ArticlePflugers Archiv : European journal of physiology2018
Effects of eugenol on respiratory burst generation in newborn rat brainstem-spinal cord preparations.
Article in Pflugers Archiv : European journal of physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed, 7 citations in OpenAlex.
- Effects of aconitine on the respiratory activity of brainstem-spinal cord preparations isolated from newborn rats.Pflugers Archiv : European journal of physiology · 2023Article
- Novel derivatives of eugenol as potent anti-inflammatory agentsRSC advances · 2022Article
- Inhibitory effects of eugenol on putative nociceptive response in spinal cord preparation isolated from neonatal rats.Experimental brain research · 2018Article
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4 authors at 1 institution in 1 country.
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Abstract
Eugenol is contained in several plants including clove and is used as an analgesic drug. In the peripheral and central nervous systems, this compound modulates neuronal activity through action on voltage-gated ionic channels and/or transient receptor potential channels. However, it is unknown whether eugenol exerts any effects on the respiratory center neurons in the medulla. We examined the effects of eugenol on respiratory rhythm generation in the brainstem-spinal cord preparation from newborn rat (P0-P3). The preparations were superfused by artificial cerebrospinal fluid at 25-26 °C, and inspiratory C4 ventral root activity was monitored. Membrane potentials of respiratory neurons were recorded in the parafacial region of the rostral ventrolateral medulla. Bath application of eugenol (0.5-1 mM) decreased respiratory rhythm accompanied by strong inhibition of the burst activity of pre-inspiratory neurons. After washout, respiratory rhythm partly recovered, but the inspiratory burst duration was extremely shortened, and this continued for more than 60 min after washout. The shortening of C4 inspiratory burst by eugenol was not reversed by capsazepine (TRPV1 antagonist) or HC-030031 (TRPA1 antagonist), whereas the depression was partially blocked by GABA
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