-
Tytuł:
-
Histamine depolarizes rat intracardiac ganglion neurons through the activation of TRPC non-selective cation channels.
-
Autorzy:
-
Sato A; Department of Pediatrics, Shiga University of Medical Science, Otsu, Shiga, 520-2192, Japan; Department of Physiology, School of Allied Health Sciences, Kitasato University, Sagamihara, Kanagawa, 252-0373, Japan; Division of Homeostatic Development, National Institute for Physiological Sciences, Okazaki, Aichi, 444-8585, Japan.
Arichi S; Department of Physiology, School of Allied Health Sciences, Kitasato University, Sagamihara, Kanagawa, 252-0373, Japan.
Kojima F; Department of Pharmacology, School of Allied Health Sciences, Kitasato University, Sagamihara, Kanagawa, 252-0373, Japan.
Hayashi T; Department of Anatomical Science, School of Allied Health Sciences, Kitasato University, Sagamihara, Kanagawa, 252-0373, Japan.
Ohba T; Division of Homeostatic Development, National Institute for Physiological Sciences, Okazaki, Aichi, 444-8585, Japan.
Cheung DL; Division of Homeostatic Development, National Institute for Physiological Sciences, Okazaki, Aichi, 444-8585, Japan.
Eto K; Department of Physiology, School of Allied Health Sciences, Kitasato University, Sagamihara, Kanagawa, 252-0373, Japan.
Narushima M; Division of Homeostatic Development, National Institute for Physiological Sciences, Okazaki, Aichi, 444-8585, Japan.
Murakoshi H; Supportive Center for Brain Research, National Institute for Physiological Sciences, Okazaki, Aichi, 444-8585, Japan.
Maruo Y; Department of Pediatrics, Shiga University of Medical Science, Otsu, Shiga, 520-2192, Japan.
Kadoya Y; Department of Anatomical Science, School of Allied Health Sciences, Kitasato University, Sagamihara, Kanagawa, 252-0373, Japan.
Nabekura J; Division of Homeostatic Development, National Institute for Physiological Sciences, Okazaki, Aichi, 444-8585, Japan.
Ishibashi H; Department of Physiology, School of Allied Health Sciences, Kitasato University, Sagamihara, Kanagawa, 252-0373, Japan. Electronic address: .
-
Źródło:
-
European journal of pharmacology [Eur J Pharmacol] 2020 Nov 05; Vol. 886, pp. 173536. Date of Electronic Publication: 2020 Sep 05.
-
Typ publikacji:
-
Journal Article
-
Język:
-
English
-
Imprint Name(s):
-
Publication: 2005- : Amsterdam : Elsevier Science
Original Publication: Amsterdam, North Holland Pub. Co.
-
MeSH Terms:
-
Ganglia/*cytology
Ganglia/*drug effects
Heart/*drug effects
Heart/*innervation
Histamine/*pharmacology
Ion Channels/*drug effects
Neurons/*drug effects
TRPC Cation Channels/*drug effects
Animals ; Calcium Signaling/drug effects ; Female ; Histamine Agonists/pharmacology ; Histamine H1 Antagonists/pharmacology ; Male ; Meglumine/pharmacology ; Patch-Clamp Techniques ; Potassium Channels/drug effects ; Pyridines/pharmacology ; Rats ; Rats, Wistar ; Triprolidine/pharmacology ; Type C Phospholipases/drug effects
-
Contributed Indexing:
-
Keywords: Acutely isolated neuron; Histamine H(1) receptor; M-current; Parasympathetic postganglionic cell; Perforated patch-clamp recording; TRPC channel
-
Substance Nomenclature:
-
0 (Histamine Agonists)
0 (Histamine H1 Antagonists)
0 (Ion Channels)
0 (Potassium Channels)
0 (Pyridines)
0 (TRPC Cation Channels)
2L8T9S52QM (Triprolidine)
6HG8UB2MUY (Meglumine)
820484N8I3 (Histamine)
ATW1AH7OJ5 (2-(2-aminoethyl)pyridine)
EC 3.1.4.- (Type C Phospholipases)
-
Entry Date(s):
-
Date Created: 20200908 Date Completed: 20210514 Latest Revision: 20210514
-
Update Code:
-
20240105
-
DOI:
-
10.1016/j.ejphar.2020.173536
-
PMID:
-
32896550
-
The cardiac plexus, which contains parasympathetic ganglia, plays an important role in regulating cardiac function. Histamine is known to excite intracardiac ganglion neurons, but the underlying mechanism is obscure. In the present study, therefore, the effect of histamine on rat intracardiac ganglion neurons was investigated using perforated patch-clamp recordings. Histamine depolarized acutely isolated neurons with a half-maximal effective concentration of 4.5 μM. This depolarization was markedly inhibited by the H 1 receptor antagonist triprolidine and mimicked by the H 1 receptor agonist 2-pyridylethylamine, thus implicating histamine H 1 receptors. Consistently, reverse transcription-PCR (RT-PCR) and Western blot analyses confirmed H 1 receptor expression in the intracardiac ganglia. Under voltage-clamp conditions, histamine evoked an inward current that was potentiated by extracellular Ca 2+ removal and attenuated by extracellular Na + replacement with N-methyl-D-glucamine. This implicated the involvement of non-selective cation channels, which given the link between H 1 receptors and G q/11 -protein-phospholipase C signalling, were suspected to be transient receptor potential canonical (TRPC) channels. This was confirmed by the marked inhibition of the inward current through the pharmacological disruption of either G q/11 signalling or intracellular Ca 2+ release and by the application of the TRPC blockers Pyr3, Gd 3+ and ML204. Consistently, RT-PCR analysis revealed the expression of several TRPC subtypes in the intracardiac ganglia. Whilst histamine was also separately found to inhibit the M-current, the histamine-induced depolarization was only significantly inhibited by the TRPC blockers Gd 3+ and ML204, and not by the M-current blocker XE991. These results suggest that TRPC channels serve as the predominant mediator of neuronal excitation by histamine.
(Copyright © 2020 Elsevier B.V. All rights reserved.)
