Involvement of TRPC4 and 5 Channels in Persistent Firing in Hippocampal CA1 Pyramidal Cells.
Action Potentials
/ drug effects
Animals
Antibodies
/ pharmacology
Benzimidazoles
/ pharmacology
CA1 Region, Hippocampal
/ drug effects
Cholinergic Agonists
/ pharmacology
Indoles
/ pharmacology
Male
Mice
Neurons
/ drug effects
Piperidines
/ pharmacology
Pyramidal Cells
/ drug effects
TRPC Cation Channels
/ antagonists & inhibitors
TRPC antagonists
TRPC channels
cholinergic modulation
hippocampus
intrinsic persistent activity
patch clamp
working memory
Journal
Cells
ISSN: 2073-4409
Titre abrégé: Cells
Pays: Switzerland
ID NLM: 101600052
Informations de publication
Date de publication:
05 02 2020
05 02 2020
Historique:
received:
01
12
2019
revised:
29
01
2020
accepted:
01
02
2020
entrez:
9
2
2020
pubmed:
9
2
2020
medline:
13
2
2021
Statut:
epublish
Résumé
Persistent neural activity has been observed in vivo during working memory tasks, and supports short-term (up to tens of seconds) retention of information. While synaptic and intrinsic cellular mechanisms of persistent firing have been proposed, underlying cellular mechanisms are not yet fully understood. In vitro experiments have shown that individual neurons in the hippocampus and other working memory related areas support persistent firing through intrinsic cellular mechanisms that involve the transient receptor potential canonical (TRPC) channels. Recent behavioral studies demonstrating the involvement of TRPC channels on working memory make the hypothesis that TRPC driven persistent firing supports working memory a very attractive one. However, this view has been challenged by recent findings that persistent firing in vitro is unchanged in TRPC knock out (KO) mice. To assess the involvement of TRPC channels further, we tested novel and highly specific TRPC channel blockers in cholinergically induced persistent firing in mice CA1 pyramidal cells for the first time. The application of the TRPC4 blocker ML204, TRPC5 blocker clemizole hydrochloride, and TRPC4 and 5 blocker Pico145, all significantly inhibited persistent firing. In addition, intracellular application of TRPC4 and TRPC5 antibodies significantly reduced persistent firing. Taken together these results indicate that TRPC4 and 5 channels support persistent firing in CA1 pyramidal neurons. Finally, we discuss possible scenarios causing these controversial observations on the role of TRPC channels in persistent firing.
Identifiants
pubmed: 32033274
pii: cells9020365
doi: 10.3390/cells9020365
pmc: PMC7072216
pii:
doi:
Substances chimiques
Antibodies
0
Benzimidazoles
0
Cholinergic Agonists
0
Indoles
0
ML 204
0
Piperidines
0
TRPC Cation Channels
0
TRPC4 ion channel
0
Trpc5 protein, mouse
0
clemizole
T97CB3796L
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Déclaration de conflit d'intérêts
The authors declare no conflict of interest.
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