by 5-HT3 receptor blockade

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Cited by 18 publications
(6 citation statements)
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“…Two kinds of stimulations (visceral and somatic) were used in our experiments. To induce visceral nociception, a colorectal distension was performed as described previously (Lyubashina et al, 2018). It was produced by inflating a 7 cm long, 2 cm diameter flexible latex balloon, which was inserted transanally and kept in position (the end of the balloon 1 cm proximal to the anus) by taping the connecting catheter to the tail.…”
Section: Methodsmentioning
confidence: 99%
“…Two kinds of stimulations (visceral and somatic) were used in our experiments. To induce visceral nociception, a colorectal distension was performed as described previously (Lyubashina et al, 2018). It was produced by inflating a 7 cm long, 2 cm diameter flexible latex balloon, which was inserted transanally and kept in position (the end of the balloon 1 cm proximal to the anus) by taping the connecting catheter to the tail.…”
Section: Methodsmentioning
confidence: 99%
“…Interestingly, in our experiments in healthy control rats alongside with the attenuation of the CRD‐evoked neuronal excitation the facilitatory action of buspirone on the CVLM neuron inhibitory responses to noxious CRD was revealed. The apparent resemblance of the CRD‐inhibited CVLM neurons to the OFF cells defined in the rostral ventromedial medulla (Fields, 2004; Fields et al, 1983; Martins & Tavares, 2017) allowed us and other authors to suggest a functional alliance between these neuronal populations, promoting antinociception (Lyubashina et al, 2016, 2018, 2019; Pinto‐Ribeiro et al, 2011). Considering this, the revealed buspirone‐induced enhancement of the abdominal nociception‐related inhibitory events within the CVLM may at least partially contribute to the antinociceptive effect of the 5‐HT1A agonist in normal conditions.…”
Section: Discussionmentioning
confidence: 88%
“…We also cannot rule out that the described post‐inflammatory intestinal hypersensitivity and its facilitation by systemic buspirone can be consequences of some alterations occurring immediately in the expression and/or sensitivity of 5‐HT1A heteroreceptors localized on glutamatergic or GABAergic targets within the raphe nuclei and other pain‐related sites such as the locus coeruleus, vagal nuclei, and spinal dorsal horn (Bagdy et al, 2000; Choi et al, 2013; Huang & Grau, 2018; Szabo & Blier, 2001; Wang et al, 2009; Wang & Ramage, 2001). Such changes may be at least partially responsible for the enhanced glutamatergic synaptic transmission and augmented nociceptive activation that have been found in these regions following gut injury (Al‐Chaer et al, 2000; Bai et al, 2019; Lyubashina et al, 2018; Ness & Gebhart, 2001; Sanoja et al, 2010; Traub et al, 2008), contributing thus to the post‐colitis amplifying of excitatory visceral nociceptive processing in the medulla and its further increase under 5‐HT1A heteroreceptor activation by buspirone, reported in the present study. Undoubtedly, special studies are needed to elucidate whether the assumptions that we made above hold true.…”
Section: Discussionmentioning
confidence: 99%
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