Abnormal transmitter release at neuromuscular junctions of mice carrying the tottering alpha1A Ca2+ channel mutation
Neurotransmitter release at many synapses is regulated synaptic potentials. We found a Ca 2⍣ -, Mg 2⍣ -and K ⍣dependent increase of spontaneous ACh release at both by P/Q-type Ca 2⍣ channels containing the α 1A poreforming subunit. Mutations in α 1A cause cerebral homo-and heterozygote tg NMJs. Furthermore, there was increased run-down of high-rate evoked release at disorders including familial hemiplegic migraine (FHM) and ataxia in humans. Tottering (tg) α 1A mutant mice homozygous tg NMJs.
... mozygous tg NMJs. In isotonic contraction experiments this led to block of synaptic transmission at lower display ataxia and epilepsy. It is not known whether α 1A mutations induce impairment of synaptic function, which concentrations of the ACh antagonist tubocurarine than were needed in wild-type muscles. Our results suggest could underlie the symptoms of these cerebral disorders. To assess whether α 1A mutations influence neuro-that in tg motor nerve terminals there is increased influx of Ca 2⍣ under resting conditions. This study shows that transmitter release, we studied P-type Ca 2⍣ channelmediated acetylcholine (ACh) release at tg neuromuscular functional consequences of α 1A mutations causing cerebral disorders can be characterized at the NMJ. junctions (NMJs) with micro-electrode measurements of Abbreviations: ACh ϭ acetylcholine; EPP ϭ endplate potential; FHM ϭ familial hemiplegic migraine; MEPP ϭ miniature endplate potential; NMJ ϭ neuromuscular junction; PCR ϭ polymerase chain reaction; tg ϭ tottering