GABA‐mediated changes in excitability of the rat lateral olfactory tract in vitro.

Abstract

SUMMARY1. Conditioning stimulation of the lateral olfactory tract (l.o.t,) in the rat olfactory cortex slice evoked a slow depolarization of the terminal regions of the l.o.t. The depolarization lasted about 150 ms and was abolished by the y-aminobutyric acid (GABA) antagonist bicuculline.2. Excitability testing of the terminal regions of the l.o.t. showed an increase in excitability which lasted for about 150 ms following a conditioning stimulus. This increase in excitability was abolished by the calcium antagonist cadmium and by the GABA antagonists bicuculline and penicillin.3. Superfused GABA caused a consistent decrease in the excitability of the terminal regions of the l.o.t. within the cortex but an increase in excitability of the axons within the tract itself. These effects were antagonized by bicuculline. K+ caused similar changes in excitability which were not antagonized by bicuculline.4. The difference between the effects of superfused GABA and the effects of orthodromic conditioning can be explained if a more restricted location of action is assumed for the GABA released by conditioning stimulation. It is suggested that GABA causes a decrease in excitability at its locus of action and that the observed increases in exictability occur in adjacent areas of neuronal membrane.

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

“…In the first, the terminals and preterminal axons of the LOT fibres were stimulated submaximally using a focally sited microelectrode and the compound action potentials propagating antidromically in the LOT recorded with a suction electrode. Application of GABA (0.1 to 1 mM) reduced the amplitude of the compound action potential (Figure 4; see also Cain & Simmonds, 1982). Application of DIP (50 pM) potentiated the effects of GABA in a picrotoxin-sensitive manner, but in concentrations up to 200yM did not mimic the actions of GABA (not shown).…”

“…The effects of DIP on the reduction in the excitability of the terminals and pre-terminal axons of the LOT fibres (Cain & Simmonds, 1982) was also assessed. The cortex adjacent and sub-adjacent to the rostral LOT of slices was dissected away and following preincubation for 2-3 h, slices were mounted cut surface up in the perfusion apparatus.…”

“…As the stimulating electrode was progressively lowered, a short duration (approximately 10ms) positive-going potential was recorded by the suction electrode. Its sensitivity to tetrodotoxin (2.25.pM) but not to Cd2+ (1 mM) suggested that it was an antidromically propagating compound action potential (see Cain & Simmonds, 1982). When assessing terminal excitability, it was essential to make certain that the site of stimulation was the terminals and pre-terminal axons but not the myelinated fibres of the LOT.…”

“…When assessing terminal excitability, it was essential to make certain that the site of stimulation was the terminals and pre-terminal axons but not the myelinated fibres of the LOT. This was routinely achieved by ensuring that (i) the latency to peak of the potential (2.5 to 4ms) was greater than that evoked when the electrode was lowered into the LOT itself (1.2 to 2.5 ms); (ii) the potential was reduced in amplitude by GABA applied to the upper cut surface of the slice (Cain & Simmonds, 1982); and (iii) the optimal depth for stimulation was between 300 and 400pm from the myelinated fibres lying on the pial surface (Price & Sprich, 1975). The stimulus current was adjusted to evoke potentials of between 40 and 50% of maximum.…”

A Study of the Possible Mechanisms Underlying the Convulsant Actions of a Linear Expanded Xanthine

“…Postsynaptic inhibition was monitored by measuring the latency of the peak amplitude of the population spike evoked by the test stimulus: changes in the latency of the populations spike, which represent changes in the synchronous firing of the pyramidal cells, reflect alterations in the intensity of the postsynaptic inhibitory actions of GABA (Pickles & Simmonds 1978). Finally, the possible effect of chloro-DCQD (2.5 and 5 mM) on the excitability of the terminals of the lateral olfactory tract was measured using the procedure described in earlier publications (Cain & Simmonds 1982;Collins 1988).…”