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G G Collins

Publications and source records attributed to G G Collins.

At least 37 records · Page 2Linked to original sources
PubMed1984

Amino acid transmitter candidates in various regions of the primary olfactory cortex following bulbectomy.

The effect of bulbectomy on amino acid levels in 5 regions of the rat primary olfactory cortex has been monitored. Glutamate levels were significantly lowered in the lateral olfactory tract only. In contrast, aspartate levels were significantly reduced in all regions except the periamygdaloid cortex. The results suggest transmitter heterogeneity of the tract fibres and confirm a likely transmitter role for aspartate for some tract terminals.

Amino Acids↗
PubMed1984

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.

Adenosine↗
PubMed1983

Endogenous adenosine inhibits excitatory transmission in the rat olfactory cortex slice.

Excitatory neurotransmission in the rat olfactory cortex slice has been monitored by measuring the amplitude of the N-wave surface field potential evoked by stimulation of the lateral olfactory tract. Application of exogenous adenosine or aspartate depressed the N-wave amplitude and evoked synthesis of cyclic AMP. These effects were partially antagonized by theophylline and the reduction of amplitude of the N-wave was potentiated by dipyridamole. When the olfactory tract slice was stimulated, dipyridamole alone reduced the amplitude of the N-wave and increased levels of cyclic AMP, both effects being antagonized by theophylline. Exogenous adenosine significantly attenuated the K+-evoked release of [3H]D-aspartate by a mechanism insensitive to either theophylline or dipyridamole. It is concluded that synaptic activation of the olfactory cortex releases adenosine, possibly as the result of the actions of the transmitter candidate of the olfactory tract, aspartate, and that this causes sufficient adenosine to accumulate to depress excitatory transmission and elevate tissue levels of cyclic AMP although there is no positive evidence that these two effects are directly related.

1-Methyl-3-isobutylxanthine↗
PubMed1982

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

A study has been made of the effects of a series of excitatory amino acid receptor antagonists on the field potentials evoked on electrical stimulation of the lateral olfactory tracts of olfactory cortex slices perfused in vitro. The antagonists studied included (+/-)-2-amino-5-phosphonovaleric acid, a potent, specific antagonist of N-methyl-D-aspartate (NMDA) receptors, gamma-D-glutamylglycine, an antagonist of NMDA and kainate receptors and (+/-)-cis-2,3-piperidine dicarboxylic acid and 2-amino-4-phosphonobutyric acid, drugs which in addition to antagonizing NMDA and kainate receptors also block responses to quisqualic acid. From the patterns of effects of the drugs it is proposed that quisqualate and NMDA but not kainate receptors are involved in mediating excitatory transmission in the olfactory cortex; quisqualate receptors are located at the lateral olfactory tract - superficial pyramidal cell synapse whereas NMDA receptors are present at the synapses of the superficial pyramidal cell collaterals with the deep pyramidal cell dendrites and/or at the synapses of the pyramidal cell collaterals and inhibitory interneurones. The results are discussed in terms of possible presynaptic and/or postsynaptic sites of antagonist action.

2-Amino-5-phosphonovalerate↗
PubMed1982

Baclofen: effects on evoked field potentials and amino acid neurotransmitter release in the rat olfactory cortex slice.

A study has been made of the in vitro effects of (+/-)- and (-)-baclofen on the evoked field potentials and release of endogenous amino acid neurotransmitter candidates (aspartate, glutamate, GABA and possibly taurine) which accompany electrical stimulation of the excitatory input to the olfactory cortex slice, the lateral olfactory tract. Baclofen appears to reduce the excitatory input to the GABA-utilizing inhibitory interneurones; this action was manifest as a drug-induced abolition of the field potential known as the P-wave (IC50 for (-)-baclofen, 1.7 +/- 0.4 microM) together with a simultaneous reduction in the synaptically evoked release of aspartase and glutamate from the cut surface of slices. Both these actions of baclofen exhibited concentration dependence and stereospecificity and were not antagonized by picrotoxin (25 microM) thereby suggesting that they are directly related. The consequence of this action of baclofen was the abolition of GABA-mediated presynaptic and postsynaptic inhibition together with their respective field potential correlates, the late N- and I-waves. (+/-)-Baclofen (5 and 25 microM) also inhibited the potassium-evoked release of aspartate and glutamate from small cubes of tissue but, except at a high concentration (1 mM), had no effect on GABA release. Baclofen (up to 1 mM) did not affect transmission either at the lateral olfactory tract-superficial pyramidal cell synapse, a site where aspartate is the likely neurotransmitter, or at the superficial pyramidal cell collateral-deep pyramidal cell excitatory synapse. It is proposed that: (i) the actions of baclofen on the olfactory cortex are the result of inhibition of aspartate and glutamate release, probably from deep pyramidal cell collaterals; and (ii) not all neurones utilizing excitatory amino acids as their neurotransmitters are subject to the inhibitory action of baclofen.

