Interaction between Calcium Chelators and the Activity of P2X7 Receptors in Mouse Motor Synapses

Autor: A. E. Gaydukov, Olga P. Balezina, Anna Miteva
Jazyk: angličtina
Rok vydání: 2020
Předmět:
0301 basic medicine
Male
Motor nerve
Synaptic Transmission
P2X7 receptors
Connexins
lcsh:Chemistry
Mice
0302 clinical medicine
Nitrendipine
L-type VDCCs
lcsh:QH301-705.5
P2x7 receptor
Egtazic Acid
Spectroscopy
Chelating Agents
Mice
Knockout
Chemistry
General Medicine
Calcium Channel Blockers
Computer Science Applications
Female
medicine.symptom
EGTA-AM
BAPTA-AM
neuromuscular junction
Acetylcholine
medicine.drug
Calcium Channels
L-Type
Neuromuscular Junction
Nerve Tissue Proteins
Neurotransmission
Catalysis
Article
Inorganic Chemistry
03 medical and health sciences
medicine
Animals
Secretion
Physical and Theoretical Chemistry
Calcium chelators
Molecular Biology
Calcium Chelating Agents
Organic Chemistry
Excitatory Postsynaptic Potentials
Mice
Inbred C57BL
030104 developmental biology
lcsh:Biology (General)
lcsh:QD1-999
Disinhibition
Synapses
Biophysics
Calcium
Receptors
Purinergic P2X7
030217 neurology & neurosurgery
Zdroj: International Journal of Molecular Sciences
Volume 21
Issue 6
International Journal of Molecular Sciences, Vol 21, Iss 6, p 2034 (2020)
ISSN: 1422-0067
DOI: 10.3390/ijms21062034
Popis: The ability of P2X7 receptors to potentiate rhythmically evoked acetylcholine (ACh) release through Ca2+ entry via P2X7 receptors and via L-type voltage-dependent Ca2+ channels (VDCCs) was compared by loading Ca2+ chelators into motor nerve terminals. Neuromuscular preparations of the diaphragms of wild-type (WT) mice and pannexin-1 knockout (Panx1&minus
/&minus
) mice, in which ACh release is potentiated by the disinhibition of the L-type VDCCs upon the activation of P2X7 receptors, were used. Miniature end-plate potentials (MEPPs) and evoked end-plate potentials (EPPs) were recorded when the motor terminals were loaded with slow or fast Ca2+ chelators (EGTA-AM or BAPTA-AM, respectively, 50 &mu
M). In WT and Panx1&minus
mice, EGTA-AM did not change either spontaneous or evoked ACh release, while BAPTA-AM inhibited synaptic transmission by suppressing the quantal content of EPPs throughout the course of the short rhythmic train (50 Hz, 1 s). In the motor synapses of either WT or Panx1&minus
mice in the presence of BAPTA-AM, the activation of P2X7 receptors by BzATP (30 &mu
M) returned the EPP quantal content to the control level. In the neuromuscular junctions (NMJs) of Panx1&minus
mice, EGTA-AM completely prevented the BzATP-induced increase in EPP quantal content. After Panx1&minus
NMJs were treated with BAPTA-AM, BzATP lost its ability to enhance the EPP quantal content to above the control level. Nitrendipine (1 &mu
M), an inhibitor of L-type VDCCs, was unable to prevent this BzATP-induced enhancement of EPP quantal content to the control level. We propose that the activation of P2X7 receptors may provide additional Ca2+ entry into motor nerve terminals, which, independent of the modulation of L-type VDCC activity, can partially reduce the buffering capacity of Ca2+ chelators, thereby providing sufficient Ca2+ signals for ACh secretion at the control level. However, the activity of both Ca2+ chelators was sufficient to eliminate Ca2+ entry via L-type VDCCs activated by P2X7 receptors and increase the EPP quantal content in the NMJs of Panx1&minus
mice to above the control level.
Databáze: OpenAIRE
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