scholarly journals THE ORGANIZATION AND INNERVATION OF THE LUMINESCENT ORGAN IN A FIREFLY, PHOTURIS PENNSYLVANICA (COLEOPTERA)

1963 ◽  
Vol 16 (2) ◽  
pp. 323-359 ◽  
Author(s):  
David S. Smith
Keyword(s):  
Electron Microscope ◽  
Synaptic Vesicles ◽  
Light Emission ◽  
Nerve Endings ◽  
Tracheal Epithelium ◽  
Nerve Terminals ◽  
Tracheal System ◽  
Physiological Evidence ◽  
Effector System

The organization of the luminescent organ of an adult firefly has been studied with the electron microscope, and particular attention has been given to the disposition of nerve terminals within the organ. The cytological structure of the cells of the tracheal system, the peripheral and terminal axons, the photocytes and the cells of the dorsal ("reflecting") layer is described. Previous observations on the peripheral course of nerve branches alongside the tracheal trunks at the level of the dorsal layer and photocyte epithelium have been confirmed, and specialised nerve endings containing axoplasmic components structurally identical with "synaptic vesicles" and "neurosecretory droplets" have been identified, not in association with the surface of the photocytes, but lying between the apposed surfaces of two components of the tracheal epithelium: the tracheal end-cell and the tracheolar cell. These cytological findings are discussed in terms of available biochemical and physiological evidence concerning the mechanism of light emission in the firefly, especially with respect to the possible role of chemical "transmitter" action in triggering a response in a luminescent effector system.

scholarly journals Submicroscopic Changes of the Nerve Endings in the Adrenal Medulla after Stimulation of the Splanchnic Nerve

1957 ◽  
Vol 3 (4) ◽  
pp. 611-614 ◽  
Author(s):  
Eduardo De Robertis ◽  
Alberto Vaz Ferreira
Keyword(s):  
Electrical Stimulation ◽  
Electron Microscope ◽  
Adrenal Medulla ◽  
Synaptic Vesicles ◽  
Splanchnic Nerve ◽  
The Other ◽  
Nerve Endings ◽  
The Mean ◽  
Increased Activity ◽  
Stimulation Of

The nerve endings of the adrenal medulla of the rabbit were studied under the electron microscope in the normal condition and after prolonged electrical stimulation of the splanchnic nerve. With a stimulus of 100 pulses per second for 10 minutes, there is an increase in the number of synaptic vesicles in the nerve ending. The mean number is of 82.6 vesicles per square micron in the normal and of 132.7 per square micron in the stimulated glands. With a stimulus of 400 pulses per second for 10 minutes, there is a considerable depletion of synaptic vesicles and other changes occur in the nerve endings. The mean number of vesicles is of 29.2 per square micron. These results are interpreted as indicative of an increased activity of the ending in one case, and as a diminished activity and fatigue of the synaptic junction in the other.

scholarly journals Motoneuron Wnts regulate neuromuscular junction development

eLife ◽  
2018 ◽  
Vol 7 ◽  
Author(s):  
Chengyong Shen ◽  
Lei Li ◽  
Kai Zhao ◽  
Lei Bai ◽  
Ailian Wang ◽  
...  
Keyword(s):  
Neuromuscular Junction ◽  
Synaptic Vesicles ◽  
Skeletal Muscles ◽  
Motor Behavior ◽  
Nerve Terminals ◽  
Presynaptic Differentiation ◽  
Gene Mutant ◽  
Postsynaptic Differentiation ◽  
Presynaptic Assembly

The neuromuscular junction (NMJ) is a synapse between motoneurons and skeletal muscles to control motor behavior. Unlike extensively investigated postsynaptic differentiation, less is known about mechanisms of presynaptic assembly. Genetic evidence of Wnt in mammalian NMJ development was missing due to the existence of multiple Wnts and their receptors. We show when Wnt secretion is abolished from motoneurons by mutating the Wnt ligand secretion mediator (Wls) gene, mutant mice showed muscle weakness and neurotransmission impairment. NMJs were unstable with reduced synaptic junctional folds and fragmented AChR clusters. Nerve terminals were swollen; synaptic vesicles were fewer and mislocated. The presynaptic deficits occurred earlier than postsynaptic deficits. Intriguingly, these phenotypes were not observed when deleting Wls in muscles or Schwann cells. We identified Wnt7A and Wnt7B as major Wnts for nerve terminal development in rescue experiments. These observations demonstrate a necessary role of motoneuron Wnts in NMJ development, in particular presynaptic differentiation.

The Role of Cholesterol in the Exo- and Endocytosis of Synaptic Vesicles in Frog Motor Nerve Endings

2010 ◽  
Vol 40 (8) ◽  
pp. 894-901 ◽  
Author(s):  
A. M. Petrov ◽  
M. R. Kasimov ◽  
A. R. Giniatullin ◽  
O. I. Tarakanova ◽  
A. L. Zefirov
Keyword(s):  
Synaptic Vesicles ◽  
Motor Nerve ◽  
Nerve Endings

Role of Mitochondrial Dysfunction in the Ca2+-Induced Decline of Transmitter Release at K+-Depolarized Motor Neuron Terminals

