Calcium channels coupled to neurotransmitter release at neonatal rat neuromuscular junctions

1. The effects of different calcium channel blockers ω-agatoxin IVA (ω-Aga IVA), ω-conotoxin GVIA (ω-CgTx GVIA) and dihydropyridines) were tested on spontaneous and evoked transmitter release at embryonic and newborn rat neuromuscular junctions (NMJs). 2. The nerve-evoked transmitter release quantal...

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Guardado en:
Detalles Bibliográficos
Publicado: 1999
Materias:
calcium channel
calcium ion
dihydropyridine
neurotransmitter
nifedipine
nitrendipine
omega agatoxin IVA
omega conotoxin GVIA
potassium ion
unclassified drug
voltage dependent calcium channel
animal cell
article
calcium transport
controlled study
embryo
embryo development
miniature endplate potential
muscle reinnervation
neuromuscular synapse
neurotransmitter release
newborn
nonhuman
perinatal development
priority journal
rat
animal tissue
Article
nerve potential
postnatal development
protein function
stimulus response
synaptic transmission
Animals
Animals, Newborn
Calcium Channel Blockers
Calcium Channels
Calcium Channels, L-Type
Calcium Channels, N-Type
Diaphragm
Embryo
Evoked Potentials
Motor Endplate
Muscle, Skeletal
Neuromuscular Junction
Neurotransmitter Agents
Nifedipine
Nitrendipine
omega-Agatoxin IVA
omega-Conotoxin GVIA
Peptides
Phrenic Nerve
Rats
Rats, Wistar
Spider Venoms
Synaptic Transmission
Acceso en línea:https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_00223751_v514_n2_p533_RosatoSiri
http://hdl.handle.net/20.500.12110/paper_00223751_v514_n2_p533_RosatoSiri
Aporte de:
Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA) de Universidad de Buenos Aires
Descripción
Sumario:1. The effects of different calcium channel blockers ω-agatoxin IVA (ω-Aga IVA), ω-conotoxin GVIA (ω-CgTx GVIA) and dihydropyridines) were tested on spontaneous and evoked transmitter release at embryonic and newborn rat neuromuscular junctions (NMJs). 2. The nerve-evoked transmitter release quantal content (m) was strongly reduced by the P/Q-type voltage-dependent calcium channel (VDCC) blocker ω-Aga IVA (100 nM) at newly formed endplates of embryos and 0- to 11-day-old rats, in agreement with the effect of this blocker on transmitter release at mature and reinnervating muscles. 3. ω-CgTx GVIA (1-5 μM), the N-type VDCC blocker, also caused a significant reduction in m at newly formed NMJs early in development (embryos and 0- to 4-day-old rats), while it was ineffective in more mature animals (5- to 11-day-old rats). 4. L-type channel blockers, nitrendipine (1 μM) and nifedipine (1 μM), did not significantly affect neurally evoked release at developing NMJs. However, nifedipine (10 μM) was able to increase m significantly at 0- to 4-day-old rat NMJs. 5. At developing NMJs, K+-evoked transmitter release was dependent on Ca2+ entry through VDCCs of the P/Q-type family (100 nM ω-Aga IVA reduced 70% of the K+-evoked miniature endplate potential frequency). N- and L-type VDCC blockers did not affect this type of release. 6. We conclude that at rat neuromuscular junctions the presynaptic calcium channel types involved in transmitter release undergo developmental changes during the early postnatal period.

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