Interaction of Pentobarbitone and Γ‐aminobutyric Acid on Mammalian Sympathetic Ganglion Cells

Brown, David A.; Constanti, Andrew

doi:10.1111/j.1476-5381.1978.tb07791.x

Cited by 55 publications

(23 citation statements)

References 19 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Recent studies on the mechanisms of action of barbiturates have revealed a GABA potentiating effect (Nicoll, 1975;Brown & Constanti, 1978;Evans, 1979) that may be mediated via an increase in the open channel lifetime of the GABA-activated ionophore (Barker & McBurney, 1979). Potentiation of synaptic inhibition in the preoptic-anterior hypothalamus by pentobarbitone provides further support for the hypothesis that such inhibition is mediated by GABA or a similar amino acid.…”

Section: Discussionmentioning

confidence: 58%

Electrophysiological analysis of inhibitory synaptic mechanisms in the preoptic area of the rat.

Mayer¹

1981

The Journal of Physiology

View full text Add to dashboard Cite

Micro-injection of tetanus toxin (100-200 MLD) into the preoptic-anterior hypothalamus signficantly reduced the frequency ofoccurrence ofinhibition evoked from both sites.6. Pentobarbitone administered acutely or as the sole anaesthetic increased both the duration and frequency of occurrence of inhibitory responses evoked from the arcuate-ventromedial nuclei.7. It is suggested that a GABA-linked inhibitory synaptic mechanism, activated by arcuate-ventromedial and periaqueductal grey stimulation, operates in the preoptic-anterior hypothalamus. Such convergent inhibition may be a result of activity in local interneurone circuitry.

show abstract

Section: Discussionmentioning

confidence: 58%

Electrophysiological analysis of inhibitory synaptic mechanisms in the preoptic area of the rat.

Mayer¹

1981

The Journal of Physiology

View full text Add to dashboard Cite

show abstract

“…The postsynaptic actions of GABA on rat sympathetic neurones in vitro have been described in detail (Adams and Brown 1975;Brown and Constanti 1978). As already discussed, the application of 4-AP resulted mainly in the spontaneous appearance of postsynaptic spikes.…”

Section: B) Effects Of Gaba In 4-aminopyridinementioning

confidence: 94%

“…Electrodes were filled with neutralised 4 M potassium acetate (pH = 7.4;Brown and Constanti 1978) and had resistances between 60 and 120 M~2. Only cells with stable resting potentials and action potentials > 60 mV were selected for study.…”

Section: Methodsmentioning

confidence: 99%

Presynaptic actions of 4-Aminopyridine and γ-aminobutyric acid on rat sympathetic ganglia in vitro

Galvan

Grafe

Bruggencate

1980

Naunyn-Schmiedeberg's Arch. Pharmacol.

View full text Add to dashboard Cite

Summary.Responses to bath-applications of 4-aminopyridine (4-AP) and y-aminobutyric acid (GABA) were recorded intracellularly from neurones in the rat isolated superior cervical ganglion.4-aminopyridine (0.1 -1.0 mmol/1) usually induced spontaneous action potentials and excitatory postsynaptic potentials (EPSPs), which were blocked by hexamethonium. Membrane potential was unchanged; spike duration was slightly increased. Vagus nerve B-and C-fibre potentials were prolonged.In 4-AP solution (0.1 -0.3 mmol/1), GABA (0.1 mmol/1), 3-aminopropanesulphonic acid or muscimol evoked "bursts" of spikes and EPSPs in addition to a neuronal depolarization. These "bursts", which were not elicited by glycine, glutamate, taurine or (+)-baclofen, were completely antagonised by hexamethonium, tetrodotoxin or bicuculline methochloride.It is concluded that: (a)4-AP has a potent presynaptic action on sympathetic ganglia; (b) presynaptic actions of GABA can be recorded postsynaptically in the presence of 4-AP; and (c) the presynaptic GABAreceptors revealed in this condition are similar to those on the postsynaptic membrane.

