THE RELATIONSHIP BETWEEN NERVE TERMINAL ADENOSINE TRIPHOSPHATASES AND NEUROTRANSMITTER RELEASE: AS DETERMINED BY THE USE OF ANTIDEPRESSANT AND OTHER CNS-ACTIVE DRUGS

This study investigated the relationship between energy failure and neurotransmitter release in the frog (Rana pipiens) brain during 1-3 h of anoxia. Unlike truly anoxia-tolerant species, the frog does not defend its brain energy charge. When exposed to anoxia at 25 degrees C, there is an immediate fall in brain ATP levels, which reach approximately 20% of normoxic levels in approximately 60 min. The frog, nevertheless, survives another 1-2 h of anoxia. At 100 min of anoxia, there is an increase in extracellular adenosine concentration, probably originating from the increased intracellular adenosine concentration caused by the breakdown of intracellular ATP. Increases in the levels of extracellular glutamate and GABA do not occur until 1-2 h after ATP depletion. This response is quite unlike that recorded for other vertebrates, anoxia-tolerant or anoxia-intolerant, where energy failure quickly results in an uncontrolled and neurotoxic release of excitatory neurotransmitters. In the frog, the delay in excitotoxic neurotransmitter release may be one of the factors that allow a period of survival after energy failure. Clearly, energy failure by itself is not a fatal event in the frog brain.

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Nerve terminal ATPase as possible trigger for neurotransmitter release

Nature ◽

10.1038/255237a0 ◽

1975 ◽

Vol 255 (5505) ◽

pp. 237-238 ◽

Cited By ~ 75

Author(s):

JOHN C. GILBERT ◽

MICHAEL G. WYLLIE ◽

DIANA V. DAVISON

Keyword(s):

Nerve Terminal ◽

Neurotransmitter Release

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Botulinum Neurotoxin a Blocks Synaptic Vesicle Exocytosis but Not Endocytosis at the Nerve Terminal

The Journal of Cell Biology ◽

10.1083/jcb.147.6.1249 ◽

1999 ◽

Vol 147 (6) ◽

pp. 1249-1260 ◽

Cited By ~ 59

Author(s):

Elaine A. Neale ◽

Linda M. Bowers ◽

Min Jia ◽

Karen E. Bateman ◽

Lura C. Williamson

Keyword(s):

Synaptic Vesicle ◽

Nerve Terminal ◽

Neurotransmitter Release ◽

Synaptic Vesicles ◽

Botulinum Neurotoxin ◽

Vesicle Membrane ◽

Botulinum Neurotoxin A ◽

Synaptic Vesicle Exocytosis ◽

Vesicle Exocytosis ◽

Botulinum Neurotoxins

The supply of synaptic vesicles in the nerve terminal is maintained by a temporally linked balance of exo- and endocytosis. Tetanus and botulinum neurotoxins block neurotransmitter release by the enzymatic cleavage of proteins identified as critical for synaptic vesicle exocytosis. We show here that botulinum neurotoxin A is unique in that the toxin-induced block in exocytosis does not arrest vesicle membrane endocytosis. In the murine spinal cord, cell cultures exposed to botulinum neurotoxin A, neither K+-evoked neurotransmitter release nor synaptic currents can be detected, twice the ordinary number of synaptic vesicles are docked at the synaptic active zone, and its protein substrate is cleaved, which is similar to observations with tetanus and other botulinal neurotoxins. In marked contrast, K+ depolarization, in the presence of Ca2+, triggers the endocytosis of the vesicle membrane in botulinum neurotoxin A–blocked cultures as evidenced by FM1-43 staining of synaptic terminals and uptake of HRP into synaptic vesicles. These experiments are the first demonstration that botulinum neurotoxin A uncouples vesicle exo- from endocytosis, and provide evidence that Ca2+ is required for synaptic vesicle membrane retrieval.

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On the relationship of neuropeptide Y Y1 receptor-immunoreactive neuronal structures to the neuropeptide Y-immunoreactive nerve terminal networks. A double immunolabelling analysis in the rat brain

Neuroscience ◽

10.1016/s0306-4522(98)00089-x ◽

1998 ◽

Vol 86 (3) ◽

pp. 827-845 ◽

Cited By ~ 24

Author(s):

L Caberlotto ◽

B Tinner ◽

B Bunnemann ◽

L Agnati ◽

K Fuxe

Keyword(s):

Neuropeptide Y ◽

Rat Brain ◽

Nerve Terminal ◽

Y1 Receptor ◽

Relationship Of ◽

The Relationship ◽

Double Immunolabelling

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The relationship of pudendal nerve terminal motor latency to squeeze pressure in patients with idiopathic fecal incontinence

Diseases of the Colon & Rectum ◽

10.1007/bf02234563 ◽

2001 ◽

Vol 44 (5) ◽

pp. 666-671 ◽

Cited By ~ 36

Author(s):

B.Ó C. Súilleabháin ◽

A. F. Horgan ◽

L. McEnroe ◽

F. W. Poon ◽

J. H. Anderson ◽

...

