GABA, Bicuculline and Central Inhibition

Curtis, D. R.; Duggan, A.W.; Felix, Dominik; Johnston, G. A. R.

doi:10.1038/2261222a0

Cited by 522 publications

(145 citation statements)

References 15 publications

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“…The ability of bicuculline to both antagonize (Curtis et al, 1970) and potentiate (Godfraind, Krnjevic & Pumain, 1970;Straughan et al, 1971) GABA on cerebral cortical neurones has been well described in the literature and will not be considered in detail, other than in the final analysis of data.…”

Section: Antagonism and Potentiationmentioning

confidence: 99%

“…Glycine and glycine-like amino acids can be used as control agonists on cat cortical neurones with moderate success (Curtis et al, 1970;Curtis, Duggan, Felix, Johnston & McLennan, 1971), although recent reports on rat cortical neurones would suggest that it is not always easy to separate antagonism of GABA and glycine (Biscoe, Duggan & Lodge, 1972). In an attempt to use glycine.…”

Section: Control Agonistsmentioning

confidence: 99%

“…As part of the search for a greater understanding of cortical inhibitory processes, the present investigation was undertaken into substances which might be capable of specifically antagonizing GABA. The substances so far reported to be GiABA antagonists include bicuculline, picrotoxin, (+)-tubocurarine and penicillin (Curtis, Duggan, Felix & Johnston, 1970;Engberg & Thaller, 1970;1972a,b;Curtis, Game, Johnston, McCulloch & MacLachlan, 1972). …”

Section: Introductionmentioning

confidence: 99%

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A comparative study of some convulsant substances as γ‐aminobutyric acid antagonists in the feline cerebral cortex

Hill

Simmonds

Straughan

1973

British J Pharmacology

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Summary1. By the use of microiontophoretic techniques, quantitative estimates were obtained of the depressant effects of y-aminobutyric acid (GABA) on single feline cortical neurones. 2. Picrotoxin, bicuculline, strychnine, ( +)-tubocurarine, penicillin and leptazol were also applied microiontophoretically to single neurones. Sequential GABA applications were made before, during and after the microiontophoresis of these substances and any effects on the time course of the GABA depression were measured as an estimate of antagonism or potentiation of GABA. 3. (+ )-Tubocurarine was found to be a potent GABA antagonist. Picrotoxin and bicuculline were rather less potent and strychnine and penicillin only weakly active as GABA antagonists. Leptazol appeared to be inactive against GABA depressions. 4. In addition, bicuculline and strychnine were found to be capable of potentiating the depressant action of GABA. This property was not shared by the other substances studied. 5. All the substances studied produced changes in neuronal firing rate that did not correlate with GABA antagonism. 6. In conclusion, several potent convulsants have been shown to be capable or GABA antagonism. It is not yet clear that this effect, rather than a direct effect on neuronal excitability, is the prime mechanism behind their convulsant properties.

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Section: Antagonism and Potentiationmentioning

confidence: 99%

Section: Control Agonistsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

A comparative study of some convulsant substances as γ‐aminobutyric acid antagonists in the feline cerebral cortex

Hill

Simmonds

Straughan

1973

British J Pharmacology

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“…Muscimol is also not a substrate for the G A B A t r a n s p o r t e r , w h i c h m a k e s i t u s e f u l f o r electrophysiological and biochemical studies. Both competitive and noncompetitive GABA A receptor antagonists also have been described 207 . Heteropentamers of α1-6, β 1 -4 , γ 1 -4 , δ , a n d ρ p r i m a r i l y i n t h e r e t i n a .…”

Section: ) Glutamatementioning

confidence: 99%

A Review of Glutamate Receptors I: Current Understanding of Their Biology

Rousseaux

2008

J Toxicol Pathol

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Seventy years ago it was discovered that glutamate is abundant in the brain and that it plays a central role in brain metabolism. However, it took the scientific community a long time to realize that glutamate also acts as a neurotransmitter. Glutamate is an amino acid and brain tissue contains as much as 5 -15 mM glutamate per kg depending on the region, which is more than of any other amino acid. The main motivation for the ongoing research on glutamate is due to the role of glutamate in the signal transduction in the nervous systems of apparently all complex living organisms, including man. Glutamate is considered to be the major mediator of excitatory signals in the mammalian central nervous system and is involved in most aspects of normal brain function including cognition, memory and learning. In this review, the basic biology of the excitatory amino acids glutamate, glutamate receptors, GABA, and glycine will first be explored. In the second part of this review, the known pathophysiology and pathology will be described. (J Toxicol Pathol 2008; 21: 25-51)

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“…This supports the suggestion that both glycine and GABA are synaptic transmitters in the spinal cord. It has been shown that the depressant effects of microiontophoretically applied y-aminobutyric acid (GABA) on feline cortical neurones can be antagonized by bicuculline or picrotoxin applied in a similar way to the same neurones (Curtis, Duggan, Felix & Johnston, 1970;Hill, Simmonds & Straughan, 1971, 1972. When given intravenously, picrotoxin and bicuculline can be shown to reduce neurally evoked inhibitions (Brooks & Asanuma, 1965;Curtis & Felix, 1971) and these observations have been used as evidence for GABA being a cortical inhibitory transmitter.…”

Section: Tjmentioning

confidence: 99%