scholarly journals Studies on the Distribution of Factor I and Acetylcholine in Crustacean Peripheral Nerve

1960 ◽  
Vol 43 (3) ◽  
pp. 509-522 ◽  
Author(s):  
Ernst Florey ◽  
M. A. Biederman
Keyword(s):  
Stretch Receptor ◽  
Aminobutyric Acid ◽  
Nerve Tissue ◽  
Inhibitory Neurons ◽  
Gamma Aminobutyric Acid ◽  
Cancer Magister ◽  
Factor I ◽  
Wet Weight ◽  
Exclusive Property ◽  
Sensory Fibers

Extracts of whole nerve (chelipeds of Cancer magister) cause inhibition of impulse generation of the crayfish stretch receptor preparation, similar to that produced by gamma-aminobutyric acid (GABA). This is not found with extracts containing only sensory or sensory and motor fibers. Extracts of inhibitory fibers inhibit the stretch receptor discharge—indicating an inhibitory action equivalent to that of up to 30,000 micrograms of GABA per gm. wet weight of inhibitor fiber. This high value is taken as an indication that the inhibitory substance in crab inhibitory fibers is not identical with gamma-aminobutyric acid. Whole nerves were found to contain 1.7 to 6.7 µg. acetylcholine per gm. nerve tissue (clam ventricle and frog rectus abdominis muscle). No acetylcholine could be detected in extracts of motor and inhibitory fibers. The acetylcholine content of sensory fibers can account for the acetylcholine activity of whole nerve extract. It is concluded that the factor I of crustacean nerve is an exclusive property of the inhibitory fibers. The results support the assumption that factor I is the transmitter substance of inhibitory neurons in these animals. The absence of acetylcholine in motor fibers indicates that this substance does not function as a transmitter of motor impulses in Crustacea, and explains the previously observed failure of the substance to elicit motor responses in these animals. The function of acetylcholine in sensory fibers is not yet clarified.

Factor I and gamma-aminobutyric acid: A summary

Neurology ◽  
1958 ◽  
Vol 8 (Supplement 1) ◽  
pp. 98-99 ◽  
Author(s):  
K. A. C. Elliott
Keyword(s):  
Aminobutyric Acid ◽  
Gamma Aminobutyric Acid ◽  
Factor I

scholarly journals THE METABOLISM OF GAMMA AMINOBUTYRIC ACID IN THE LOBSTER NERVOUS SYSTEM

1970 ◽  
Vol 46 (2) ◽  
pp. 290-299 ◽  
Author(s):  
Z. W. Hall ◽  
M. D. Bownds ◽  
E. A. Kravitz
Keyword(s):  
Aminobutyric Acid ◽  
Inhibitory Neurons ◽  
Decarboxylase Activity ◽  
Succinic Semialdehyde ◽  
Gamma Aminobutyric Acid ◽  
Succinic Semialdehyde Dehydrogenase ◽  
Gaba Metabolism ◽  
Semialdehyde Dehydrogenase ◽  
Electrophoretic Behavior ◽  
Inhibitory Transmitter

γ-aminobutyric acid (GABA) is the inhibitory transmitter compound at the lobster neuromuscular junction. This paper presents a comparison of the enzymes of GABA metabolism in single identified inhibitory and excitatory axons from lobster walking legs. Inhibitory axons contain more than 100 times as much glutamic decarboxylase activity as do excitatory axons. GABA-glutamic transaminase is found in both excitatory and inhibitory axons, but about 50% more enzyme is present in inhibitory axons. The kinetic and electrophoretic behavior of the transaminase activity in excitatory and inhibitory axons is similar. Succinic semialdehyde dehydrogenase is found in both axon types, as is an unknown enzyme which converts a contaminant in radioactive glutamic acid to GABA. In lobster inhibitory neurons, therefore, the ability to accumulate GABA ultimately rests on the ability of the neuron to accumulate the enzyme glutamic decarboxylase.

scholarly journals Effect of gamma-aminobutyric acid on intracellular pH in the crayfish stretch-receptor neurone

1991 ◽  
Vol 156 (1) ◽  
pp. 349-360 ◽  
Author(s):  
J. Voipio ◽  
M. Pasternack ◽  
B. Rydqvist ◽  
K. Kaila
Keyword(s):  
Intracellular Ph ◽  
Action Potentials ◽  
Initial Rate ◽  
Reversal Potential ◽  
Stretch Receptor ◽  
Aminobutyric Acid ◽  
Gamma Aminobutyric Acid ◽  
Anion Channels ◽  
Co2 Partial Pressure ◽  
Crayfish Stretch Receptor

The effect of gamma-aminobutyric acid (GABA) on intracellular pH (pHi) was examined in the crayfish stretch-receptor neurone using H(+)-selective microelectrodes and a two-microelectrode voltage clamp. In the presence of 30 mmol l-1 HCO3- (pH 7.4), application of GABA (0.5 mmol l-1) produced a mean fall in pHi of 0.26 units. The initial rate of fall of pHi was attributable to a net influx of acid equivalents of 6.3 mmol l-1 min-1. In the nominal absence of HCO3-, GABA had little effect on pHi. The HCO3(−)-dependent acidosis caused by GABA was inhibited by picrotoxin (0.1 mmol l-1) but not by depletion of extracellular and intracellular Cl-. Acetazolamide (0.1 mmol l-1) decreased the rate of fall of pHi caused by a step increase in CO2 partial pressure as well as by GABA, which indicates that the neurone contains carbonic anhydrase. In the presence of both Cl- and HCO3-, the reversal potential of the GABA-activated current was more positive than under nominally HCO3(−)-free conditions. In line with this, GABA induced a marked HCO3(−)-dependent depolarization, and this depolarizing action was enhanced in the absence of Cl- so as to lead to triggering of action potentials. All these observations support the conclusion that the GABA-induced fall in pHi is due to a net efflux of HCO3- through the inhibitory anion channels.

THE RELATION OF GAMMA-AMINOBUTYRIC ACID TO FACTOR I IN BRAIN EXTRACTS

1961 ◽  
Vol 7 (2) ◽  
pp. 147-154 ◽  
Author(s):  
Emanuel Levin ◽  
R. A. Lovell ◽  
K. A. C. Elliott
Keyword(s):  
Aminobutyric Acid ◽  
Gamma Aminobutyric Acid ◽  
Factor I ◽  
Brain Extracts
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