Primary afferent depolarization induced by ?-aminobutyric acid injected into the central canal of the cat spinal cord

1981 ◽  
Vol 92 (6) ◽  
pp. 1678-1680 ◽  
Author(s):  
S. N. Kozhechkin ◽  
T. Yu Ruchinskaya ◽  
G. S. Sanadiradze ◽  
Yu. S. Sverdlov

1979 ◽  
Vol 57 (10) ◽  
pp. 1157-1167 ◽  
Author(s):  
B. R. Sastry

The effects of iontophoretically applied γ-aminobutyric acid (GABA), (−)-nipecotic acid (NCA), 2,4-diaminobutyric acid (DABA), and pentobarbital were examined on the thresholds for antidromic activation of single group I muscle afferents, in decerebrated spinal cats. GABA decreased the threshold for antidromic activation of the majority of the afferents. During this decrease in the threshold, the preterminal axons were depolarized. This depolarization was decreased by a prior depolarization, but increased by a hyperpolarization, of the afferent. During the depolarization of the afferent produced by GABA, the size of the orthodromic action potential was decreased. Iontophoretically applied bicuculline antagonized the effect of GABA on the threshold for antidromic activation of the afferents. NCA, DABA, and pentobarbital potentiated the action of GABA on the afferent terminal excitability. Pre-treatment of the animals with semicarbazide, which reportedly depletes spinal GABA, resulted in a reduction in the threshold produced by a conditioning stimulation of other group I afferents. GABA decreased the threshold for antidromic activation of the nonterminal regions of the afferents when applied near the stimulation sites. The amounts of GABA required to produce a decrease in the threshold of the nonterminal afferents were greater than those required to produce a comparable effect on the terminal regions of the fibres. Iontophoretically applied NCA and bicuculline, in amounts that were adequate to alter the effects of applied GABA, failed to affect the nerve stimulation-induced decrease in the threshold for antidromic activation of the fibres. Intravenously injected bicuculline, however, antagonized the actions of GABA as well as of the reduction in the threshold produced by nerve stimulation.These results indicate that (1) GABA-induced increase in the excitability of group I afferent terminals is associated with a depolarization of the afferent, (2) the uptake of iontophoretically applied amino acid into the spinal cord tissue appears to limit its action on the afferent terminal excitability, (3) GABA has a preterminal depolarizing action on group I muscle afferents, and (4) primary afferent depolarization produced by nerve stimulation may be of diffuse origin and, hence, cannot be significantly affected by iontophoretically applied NCA and bicuculline.



1980 ◽  
Vol 5 (9) ◽  
pp. 1037-1045 ◽  
Author(s):  
S. Glusman ◽  
M. Pacheco ◽  
D. McAdoo ◽  
B. Haber




1982 ◽  
Vol 60 (6) ◽  
pp. 850-855 ◽  
Author(s):  
Radan Čapek ◽  
Barbara Esplin

Effects of taurine and homotaurine (3-aminopropancsuIfonic acid), on excitability of primary afferents were compared with effects of γ-aminobutyric acid (GABA) in spinal unanaesthesized cats. Homotaurine and GABA, administered intravenously or topically, produced a marked increase in afferent excitability. Homotaurine was about 10 times more potent than GABA. Taurine (up to 2 mmol/kg i.v., or 10 mM topically) did not produce a consistent change in afferent excitability. The effect of homotaurine was antagonized by bicuculline or picrotoxin in doses which suppressed the primary afferent depolarization, as indicated by an increase of afferent excitability, evoked by conditioning stimulation of an antagonistic muscle nerve. Semicarbazidc, an inhibitor of GABA synthesis, did not attenuate the homotaurine-induced excitability changes of afferents while suppressing entirely the primary afferent depolarization. These findings suggest that homotaurine exerts a direct GABA-like action on feline primary afferents.





1992 ◽  
Vol 15 (12) ◽  
pp. 1354-1363 ◽  
Author(s):  
Jeremy M. Shefner ◽  
Fritz Buchthal ◽  
Christian Krarup




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