show abstract

“…A post-synaptic mechanism is perhaps the most favoured (e.g. Jessel & Richards, 1977;Barker & Ransom, 1978;Brown & Constanti, 1978; Lodge & Curtis, 1978, Scholfield, 1978, and some authors have even reported a GABA-mimetic action of PB (Nicoll, 1975;Nicoll & Iwamoto, 1978;MacDonald & Barker, 1978;Evans, 1979).…”

Section: Introductionmentioning

confidence: 99%

“…Potentiation of the response under these conditions is most simply explained by either a post-synaptic action or delayed removal of GABA by inhibition of the uptake mechanism. Since nipecotic acid, an inhibitor of GABA uptake (Johnston, Krogsgaard-Larsen & Stephanson, 1975), failed to duplicate all the observed PB effects (Bowery & Dray, 1977;Brown & Constanti, 1978;Evans, 1979), potentiation was considered unlikely to have been mediated by the latter mechanism. Further evidence for a post-synaptic action has been interpreted from the reversal of the action of GABA antagonists by PB, first reported for picrotoxin (PTX) by Eccles, Schmidt & Willis (1963) and later for bicuculline by Bowery & Dray (1976).…”

Section: Introductionmentioning

confidence: 99%

Pentobarbitone interference with inhibitory synaptic transmission in crayfish stretch receptor neurones.

Aickin¹,

Deisz²

1981

The Journal of Physiology

View full text Add to dashboard Cite

1. The effect of pentobarbitone (PB) on GABA‐ergic inhibition was investigated in the isolated crayfish stretch receptor. The soma of the slowly adapting neurone was impaled with two micro‐electrodes to give an accurate determination of membrane conductances. 2. Application of PB in concentrations from 10(‐6) to 10(‐3) M increased the rise time constant of the inhibitory post‐synaptic potential (i.p.s.p.). The i.p.s.p. percentage amplitude and decay time constant were also increased in eight out of twelve neurones. On prolonged exposure, the percentage amplitude declined at a rate dependent upon the dose and the frequency of stimulation until the i.p.s.p. became undetectable. 3. The response to ionophoretically applied GABA remained essentially unaltered in the presence of PB, but the falling phase was prolonged by up to 8% in four of the ten neurones tested. Resting membrane conductance, i.p.s.p. driving force (i.p.s.p. reversal potential minus resting membrane potential), and parameters of the anti‐ and orthodromic action potential were not significantly affected. 4. Removal of PB after prolonged exposure usually caused an immediate increase in i.p.s.p. percentage amplitude but the i.p.s.p. rising phase remained slowed. 5. Application of excess extracellular GABA only affected the i.p.s.p. percentage amplitude after it had been reduced by PB. It transiently increased the attenuated i.p.s.p. percentage amplitude in the presence of PB, and after the removal of PB permanently increased the amplitude to its original value. 6. Nipecotic acid and cis‐1,3‐aminocyclohexane carboxylic acid, inhibitors of GABA re‐uptake, slightly increased the i.p.s.p. percentage amplitude, and prolonged the falling phase but did not affect the rising phase. The percentage amplitude declined on prolonged exposure. 7. We conclude that PB has no electrophysiologically demonstrable post‐synaptic action in the crayfish stretch receptor neurone, but it inhibits the presynaptic release and re‐uptake of GABA.

show abstract

Interaction of Pentobarbitone and Γ‐aminobutyric Acid on Mammalian Sympathetic Ganglion Cells

Cited by 55 publications

References 19 publications

Electrophysiological analysis of inhibitory synaptic mechanisms in the preoptic area of the rat.

Electrophysiological analysis of inhibitory synaptic mechanisms in the preoptic area of the rat.

Presynaptic actions of 4-Aminopyridine and γ-aminobutyric acid on rat sympathetic ganglia in vitro

Pentobarbitone interference with inhibitory synaptic transmission in crayfish stretch receptor neurones.

Contact Info

Product

Resources

About