Excitatory and inhibitory effects of dopamine on synaptic transmission in the rat olfactory cortex slice.

A study has been undertaken of the effects of dopamine on excitatory transmission at the lateral olfactory tract (LOT)-superficial pyramidal cell synapse of the rat olfactory cortex slice by measuring the effects of bath-applied dopamine on the amplitudes and latencies of the surface field potentials evoked on submaximal LOT stimulation in a total of 32 preparations. In 7 (22%) slices, dopamine had no detectable effects on transmission. In the remaining preparations, dopamine (1-250 microM) depressed transmission in a concentration-dependent manner. This action was unaffected by nadolol (10 microM), phentolamine (10 microM) and picrotoxin (25 microM) but was antagonized by chlorpromazine (10 microM) and trifluoperazine (0.2 and 0.5 microM) and mimicked by bromocriptine (0.01-5 microM) and apomorphine (0.25-25 microM). Investigation of the effects of dopamine on stimulus input-evoked potential output relationships indicated that the inhibitory effect of dopamine on transmission was mediated by a reduction in pyramidal cell excitability. In 6 slices (24% of those sensitive to dopamine) low dopamine concentrations (0.1-1 microM) facilitated transmission at the LOT-superficial pyramidal cell synapse. This excitatory effect was antagonized by nadolol and phentolamine (10 microM) and also by 100 microM 2-amino-5-phosphonovalerate (an antagonist of excitatory amino acid receptors of the N-methyl-D-aspartate type) but was unaffected by chlorpromazine (10 microM) and trifluoperazine (0.2 and 0.5 microM). By a comparison with the effects of noradrenaline on transmission, it is concluded that the excitatory effects of dopamine are mediated either indirectly by the release of noradrenaline or by a direct interaction of dopamine with adrenoceptors.(ABSTRACT TRUNCATED AT 250 WORDS)

Excitatory and inhibitory effects of noradrenaline on synaptic transmission in the rat olfactory cortex slice.

An investigation has been made of the effects of noradrenaline on excitatory transmission at the lateral olfactory tract (LOT)-superficial pyramidal cell synapse of the rat olfactory cortex slice by measuring the effects of bath-applied noradrenaline on the amplitudes and latencies of the field potentials evoked on LOT stimulation. Low concentrations of noradrenaline (0.1-5 microM) facilitate transmission whereas higher doses (20-250 microM) depress transmission. Both these effects were completely blocked by non-selective alpha- and beta-adrenoceptor antagonists, by 2-amino-5-phosphonovaleric acid (an antagonist of excitatory amino acid receptors of the N-methyl-D-aspartate type) and by the methylxanthine theophylline. The depressant effects of noradrenaline were mimicked by bath application of GABA or adenosine and specifically antagonized by bicuculline and picrotoxin. In parallel experiments, noradrenaline (100 microM) significantly increased the potassium-evoked release of endogenous aspartate, glutamate and GABA, proposed transmitters of the olfactory cortex, although the effect on GABA release was specifically antagonized by 2-amino-5-phosphonovaleric acid. Noradrenaline (100 microM) also significantly increased the potassium-evoked release of D-[3H]aspartate, an effect antagonized by a number of alpha- and beta-adrenoceptor antagonists. It is concluded that at low concentrations, noradrenaline facilitates transmission at the LOT-superficial pyramidal cell synapse by increasing excitatory amino acid neurotransmitter release. This effect is mediated by both alpha- and beta-adrenoceptors although the primary site of release is unknown. At higher concentrations of noradrenaline, the increased levels of excitatory transmitters release sufficient endogenous GABA (and possibly adenosine) to cause an overall depression of transmission. These conclusions are supported by the results of a series of experiments in which the effects of noradrenaline on stimulus input-evoked field potential output relationships were assessed. It is not possible to exclude additional direct effects of noradrenaline on membrane excitability.

Aspartate and not glutamate is the likely transmitter of the rat lateral olfactory tract fibres.

The protoveratrine A-evoked release of endogenous amino acid neurotransmitter candidates from olfactory cortex slices taken from control and bulbectomized rats has been monitored. Bulbectomy is accompanied by a statistically significant and specific attenuation of drug-evoked aspartate release suggesting that the excitatory transmitter of the lateral olfactory tract fibres is aspartate rather than glutamate.

Patterns of endogenous amino acid release from slices of rat and guinea-pig olfactory cortex.

A study has been made of the effects of depolarizing stimuli on the release of endogenous amino acid neurotransmitter candidates (aspartate, glutamate, GABA and taurine) from in vitro preparations of rat and guinea pig olfactory cortex. Exposure of small cubes of olfactory cortex tissue from either species to potassium chloride (50 mM) was accompanied by a calcium-dependent release of aspartate, glutamate and GABA. A similar release pattern was evoked by protoveratrine A (100 muM) although the release was largely calcium-independent. Neither agent led to increased release of taurine. Electrical stimulation of the excitatory input (lateral olfactory tract) of freshly prepared, synaptically intact olfactory cortex slices of both species induced significant release of aspartate and GABA from the uncut pial surface and of aspartate, GABA and glutamate from the cut surface. Evoked taurine release occurred from both surfaces of rat olfactory cortex slices but no release was detected from guinea pig olfactory cortex slices. These patterns of release were unaffected by changes in stimulus frequency and were mimicked by protoveratrine A (100 muM) applied to one or other surface. Preincubation of slices from rats for 2 led to loss of tissue amino acids and to changes in their release patterns; the presence of glutamine (5 mM) during preincubation prevented the loss of amino acids but did not alter their pattern of release. Because of the close similarities between both the electrophysiological properties and the patterns of amino acid release it is concluded that there is probably an identity of amino acid neurotransmitters (aspartate, glutamate and GABA) in rat and guinea pig olfactory cortex. The role of taurine in the rat olfactory cortex is unknown but would seem unlikely to be that of a neurotransmitter. The results are discussed: (i) in terms of the cellular origins of the released amino acids; and (ii) wit respect to apparent experimental discrepancies which have appeared in the literature.