SYNTHESIS AND STORAGE OF ACETYLCHOLINE IN NERVOUS TISSUE

1963 ◽  
Vol 41 (1) ◽  
pp. 2555-2571 ◽  
Author(s):  
F. C. MacIntosh
Keyword(s):  
Nervous Tissue ◽  
Nerve Endings ◽  
And Storage

A discussion of the factors involved in the physiological synthesis of acetylcholine in nerve endings, and of the action thereon of hemicholinium No. 3.

SYNTHESIS AND STORAGE OF ACETYLCHOLINE IN NERVOUS TISSUE

1963 ◽  
Vol 41 (12) ◽  
pp. 2555-2571 ◽  
Author(s):  
F. C. MacIntosh
Keyword(s):  
Nervous Tissue ◽  
Nerve Endings ◽  
And Storage

A discussion of the factors involved in the physiological synthesis of acetylcholine in nerve endings, and of the action thereon of hemicholinium No. 3.

Implications of uptake and storage of norepinephrine by sympathetic nerve endings

Life Sciences ◽  
1963 ◽  
Vol 2 (12) ◽  
pp. 953-958 ◽  
Author(s):  
R.P. Maickel ◽  
M.A. Beaven ◽  
B.B. Brodie
Keyword(s):  
Sympathetic Nerve ◽  
Nerve Endings ◽  
And Storage

EFFECTS OF QUATERNARY BASES AND INORGANIC CATIONS ON ACETYLCHOLINE SYNTHESIS IN NERVOUS TISSUE

1967 ◽  
Vol 45 (2) ◽  
pp. 249-268 ◽  
Author(s):  
S. P. Bhatnagar ◽  
F. C. MacIntosh
Keyword(s):  
Nervous Tissue ◽  
Inhibitory Effect ◽  
Sympathetic Ganglia ◽  
Direct Inhibition ◽  
Inorganic Cations ◽  
Tetrabutyl Ammonium ◽  
Cervical Ganglion ◽  
Choline Acetylase ◽  
High Concentrations ◽  
And Storage

A number of quaternary bases were tested for their ability to inhibit the synthesis of acetylcholine (ACh) by incubated minced mouse brain. Tetramethyl-, tetraethyl-, tetrapropyl-, and tetrabutyl-ammonium were moderately active as inhibitors, the strongest being the tetraethyl base (TEA), which was 1–2% as active as the hemicholinium HC-3. Weaker activity was exhibited by hexamethonium, d-tubocurarine, and tolazoline; NH4Cl and N-methylnicotinamide were inactive at concentrations up to 10−2 M. Except in high concentrations, none of the bases significantly affected the release of ACh from the tissue into the eserinized medium. The addition of choline to the medium somewhat increased the rate of ACh formation when the bases were absent and strikingly antagonized the inhibitory action of HC-3 and TEA. TEA also resembled HC-3 in that (i) it reduced the ACh content of the preganglionically excited superior cervical ganglion of the cat, though neither stimulation alone nor the drug alone has such an effect; (ii) it killed mice by paralyzing respiration, and this effect was antagonized by choline; (iii) its inhibitory effect on ACh synthesis by intact nervous tissue was not due to direct inhibition of choline acetylase. The finding of Birks and Quastel that extracellular Na+is essential for the synthesis and storage of ACh by perfused sympathetic ganglia was confirmed for incubated brain tissue. Neither the action of HC-3 and TEA in inhibiting ACh synthesis, nor that of Na+in promoting it, has as yet been clarified.

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