Animals↗
PubMed1981

The effects of chlordiazepoxide on synaptic transmission and amino acid neurotransmitter release in slices of rat olfactory cortex.

The rat olfactory cortex slice has been used to investigate the effects of chlordiazepoxide on evoked field potentials and the release of endogenous amino acid neurotransmitters (aspartate, glutamate, GABA and possibly taurine) which accompany electrical stimulation of the lateral olfactory tract. When single, low frequency stimuli were employed, chlordiazepoxide (2 microM-1 mM) depressed the amplitude of the field potential correlate of the depolarizing actions of the lateral olfactory tract excitatory transmitter (aspartate?) although aspartate release was unaffected. The field potential correlate of GABA-mediated presynaptic inhibition (late N-wave) was also depressed in amplitude but low drug concentrations (between approximately 2 and 50 microM) increased its peak duration . Effects of chlordiazepoxide on evoked inhibition were analyzed by giving paired stimuli such that the second stimulus occurred during the field potentials evoked by the first stimulus. Chlordiazepoxide (1-20 microM) increased the depression in amplitudes of the presynaptic massed action potential and late N-wave evoked by the second of a pair of stimuli compared with those evoked by the first stimulus suggesting that presynaptic inhibition was potentiated. These effects of chlordiazepoxide were accompanied by a significant reduction in aspartate release from the lateral olfactory tract terminals. Moreover, the drug effects on presynaptic inhibition and aspartate release were antagonized by picrotoxin (5 microM). On the other hand, chlordiazepoxide (1-50 microM) had no significant effect on postsynaptic inhibition. The results are discussed in terms of both the sites (presynaptic or postsynaptic) and mechanisms of action of chlordiazepoxide.

4-Aminobutyrate Transaminase↗
PubMed1981

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.

Animals↗
PubMed1981

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.

Amino Acids↗
PubMed1981

Effects of pentobarbitone on the synaptically evoked release of the amino acid neurotransmitter candidates aspartate and GABA from rat olfactory cortex.

1. In the rat olfactory cortex slice, sub-anaesthetic concentrations of pentobarbitone reduce the amplitude of the N-wave with a concomitant reduction in the release of the excitatory transmitter aspartate. The pentobarbitone induced potentiation of the GABA-mediated I-wave is accompanied by increased GABA release. Although the changes in transmitter release and evoked electrical activity are consistent, there is only circumstantial evidence that the phenomena are related. 2. Pentobarbitone also reduced release of taurine although the significance (if any) of this finding is obscure. 3. The results are discussed in terms of the mechanisms by which pentobarbitone induces the changes in amino acid release.

Animals↗
PubMed1980

Release of endogenous amino acid neurotransmitter candidates from rat olfactory cortex slices: possible regulatory mechanisms and the effects of pentobarbitone.

A study has been made of the regulation of evoked release of the amino acid neurotransmitter candidates (aspartate, GABA and taurine) from rat olfactory cortex slices. The effects of pentobarbitone (10-1000 microM) on release have also been assessed. Release of aspartate, the presumed excitatory transmitter of some of the lateral olfactory tract fibres, is reduced by muscimol (10 microM) and this effect is antagonized by picrotoxin (15 microM): it is concluded that presynaptic GABA receptors may modulate aspartate release. Low concentrations of pentobarbitone also reduce aspartate release, but this effect is picrotoxin-insensitive. Release of GABA, the presumed transmitter of inhibitory interneurones, is reduced by muscimol (10 microM) and this effect is antagonized by picrotoxin (15 microM): it is suggested that GABA release may be regulated by presynaptic autoreceptors. Pentobarbitone significantly increases release of GABA when slices are synaptically activated although the mechanism of this effect is unclear. Release of taurine, not hitherto considered a neurotransmitter in this brain area, is depressed by muscimol (10 microM) and pentobarbitone and increased by picrotoxin (15 microM). Results are discussed in terms of (i) mechanisms of regulation of amino acid release in the olfactory cortex, (ii) effects of pentobarbitone on release and (iii) the compatibility of the present results with previously published electrophysiological studies.

