Primary afferent depolarization distribution of the ?-aminobutyric acid system in frog spinal cord

1980 ◽  
Vol 5 (9) ◽  
pp. 1037-1045 ◽  
Author(s):  
S. Glusman ◽  
M. Pacheco ◽  
D. McAdoo ◽  
B. Haber
Keyword(s):  
Spinal Cord ◽  
Aminobutyric Acid ◽  
Primary Afferent Depolarization ◽  
Acid System ◽  
Primary Afferent ◽  
Frog Spinal Cord

Primary afferent depolarization in frog spinal cord is associated with an increase in membrane conductance

1983 ◽  
Vol 61 (6) ◽  
pp. 626-631 ◽  
Author(s):  
Ante L. Padjen ◽  
Toshio Hashiguchi
Keyword(s):  
Spinal Cord ◽  
Linear Part ◽  
Membrane Conductance ◽  
Potassium Sulfate ◽  
Equilibrium Potential ◽  
Primary Afferent Depolarization ◽  
Primary Afferent ◽  
Frog Spinal Cord ◽  
Voltage Dependent ◽  
Afferent Terminals

The mechanism of primary afferent depolarization (PAD) was studied in the isolated frog spinal cord using intrafibre recording (microelectrodes filled with 0.6 M potassium sulfate) from large myelinated axons of dorsal roots. Standard current–clamp technique was used to obtain voltage–current (V–I) relationship. It was found that: (i) PAD is voltage dependent: its amplitude and rate of rise are increased with hyperpolarization; (ii) the slope of the linear part of the V–I curve obtained during PAD is decreased compared with the V–I curve at rest; (iii) the PAD equilibrium potential, estimated by extrapolation, ranged from −66 to −40 mV. These results suggest that PAD is associated with an increase in conductance of primary afferent terminals and thus seem to provide the first experimental evidence for the hypothesis that shunting of primary afferent membrane is the mechanism of presynaptic inhibition in the vertebrate nervous system.

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
Keyword(s):  
Spinal Cord ◽  
Central Canal ◽  
Aminobutyric Acid ◽  
Primary Afferent Depolarization ◽  
Primary Afferent

Ultrastructural observations in the frog spinal cord in relation to the generation of primary afferent depolarization

1976 ◽  
Vol 2 (3) ◽  
pp. 137-145 ◽  
Author(s):  
S. Glusman ◽  
G. Vázquez ◽  
P. Rudomín
Keyword(s):  
Spinal Cord ◽  
Primary Afferent Depolarization ◽  
Primary Afferent ◽  
Frog Spinal Cord

γ-Aminobutyric acid and primary afferent depolarization in feline spinal cord

1979 ◽  
Vol 57 (10) ◽  
pp. 1157-1167 ◽  
Author(s):  
B. R. Sastry
Keyword(s):  
Spinal Cord ◽  
Nerve Stimulation ◽  
Muscle Afferents ◽  
Aminobutyric Acid ◽  
Primary Afferent Depolarization ◽  
Antidromic Activation ◽  
Primary Afferent ◽  
Afferent Terminal ◽  
Group I ◽  
Terminal Excitability

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.

Effects of γ-aminobutyrate and bicuculline on primary afferent depolarization of cutaneous fibres in the cat spinal cord

Neuroscience ◽  
1983 ◽  
Vol 10 (3) ◽  
pp. 869-874 ◽  
Author(s):  
G. Gmelin ◽  
M. Zimmermann
Keyword(s):  
Spinal Cord ◽  
Primary Afferent Depolarization ◽  
Primary Afferent

Excitability of primary afferents in feline spinal cord: taurine, homotaurine, and γ-aminobutyric acid compared

1982 ◽  
Vol 60 (6) ◽  
pp. 850-855 ◽  
Author(s):  
Radan Čapek ◽  
Barbara Esplin
Keyword(s):  
Primary Afferents ◽  
Aminobutyric Acid ◽  
Primary Afferent Depolarization ◽  
Conditioning Stimulation ◽  
Primary Afferent ◽  
Antagonistic Muscle ◽  
Consistent Change ◽  
Muscle Nerve ◽  
Gaba Synthesis ◽  
Stimulation Of

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.

Evidence for release of glutamic acid, aspartic acid and substance P but not γ-aminobutyric acid from primary afferent fibres in rat spinal cord

1996 ◽  
Vol 302 (1-3) ◽  
pp. 27-36 ◽  
Author(s):  
Hwee Teoh ◽  
Marzia Malcangio ◽  
Leslie J. Fowler ◽  
Norman G. Bowery
Keyword(s):  
Spinal Cord ◽  
Substance P ◽  
Glutamic Acid ◽  
Aspartic Acid ◽  
Aminobutyric Acid ◽  
Rat Spinal Cord ◽  
Primary Afferent
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