1999 ◽  
Vol 81 (2) ◽  
pp. 498-506 ◽  
Author(s):  
Michelle A. Calupca ◽  
Gregory M. Hendricks ◽  
Jean C. Hardwick ◽  
Rodney L. Parsons
Keyword(s):  
Motor Neuron ◽  
Mitochondrial Dysfunction ◽  
Transmitter Release ◽  
Synaptic Vesicles ◽  
Prolonged Exposure ◽  
Nerve Terminals ◽  
Atp Production ◽  
Neuron Terminals ◽  
Nerve Muscle

Role of mitochondrial dysfunction in the Ca2+-induced decline of transmitter release at K+-depolarized motor neuron terminals. The present study tested whether a Ca2+-induced disruption of mitochondrial function was responsible for the decline in miniature endplate current (MEPC) frequency that occurs with nerve-muscle preparations maintained in a 35 mM potassium propionate (35 mM KP) solution containing elevated calcium. When the 35 mM KP contained control Ca2+(1 mM), the MEPC frequency increased and remained elevated for many hours, and the mitochondria within twitch motor neuron terminals were similar in appearance to those in unstimulated terminals. All nerve terminals accumulated FM1–43 when the dye was present for the final 6 min of a 300-min exposure to 35 mM KP with control Ca2+. In contrast, when Ca2+ was increased to 3.6 mM in the 35 mM KP solution, the MEPC frequency initially reached frequencies >350 s− 1 but then gradually fell approaching frequencies <50 s−1. A progressive swelling and eventual distortion of mitochondria within the twitch motor neuron terminals occurred during prolonged exposure to 35 mM KP with elevated Ca2+. After ∼300 min in 35 mM KP with elevated Ca2+, only 58% of the twitch terminals accumulated FM1–43. The decline in MEPC frequency in 35 mM KP with elevated Ca2+ was less when 15 mM glucose was present or when preparations were pretreated with 10 μM oligomycin and then bathed in the 35 mM KP with glucose. When glucose was present, with or without oligomycin pretreatment, a greater percentage of twitch terminals accumulated FM1–43. However, the mitochondria in these preparations were still greatly swollen and distorted. We propose that prolonged depolarization of twitch motor neuron terminals by 35 mM KP with elevated Ca2+ produced a Ca2+-induced decrease in mitochondrial ATP production. Under these conditions, the cytosolic ATP/ADP ratio was decreased thereby compromising both transmitter release and refilling of recycled synaptic vesicles. The addition of glucose stimulated glycolysis which contributed to the maintenance of required ATP levels.

The role of extracellular calcium in exo- and endocytosis of synaptic vesicles at the frog motor nerve terminals

Neuroscience ◽  
2006 ◽  
Vol 143 (4) ◽  
pp. 905-910 ◽  
Author(s):  
A.L. Zefirov ◽  
M.M. Abdrakhmanov ◽  
M.A. Mukhamedyarov ◽  
P.N. Grigoryev
Keyword(s):  
Synaptic Vesicles ◽  
Motor Nerve ◽  
Extracellular Calcium ◽  
Nerve Terminals ◽  
Motor Nerve Terminals

scholarly journals The Role of GSK3 in Presynaptic Function

2011 ◽  
Vol 2011 ◽  
pp. 1-8 ◽  
Author(s):  
Karen Janet Smillie ◽  
Michael Alan Cousin
Keyword(s):  
Synaptic Vesicles ◽  
Glycogen Synthase ◽  
Glycogen Synthase Kinase 3 ◽  
Nerve Terminals ◽  
The Past ◽  
Presynaptic Function ◽  
Signalling Cascades ◽  
Synaptic Failure ◽  
Activity Dependent

The past ten years of research have identified a number of key roles for glycogen synthase kinase 3 (GSK3) at the synapse. In terms of presynaptic physiology, critical roles for GSK3 have been revealed in the growth and maturation of the nerve terminal and more recently a key role in the control of activity-dependent bulk endocytosis of synaptic vesicles. This paper will summarise the major roles assigned to GSK3 in both immature and mature nerve terminals, the substrates GSK3 phosphorylates to exert its action, and how GSK3 activity is regulated by different presynaptic signalling cascades. The number of essential roles for GSK3, coupled with the numerous signalling cascades all converging to regulate its activity, suggests that GSK3 is a key integrator of multiple inputs to modulate the strength of neurotransmission. Modulation of these pathways may point to potential mechanisms to overcome synaptic failure in neurodegenerative disorders such as Alzheimer's disease.

scholarly journals The role of V-ATPase in neuronal and endocrine systems.

1992 ◽  
Vol 172 (1) ◽  
pp. 171-178 ◽  
Author(s):  
Y Moriyama ◽  
M Maeda ◽  
M Futai
Keyword(s):  
Synaptic Vesicles ◽  
Recent Progress ◽  
Energy Coupling ◽  
Transport Systems ◽  
Nerve Terminals ◽  
Electrochemical Gradient ◽  
Neural Transmission ◽  
Structural Aspects ◽  
Endocrine Tissues

Synaptic vesicles have important roles in the neural transmission at nerve terminals: the storage and the controlled exocytosis of neurotransmitters. At least two different factors are responsible for the concentration process: the vacuolar-type H(+)-ATPase (V-ATPase), establishing an electrochemical gradient of protons, and specific transport systems for transmitters. We will discuss our recent progress on the energy-transducing systems in synaptic vesicles: (1) structural aspects of V-ATPase; (2) energy coupling of transport of transmitters; (3) reconstitution of transporters; (4) effects of neurotoxins and neuron blocking agents; (5) function of synaptic-vesicle-like microvesicles from endocrine tissues.

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