Pharmacological studies on inhibition in the cuneate nucleus of the cat

Banna, N. R.; Jabbur, Suhayl J.

doi:10.1016/0028-3908(69)90051-3

Cited by 55 publications

(22 citation statements)

References 9 publications

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“…It may be relevant that all the substances found capable of antagonizing GABA have been shown to reduce the P-wave or dorsal root potential correlates of pre-synaptic inhibition (Banna & Jabbur, 1969;Banna et al, 1972;Davidoff, 1972;Hill, Simmonds & Straughan, 1973c, 1974. But other substances such as leptazol and bemegride can reduce pre-synaptic inhibition (Banna & Jabbur, 1970;Hill et al, 1974) although we have been unable to show that either substance can antagonize GABA in the cuneate nucleus or the cerebral cortex (Hill et al, 1973a).…”

Section: Experimentalproceduresmentioning

confidence: 65%

“…An alternative explanation could involve the possibly different distributions of GABA receptors at pre-and post-synaptic sites in cuneate nucleus and cerebral cortex. Both pre-and post-synaptic inhibition have been demonstrated in the cuneate nucleus (Andersen, Etholm & Gordon, 1970) and GABA has been suggested as the transmitter for both mechanisms (Banna & Jabbur, 1969;Davidson & Reisine, 1971;Kelly & Renaud, 1971;Banna, Naccache & Jabbur, 1972;Kelly & Renaud, 1973c). In the cortex, however, only a post-synaptic action of GABA has been shown to occur, as yet (Krnjevic & Schwartz, 1968).…”

Section: Experimentalproceduresmentioning

confidence: 99%

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Antagonism of Γ‐aminobutyric Acid and Glycine by Convulsants in the Cuneate Nucleus of Cat

Hill

Simmonds

Straughan

1976

British J Pharmacology

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1Some convulsant substances have been applied-to single neurones in the cat cuneate nucleus by microiontophoresis. Numerical values were derived for the effectiveness and selectivity of the substances as antagonists of y-aminobutyric acid (GABA) and glycine. 2 (+)-Bicuculline methochloride was the most effective GABA antagonist and it also excited many neurones. It antagonized GABA in 93% of experiments but also antagonized glycine in 41% of experiments. In most experiments the antagonism of GABA was greater than the antagonism of glycine resulting in an overall selective antagonism of GABA that was statistically significant. Nevertheless, in only about one quarter of the individual experiments was the GABA antagonism substantial and the selectivity clearcut. 3 (+)-Bicuculline and picrotoxin were less easily applied to neurones by microiontophoresis and were found to antagonize GABA in 30% and 35% of experiments, respectively. They also antagonized glycine in 25% and 30% of experiments, respectively. Overall, neither substance could be shown to be selective, statistically, although in the few individual experiments where the GABA antagonism was substantial the antagonism was clearly selective. 4 (+)Tubocurarine antagonized GABA in 59% and glycine in 32% of experiments and it also excited many neurones. Penicillin antagonized GABA in 33% of experiments without antagonizing glycine. Neither antagonist caused any substantial antagonisms of GABA and neither showed significant selectivity overall. (-)-Bicuculline methochloride, leptazol and bemegride antagonized GABA or glycine in less than 10% of experiments, although (-)-bicuculline methochloride excited most neurones. SStrychnine antagonized glycine in every experiment while antagonizing GABA in only 5% of experiments. In each individual experiment the antagonism of glycine was substantial and clearly selective, resulting in a statistically significant selectivity overall. 6 It is concluded that the selective glycine antagonist strychnine is considerably better than the presently available GABA antagonists for distinguishing between responses to GABA and glycine, when the antagonists are applied by microiontophoresis.

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Section: Experimentalproceduresmentioning

confidence: 65%

Section: Experimentalproceduresmentioning

confidence: 99%

Antagonism of Γ‐aminobutyric Acid and Glycine by Convulsants in the Cuneate Nucleus of Cat

Hill

Simmonds

Straughan

1976

British J Pharmacology

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“…However, evidence concerning the nature of the transmitter at the vertebrate axo-axonic synapse is lacking. Eccles, Schmidt & Willis (1963) and Banna & Jabbur (1969) A wide variety of cholinergic drugs, including acetylcholine, dihydro-flerythroidine, gallamine triethiodide, nicotine, eserine and tetraethyl pyrophosphate have been shown to have no effect on presynaptic inhibition in the spinal cord when topically applied or administered intravenously (Eccles et al 1963;Schmidt, 1963). Similarly, microiontophoresis of dopamine, noradrenaline or 5-HT has not been shown to exert any specific effect on presynaptic inhibition in the spinal cord or cuneate nucleus Salmoiraghi & Weight, 1966;Galindo, Krnjevinc & Schwartz, 1967, Curtis & Crawford, 1969.…”

Section: Introductionmentioning

confidence: 99%

Amino acids and presynaptic inhibition in the rat cuneate nucleus

Davidson¹,

Southwick²

1971

The Journal of Physiology

132

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SUMMARY1. Presynaptic inhibition was evoked in the rat cuneate nucleus by a peripheral conditioning stimulus. The dicarboxylic amino acid salts glutamate and aspartate and the neutral amino acids glycine and yaminobutyric acid (GABA) were topically applied to a restricted area of the cuneate nucleus and their effects on both resting primary afferent terminal excitability and the increase in excitability of afferent terminals during presynaptic inhibition determined.2. Aspartate had no effect on either resting primary afferent terminal excitability or on the increase in excitability during presynaptic inhibition.3. Glycine reduced both resting primary afferent terminal excitability and presynaptic inhibition.4. Glutamate increased both resting primary afferent terminal excitability and presynaptic inhibition while GABA increased resting primary afferent terminal excitability but reduced the increase in excitability during presynaptic inhibition.5. The convulsant alkaloids picrotoxin (given intravenously) and bicuculline (topically applied) blocked presynaptic inhibition. The blocking action of picrotoxin was overcome by topical application of GABA but not glutamate.6. Simultaneous measurement of pre-and post-synaptic excitability in the cuneate nucleus showed that while glutamate increased excitability at both sites, GABA increased primary afferent terminal excitability but depressed post-synaptic excitability.7. It is concluded that glycine and glutamate exert non-specific actions on primary afferent terminals similar to their effects at post-synaptic sites elsewhere in the c.N.s. while GABA depolarizes primary afferent terminals by a specific action at the same receptor site as the presynaptic inhibitory transmitter. The possibility is discussed that the presynaptic inhibitory transmitter in the cuneate nucleus is GABA or a closely related substance.

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“…Using a small laboratory computer (Biomac 1000, Datalabs Ltd), 32 potentials were averaged over a sweep time of 160 ms at regular intervals of 2 or 3 min and each complete average was written out on an X-Y recorder. Potentials were analysed by measuring the N-and P-wave components as described by Banna & Jabbur (1969) and the amplitude of the P-wave was taken to be representative of the depolarization of primary afferent fibres associated with presynaptic inhibition. Drugs were applied to the surface of the cuneate nucleus from a fine polyethylene cannula as solutions in physiological saline at neutral pH.…”

Section: Methodsmentioning

confidence: 99%

“…The presynaptic inhibitory process of the cuneate nucleus is blocked by a number of other convulsant substances (Banna & Jabbur, 1969;Davidson & Southwick, 1971) and accordingly we have examined the effect of topical application of folic acid solutions upon this inhibition.…”

Section: Introductionmentioning

confidence: 99%