Neurochemistry of the vertebrate olfactory bulb

Pentobarbitone, phenobarbitone, methohexitone, chloralose and alphaxalone produced 10-fold increases in the duration of an inhibitory post-synaptic conductance (i.p.s.c.) as recorded intracellularly from neurones of the guinea-pig olfactory cortex in vitro. Higher concentrations slightly depolarised these neurones and reduced their input resistances (Ri), presumably a spontaneous activation of the inhibitory conductance. The excitatory potentials were also depressed. Ketamine, halothane and urethane doubled the i.p.s.c. duration. Higher concentrations depressed synaptic activity and the action potential, as did lignocaine. Ketamine also increased Ri. These results confirm the idea that these compounds produced anaesthesia by prolonging inhibition (accompanied by a depression of the e.p.s.p. with some anaesthetics).

Potentiation of inhibition by general anaesthetics in neurones of the olfactory cortex in vitro

Stereoisomers of the barbiturate anesthetic pentobarbital were applied to mouse spinal neurons growing in tissue culture. Intracellular recordings of neuronal membrane properties revealed that the (+) and (-) isomers caused direct changes in membrane potential and conductance on some but not all of the cells tested. The action of the (+) isomer was predominantly excitatory, whereas the (-) isomer produced predominantly inhibitory responses. The (-) isomer was considerably more effective in potentiating inhibitory responses to the transmitter gamma-aminobutyric acid. The results show that pentobarbital has multiple effects on neuronal excitability and demonstrate the presence of stereospecific sites of barbiturate action on central neurons.

https://science.sciencemag.org/content/sci/207/4427/195.full.pdf

Pentobarbital: stereospecific actions of (+) and (-) isomers revealed on cultured mammalian neurons

Some effects of excitatory amino acid receptor antagonists on synaptic transmission in the rat olfactory cortex slice

1. The effects of the general anaesthetic 2,6-diisopropylphenol (DIP) on synaptic transmission and the actions of amino acid transmitter candidates have been investigated in rat olfactory cortex slices. 2. On electrical stimulation of the lateral olfactory tract (LOT), DIP (20 to 200 microM) increased the area of those surface field potentials which reflect gamma-aminobutyric acid (GABA)-mediated transmission in a concentration-dependent manner in 6 out of 12 slices. In a series of conditioning experiments, DIP (50 microM) also potentiated GABA-mediated pre- and post-synaptic inhibition. 3. Perfusion of slices with DIP (50 microM) potentiated the reduction in the excitability of the terminals of the LOT produced by exogenous GABA in a picrotoxin-sensitive manner. 4. DIP (50 microM) markedly potentiated the surface depolarizations evoked by GABA, muscimol and 3-aminopropanesulphonic acid. The effect on the response to 3-aminopropanesulphonic acid was observed over a concentration range of DIP of 6.25 to 50 microM and was not blocked by the benzodiazepine receptor antagonist Ro 15-1788. 5. In slices in which GABA-mediated transmission was abolished by picrotoxin (25 microM), DIP (50 microM) had no significant effect on monosynaptically-evoked excitatory transmission but depressed the areas of those field potentials which reflect di-/polysynaptic excitations in a concentration-dependent manner (from between 1.6 and 6.25 to 50 microM). 6. In a series of conditioning experiments DIP (50 microM) abolished the increase in the excitability of the pyramidal cells evoked on stimulation of deep association fibres. 7. DIP (50 microM) had no significant effect on surface depolarizations evoked by N-methyl-D-aspartate, quisqualate and kainate or by the transmitter candidates L-glutamate and L-aspartate. 8. It is concluded that, at clinically relevant concentrations, DIP potentiates GABA-mediated transmission probably by an interaction with the GABA receptor complex and inhibits di-/polysynaptic excitations, possibly by inhibiting the release of excitatory transmitters.

Effects of the anaesthetic 2,6-diisopropylphenol on synaptic transmission in the rat olfactory cortex slice.

1. Field potentials were evoked in slices of rat olfactory cortex by stimulating the lateral olfactory tract. In addition to previously described components of the wave-form, a further distinct surface-negative potential of low amplitude and long duration (I-wave) has been described. 2. Pentobarbitone, at concentrations of 10(-5) M and above, markedly enhanced enhanced the amplitude and duration of the I-wave with only minimal effect on other components of the field potential. 3. The I-wave was reversibly reduced by the GABA antagonists bicuculline and picrotoxin and was also attenuated at rapid rates of stimulation. Low chloride medium usually caused a transient increase in amplitude of the I-wave followed by a gradual reduction, suggesting that a chloride-mediated depolarization was involved. 4. Evoked inhibition, which was most probably post-synaptic, occurred in parallel with the I-wave. This was monitored as a suppression of, or increase in latency of the population spike evoked by a second stimulus at appropriate intervals after the first. Pentobarbitone substantially increased the duration of the post-synpatic inhibition, without obvious changes in the presynaptic inhibitory phenomenon associated with antidromic firing in the lateral olfactory tract. 5. It is proposed that the I-wave is the field potential representation of a population depolarizing i.p.s.p. and that the main action of pentobarbitone is to enhance this inhibition.

https://physoc.onlinelibrary.wiley.com/doi/pdf/10.1113/jphysiol.1978.sp012181

Field potentials, inhibition and the effect of pentobarbitone in the rat olfactory cortex slice.

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Field potentials, inhibition and the effect of pentobarbitone in the rat olfactory cortex slice.