Coordinated release of ATP and ACh from cholinergic synaptosomes and its inhibition by calmodulin antagonists

Schweitzer, Erik S.

doi:10.1523/jneurosci.07-09-02948.1987

Cited by 67 publications

(37 citation statements)

References 35 publications

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“…muscular junction (15) or from Torpedo electric organ nerve terminals (24,25). The corelease of ACh and ATP has been measured directly in mouse neuromuscular junction after a single stimulus of the presynaptic nerve trunk (15), reinforcing the view of coincident release of ACh and ATP from single synaptic vesicles.…”

Section: (F and H) Western Blot Detection Of Sv2 Content In Immunoprementioning

confidence: 83%

Control of neurotransmitter release by an internal gel matrix in synaptic vesicles

Reigada

Díez‐Pérez

Gorostiza

et al. 2003

Proc. Natl. Acad. Sci. U.S.A.

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Neurotransmitters are stored in synaptic vesicles, where they have been assumed to be in free solution. Here we report that in Torpedo synaptic vesicles, only 5% of the total acetylcholine (ACh) or ATP content is free, and that the rest is adsorbed to an intravesicular proteoglycan matrix. This matrix, which controls ACh and ATP release by an ion-exchange mechanism, behaves like a smart gel. That is, it releases neurotransmitter and changes its volume when challenged with small ionic concentration change. Immunodetection analysis revealed that the synaptic vesicle proteoglycan SV2 is the core of the intravesicular matrix and is responsible for immobilization and release of ACh and ATP. We suggest that in the early steps of vesicle fusion, this internal matrix regulates the availability of free diffusible ACh and ATP, and thus serves to modulate the quantity of transmitter released.

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Section: (F and H) Western Blot Detection Of Sv2 Content In Immunoprementioning

confidence: 83%

Control of neurotransmitter release by an internal gel matrix in synaptic vesicles

Reigada

Díez‐Pérez

Gorostiza

et al. 2003

Proc. Natl. Acad. Sci. U.S.A.

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“…These results provide further evidence for coordinated ACh and adenine nucleotide release (cf. Silinsky, 1975;Schweitzer, 1987), independent of adenosine release.…”

Section: Adenosinementioning

confidence: 94%

Sources of adenosine released during neuromuscular transmission in the rat.

Smith

1991

The Journal of Physiology

106

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SUMMARY1. The levels of adenine nucleotides and adenosine which accumulate in the neuromuscular junction during nerve stimulation of the rat extensor digitorum longus (EDL) muscle were assayed biochemically. The sources were also determined by the use of different inhibitors.2. ATP and total adenine nucleotide release increased as stimulation frequency increased, consistent with previous evidence indicating ATP release from presynaptic sources.3. Adenosine levels also increased during nerve stimulation. However, accumulation decreased by 46-58 % when muscle activation was blocked by the addition of d-tubocurarine (dTC). Adenosine levels also decreased by 40-59% when adenine nucleotide hydrolysis to adenosine was blocked by the addition of 1 mM-X,fmethyladenosine 5'-diphosphate. Thus, approximately half of the extracellular adenosine is released from activated muscle while the other half is derived from adenine nucleotide hydrolysis.4. Similar quantities of adenine nucleotide and acetylcholine (ACh) accumulated during nerve stimulation. With adenine nucleotide and ACh hydrolysis blocked by a,,-methyladenosine 5'-diphosphate and eserine, respectively, the calculated amounts of adenine nucleotide and ACh released were 1-2 x 10-18 and 1 5 x 101 mol (stimulus impulse)-' endplate-1.5. AH5183 (vesamicol), which blocks ACh release, reduced extracellular ACh and adenine nucleotide accumulation by 40 and 45%, respectively. It did not affedt adenosine release from the activated muscle.6. Theophylline (100,M), which blocks adenosine receptors, caused ATP accumulation to increase by 38 %; extracellular levels of adenosine derived from adenine nucleotide hydrolysis also increased by 17 %. These results are consistent with the presence of adenosine-mediated inhibition of adenine nucleotide release.7. It is concluded that adenine nucleotides (presumably in the form of ATP) and ACh are released jointly, and that ATP is hydrolysed fairly rapidly to adenosine. Adenosine resulting from ATP hydrolysis accounts for about half of the extracellular adenosine accumulating during nerve stimulation, while the other half is released directly by the underlying muscle.

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“…Finally, chemical substances released by the conditioning stimulus might directly interfere with transmitter release by the test stimulus. Two substances known to be released by vertebrate motor nerve terminals are ACh and ATP (Schweitzer, 1987). Adenosine, a metabolite of ATP, has been shown to inhibit transmitter release (Silinsky, 1984;Silinsky, Ginsborg & Hirsh, 1987).…”

Section: Presynaptic Inhibition Of Transmitter Releasementioning

confidence: 99%

Inhibitory interactions between motoneurone terminals in neonatal rat lumbrical muscle.

Betz

Chua

Ridge

1989

The Journal of Physiology

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SUMMARY1. Evoked synaptic potentials and currents were recorded in neonatal rat fourth deep lumbrical muscle during the period of polyneuronal innervation. Signs of inhibitory interactions between converging mononeurone terminals were detected.2. Muscle fibres innervated bv axons from the lateral plantar nerve (LPN) and from the sural nerve (SN) were studied. In unblocked preparations the muscle contracted, and electrode tips were mounted on flexible wires to prevent loss of impalements.3. In voltage recordings from unblocked preparations, paired two-shock stimulation of one nerve revealed synaptic depression: the second response was smaller than the first. XVhen the two stimuli were delivered to different nerves (SN and LPN), the second response was smaller than its own control. 4 5. The inhibition was not constant during the tail of the test end-plate current (EPC). Instead, it declined during the EPC tail, suggesting that the mechanism of inhibition was active, though diminishing, throughout the time course of the test EPC.6. The amount of inhibition was not noticeably affected by altering the muscle membrane potential (two cells studied).7. Treatment with curare or a-bungarotoxin to block most ACh receptors reduced the inhibition. In about half of the fibres studied, no inhibition was evident: in the others, up to 50% inhibition was observed. The average inhibition for all receptorblocked fibres was about 15 %.8. In six a-bungarotoxin-treated cells. multiple conditioning stimuli were t To whom all correspondence should be addressedl.II1Is5 7i

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Coordinated release of ATP and ACh from cholinergic synaptosomes and its inhibition by calmodulin antagonists

Cited by 67 publications

References 35 publications

Control of neurotransmitter release by an internal gel matrix in synaptic vesicles

Control of neurotransmitter release by an internal gel matrix in synaptic vesicles

Sources of adenosine released during neuromuscular transmission in the rat.

Inhibitory interactions between motoneurone terminals in neonatal rat lumbrical muscle.

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