Morphological studies of neurotransmitter release and membrane recycling in sympathetic nerve terminals in culture

1983 ◽  
Vol 12 (1) ◽  
pp. 93-116 ◽  
Author(s):  
Kathleen M. Buckley ◽  
Story C. Landis
Keyword(s):  
Sympathetic Nerve ◽  
Neurotransmitter Release ◽  
Nerve Terminals ◽  
Membrane Recycling ◽  
Morphological Studies

Evidence for Presynaptic Parasympathetic Receptors on Nasal Blood Vessels

1982 ◽  
Vol 91 (2) ◽  
pp. 216-219 ◽  
Author(s):  
Richard T. Jackson
Keyword(s):  
Smooth Muscle ◽  
Blood Vessels ◽  
Muscarinic Receptor ◽  
Sympathetic Nerve ◽  
Neurotransmitter Release ◽  
Present Experiment ◽  
Presynaptic Receptors ◽  
Nerve Terminals ◽  
Norepinephrine Release ◽  
Nasal Blood Vessels

Noradrenergic synapses in the heart and several blood vessels have been shown to possess prejunctional receptors that modulate the release of norepinephrine from the synapse. The present experiment attempted to find evidence for presynaptic receptors for acetylcholine that modulated norepinephrine release. From the evidence obtained, it appears that the acetylcholine released from nasal parasympathetic fibers does not directly affect the smooth muscle of nasal blood vessels. Acetylcholine does, however, appear to inhibit the release of norepinephrine from nasal sympathetic nerve terminals. It appears that any nasal vasodilation produced by nasal parasympathetic fibers is caused by acetylcholine acting on an inhibitory, presynaptic, muscarinic receptor on the sympathetic nerve terminals. Acetylcholine would exert its control over nasal vessels by regulating the degree of sympathetic neurotransmitter release.

scholarly journals Sympathetic nerve terminals in the tunica media of human superficial temporal and middle cerebral arteries: wet histofluorescence.

Stroke ◽  
1983 ◽  
Vol 14 (1) ◽  
pp. 62-66 ◽  
Author(s):  
I Akiguchi ◽  
H Fukuyama ◽  
M Kameyama ◽  
T Koyama ◽  
H Kimura ◽  
...  
Keyword(s):  
Sympathetic Nerve ◽  
Cerebral Arteries ◽  
Nerve Terminals ◽  
Tunica Media ◽  
Middle Cerebral Arteries

Chronic exposure to neuropeptide Y determines cardiac alpha 1-adrenergic responsiveness

1991 ◽  
Vol 261 (3) ◽  
pp. H969-H973 ◽  
Author(s):  
L. S. Sun ◽  
P. C. Ursell ◽  
R. B. Robinson
Keyword(s):  
Neuropeptide Y ◽  
Sympathetic Nerve ◽  
Chronic Exposure ◽  
Developmental Change ◽  
Sympathetic Innervation ◽  
Nerve Terminals ◽  
Cardiac Sympathetic Nerve ◽  
Cardiac Sympathetic Innervation ◽  
Chronotropic Response ◽  
Npy Antagonist

The onset of sympathetic innervation induces a developmental change in the cardiac alpha 1-adrenergic chronotropic response from an increase to a decrease in rate. The mechanism by which innervation induces this alteration is unknown. Neuropeptide Y (NPY), which is found abundantly in cardiac sympathetic nerve terminals, was considered as a possible mediator for this effect. Chronic conditioning by NPY in noninnervated myocyte cultures stimulated the effect of sympathetic innervation in inducing the alpha 1-inhibitory chronotropic response. Chronic conditioning by the NPY antagonist PYX-2 blocked the effect of innervation. Thus endogenous NPY may modulate alpha 1-adrenergic responsiveness during the ontogeny of cardiac sympathetic innervation.

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