Acute Complexin Knockout Abates Spontaneous and Evoked Transmitter Release

The Ca2+ that promotes transmitter release is generally thought to enter presynaptic terminals through voltage-gated Ca2+channels. Using electrophysiology and Ca2+ imaging, we show that, in amacrine cell dendrites, at least some of the Ca2+ that triggers transmitter release comes from endoplasmic reticulum Ca2+ stores. We show that both inositol 1,4,5-trisphosphate receptors (IP3Rs) and ryanodine receptors (RyRs) are present in these dendrites and both participate in the elevation of cytoplasmic [Ca2+] during the brief depolarization of a dendrite. Only the Ca2+ released through IP3Rs, however, seems to promote the release of transmitter. Antagonists for the IP3R reduced transmitter release, whereas RyR blockers had no effect. Application of an agonist for metabotropic glutamate receptor, known to liberate Ca2+ from internal stores, enhanced both spontaneous and evoked transmitter release.

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The Neuromuscular Junction Revisited: Ca2+ Channels and Transmitter Release in Cholinergic Neurones in Xenopus Nerve and Muscle Cell Culture

Journal of Experimental Biology ◽

10.1242/jeb.153.1.129 ◽

1990 ◽

Vol 153 (1) ◽

pp. 129-140 ◽

Cited By ~ 1

Author(s):

T. P. FENG ◽

ZHENG-SHAN DAI

Keyword(s):

Neuromuscular Junction ◽

Transmitter Release ◽

Single Channel ◽

Calcium Currents ◽

Patch Clamps ◽

Whole Cell ◽

Voltage Gated ◽

Cholinergic Neurones ◽

Ca2 Channels ◽

Evoked Transmitter Release

Although the entry of calcium ions into the presynaptic nerve terminals through voltage-gated Ca2+ channels is now universally recognized as playing an essential role in evoked transmitter release at the neuromuscular junction (NMJ), and indeed in chemical synapses generally, we have as yet very little direct knowledge of the Ca2+ channels of the presynaptic terminals. In this work, making use of cocultured nerve and muscle cells from Xenopus embryos, we studied the NMJ formed between the soma of identified cholinergic neurones and myoball, which allowed the use of patch-clamps on both the pre- and postsynaptic components. Both whole-cell and single-channel recordings of Ca2+ channels in the presynaptic cell were made. We found only one type of voltage-gated Ca2+ channel with highvoltage activation and slow inactivation characteristics, allowing its classification either as the L or the N type. The channels were susceptible to block by metenkephalin but not to block by nifedipine or to enhancement by Bay K 8644. This combination of pharmacological properties favours their classification as the N type. Preliminary observations on the correlation between calcium currents and transmitter release disclosed a strikingly rapid run-down of the evoked release with unchanged calcium currents and spontaneous release during whole-cell recording, indicating a specific wash-out effect on some link between calcium entry and evoked transmitter release.

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Structural and functional changes of frog neuromuscular junctions in high calcium solutions

Proceedings of the Royal Society of London Series B Biological Sciences ◽

10.1098/rspb.1971.0072 ◽

1971 ◽

Vol 178 (1053) ◽

pp. 407-415 ◽

Cited By ~ 29

Keyword(s):

Transmitter Release ◽

Synaptic Vesicles ◽

Neuromuscular Junctions ◽

Motor Nerve ◽

Secretory Response ◽

Spontaneous Release ◽

Functional Changes ◽

High Calcium ◽

Release Of Acetylcholine ◽

Evoked Transmitter Release

When frog muscles are exposed for several hours to a solution of isotonic calcium chloride, the secretory response of the motor nerve terminals to imposed depolarization ultimately fails and the rate of spontaneous release of acetylcholine also declines towards zero. The failure of depolarization-evoked transmitter release is irreversible while spontaneous release reappears, though in highly abnormal fashion, when the muscle is returned to a normal ionic medium. Examination of motor end-plates, during various stages of calcium treatment, shows that there is gradual intra-axonal agglutination of synaptic vesicles which is only very incompletely reversible. This effect is presumably the consequence of gradual entry and intracellular accumulation of calcium ions. Analogous treatment with isotonic magnesium, while resulting in immediate loss of evoked transmitter release, does not lead to progressive agglutination of synaptic vesicles, nor to irreversible impairment of the secretory response of the nerve terminal. The possible relations between structural and functional changes during calcium and magnesium treatment are discussed.

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