Keyword(s):

Fecal Incontinence ◽

Nerve Terminal ◽

Pudendal Nerve ◽

Squeeze Pressure ◽

Motor Latency ◽

Idiopathic Fecal Incontinence ◽

Relationship Of ◽

The Relationship

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Calcium, Calmodulin, and Synaptic Function: Modulation of Neurotransmitter Release, Nerve Terminal Protein Phosphorylation, and Synaptic Vesicle Morphology by Calcium and Calmodulin

Regulatory Mechanisms of Synaptic Transmission ◽

10.1007/978-1-4684-3968-7_11 ◽

1981 ◽

pp. 205-239 ◽

Cited By ~ 7

Author(s):

Robert J. DeLorenzo

Keyword(s):

Protein Phosphorylation ◽

Synaptic Vesicle ◽

Nerve Terminal ◽

Neurotransmitter Release ◽

Synaptic Function ◽

Terminal Protein

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Presynaptic Proteins as Markers of the Neurotoxic Activity of BmjeTX-I and BmjeTX-II Toxins fromBothrops marajoensis(Marajó Lancehead) Snake Venom

Biochemistry Research International ◽

10.1155/2016/2053459 ◽

2016 ◽

Vol 2016 ◽

pp. 1-10

Author(s):

Antonio Lisboa ◽

Rodolfo Melaré ◽

Junia R. B. Franco ◽

Carolina V. Bis ◽

Marta Gracia ◽

...

Keyword(s):

Nerve Terminal ◽

Neurotransmitter Release ◽

Acetylcholine Receptors ◽

Motor Nerve ◽

Synaptic Proteins ◽

Muscle Fibres ◽

Motor Nerve Terminal ◽

Transmission Electron ◽

Skeletal Muscle Fibres

Neuromuscular preparations exposed toB. marajoensisvenom show increases in the frequency of miniature end-plate potentials and twitch tension facilitation followed by presynaptic neuromuscular paralysis, without evidences of muscle damage. Considering that presynaptic toxins interfere into the machinery involved in neurotransmitter release (synaptophysin, synaptobrevin, and SNAP25 proteins), the main objective of this communication is to analyze, by immunofluorescence and western blotting, the expression of the synaptic proteins, synaptophysin, synaptobrevin, and SNAP25 and by myography, light, and transmission electron microscopy the pathology of motor nerve terminals and skeletal muscle fibres of chick biventer cervicis preparations (CBC) exposedin vitroto BmjeTX-I and BmjeTX-II toxins fromB. marajoensisvenom. CBC incubated with toxins showed irreversible twitch tension blockade and unaffected KCl- and ACh-evoked contractures, and the positive colabelling of acetylcholine receptors confirmed that their action was primarily at the motor nerve terminal. Hypercontraction and loose myofilaments and synaptic vesicle depletion and motor nerve damage indicated that the toxins displayed both myotoxic and neurotoxic effect. The blockade resulted from interference on synaptophysin, synaptobrevin, and SNAP25 proteins leading to the conclusion that BmjeTX-I and BmjeTX-II affected neurotransmitter release machinery by preventing the docking of synaptic vesicles to the axolemma of the nerve terminal.

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Presynaptic roles of intracellular Ca2+ stores in signalling and exocytosis

Biochemical Society Transactions ◽

10.1042/bst0380529 ◽

2010 ◽

Vol 38 (2) ◽

pp. 529-535 ◽

Cited By ~ 16

Author(s):

Sohaib Nizami ◽

Vivian W.Y. Lee ◽

Jennifer Davies ◽

Philip Long ◽

Jasmina N. Jovanovic ◽

...

Keyword(s):

Protein Kinases ◽

G Protein ◽

Nerve Terminal ◽

Neurotransmitter Release ◽

Glutamate Release ◽

Neuronal Cells ◽

Receptor Activation ◽

Pivotal Role ◽

Presynaptic Function ◽

G Protein Coupled

The signalling roles of Ca2+ic (intracellular Ca2+) stores are well established in non-neuronal and neuronal cells. In neurons, although Ca2+ic stores have been assigned a pivotal role in postsynaptic responses to Gq-coupled receptors, or secondarily to extracellular Ca2+ influx, the functions of dynamic Ca2+ic stores in presynaptic terminals remain to be fully elucidated. In the present paper, we review some of the recent evidence supporting an involvement of Ca2+ic in presynaptic function, and discuss loci at which this source of Ca2+ may impinge. Nerve terminal preparations provide good models for functionally examining putative Ca2+ic stores under physiological and pathophysiological stimulation paradigms, using Ca2+-dependent activation of resident protein kinases as sensors for fine changes in intracellular Ca2+ levels. We conclude that intraterminal Ca2+ic stores may, directly or indirectly, enhance neurotransmitter release following nerve terminal depolarization and/or G-protein-coupled receptor activation. During conditions that prevail following neuronal ischaemia, increased glutamate release instigated by Ca2+ic store activation may thereby contribute to excitotoxicity and eventual synaptopathy.

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