Animals↗
PubMed1980

Influence of cellular transport on the interaction of amino acids with gamma-aminobutyric acid (GABA)-receptors in the isolated olfactory cortex of the guinea-pig.

1 Freshly cut guniea-pig olfactory cortex slices contained 2.2 mmol gamma-aminobutyric acid (GABA)/kg tissue weight. This declined during in vitro incubation at 25 degrees C in the absence of exogenous GABA, but increased to 6.95 mmol/kg after 1.5 h incubation in 1 mM GABA. 2 Uptake of [3H]-GABA (1 microM) was inhibited by 1 mM (+/-)-nipecotic acid (-83%), beta-amino-n-butyric acid (BABA) (-59%), L-2,4-diaminobutyric acid (DABA) (-63%), (+/-)cis-3-aminocyclohexane carboxylic acid (ACHC) (-53%), and 3-aminopropanesulphonic acid (3-APS) (-26%), but was increased by beta-alanine (BALA) (+23%). 3 Autoradiographs showed steep concentration gradients of radioactivity across slices incubated for short periods in [3H]-GABA. 4 Efflux of [3H]-GABA from pre-loaded slices was accelerated strongly by nipecotic acid, BABA, DABA and ACHC but weakly or not all by BALA or 3-APS. 5 Nipecotic acid (1 mM) potentiated the surface-depolarization of the slice produced by GABA but not that produced by 3-APS. 6 The depolarizing actions of DABA, BABA, nipecotic acid and ACHC, but not that of 3-APS or BALA, were potentiated when the endogenous GABA content of slices was raised. 7 It is concluded that: (a) the depolarizing action of exogenous GABA is limited by cellular uptake; (b) surface-depolarizations produced by nipecotic acid, DABA, BABA and ACHC may be mediated by the release of GABA; and (c) neuronal, rather than glial, transport systems are responsible for these effects.

Amino Acids↗
PubMed1979

Inhibition of aspartate release from the retina of the anaesthetised rabbit by stimulation with light flashes.

Rabbits were anaesthetised and the cornea, iris, lens and vitreous were removed from eyes to form an eye-cup which was filled with Krebs-bicarbonate Ringer. The medium in the eye-cup was replaced at 10-min intervals and the amino acids in each resulting sample were assayed. Exposure of the dark-adapted retina to flashes of light (3 Hz) did not alter the efflux of glutamate glutamine, alanine, glycine or GABA. The efflux of taurine and ACh was greatly increased by light flashes, but in contrast, the release of aspartate was reduced by more than 50%, a result consistent with the suggestion that aspartate may be a photoreceptor transmitter substance.

Anesthesia, General↗
PubMed1979

Evidence of a neurotransmitter role for aspartate and gamma-aminobutyric acid in the rat olfactory cortex.

1. Using a cortical cup technique, the release of seven endogenous amino acids from the isolated rat olfactory cortex slice has been monitored.2. Electrical stimulation of the lateral olfactory tract at a frequency of 4 min(-1) was accompanied by a significant increase in the release of aspartate, GABA and taurine; the release of GABA and aspartate but not that of taurine was Ca(2+)-dependent.3. Chronic unilateral bulbectomy was accompanied by a specific, significant fall in the aspartate content of the olfactory cortex which reached a maximum 5 days after surgery and persisted for at least a further 5 days. Electrical stimulation of the lateral olfactory tract of such preparations did not release any of the amino acids under investigation.4. When slices from the unoperated side were exposed to solutions containing 25 mM-K+ or stimulated with electrodes placed directly on the cortex enclosed by the cup there was a Ca(2+)-dependent release of aspartate and GABA accompanied by a Ca(2+)-independent release of taurine. Following chronic bulbectomy, these procedures failed to evoke significant release of aspartate whereas the characteristics of GABA and taurine release were unaltered.5. It is concluded that aspartate may be the excitatory transmitter of some of the terminals of the lateral olfactory tract fibres and that GABA may be a transmitter at some inhibitory synapses of the rat olfactory cortex.

Amino Acids↗