Evidence of a neurotransmitter role for aspartate and γ‐aminobutyric acid in the rat olfactory cortex

Collins, G.G.S.

doi:10.1113/jphysiol.1979.sp012799

Cited by 98 publications

(17 citation statements)

References 17 publications

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“…Stimulation of the LOT elicited a surface negative waveform which is the result of the release of acidic amino-acid (Collins, 1979) acting on x-amino-3-hydroxy-5-methyl-4-isoxazoleproprionic acid (AMPA) type receptors (Collins & Buckley, 1989). NMDA receptors are present in olfactory cortex (Tacconi et al, 1993) and they may also be involved in synaptic transmission (Collins, 1991) Figure 1 but can be seen with both preparations in Figure 2.…”

Section: Resultsmentioning

confidence: 99%

NMDA antagonists increase recovery of evoked potentials from slices of rat olfactory cortex after anoxia

Yassin

Scholfield

1994

British J Pharmacology

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1 The role of glutamate in producing tissue damage during cerebral anoxia was investigated in brain slices using antagonists to the NMDA and AMPA receptor types. 2 Tissue function was assessed by field recordings of the synaptically evoked potentials elicited by stimulating the main afferent input to the olfactory cortex, the lateral olfactory tract. Anoxia was produced by bathing the slice in glucose-free solution equilibrated with 95% N2/5% CO2. 3 The amount of recovery of the evoked potential was inversely dependent on the period of anoxia and temperature: at 24°C, 15 min of anoxia followed by reoxygenation produced a 14.6 ± 4.1 % recovery whereas there was no recovery at 35°C. 4 Dizocilpine and ketamine had no effect on synaptic transmission in oxygenated media but following anoxia they produced an increased recovery of the responses: from 14.6 ± 4.1 % to 48.3 ± 7.8% for dizocilpine (10 AM) and 21.6 ± 7.7% to 87.2 ± 7.1% for ketamine (200,M)

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Section: Resultsmentioning

confidence: 99%

NMDA antagonists increase recovery of evoked potentials from slices of rat olfactory cortex after anoxia

Yassin

Scholfield

1994

British J Pharmacology

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“…There are two possible explanations for the discrepancy between the effects of baclofen and bicuculline: (1) GABA does not mediate the inhibitory conductance, or (2) baclofen acts in the chain of synaptic events at some point before the postsynaptic inhibitory site. A large body of evidence favours GABA as the /x u inhibitory substance in the olfactory cortex (Pickles p o & Simmonds, 1978;Brown & Galvan, 1979;Brown & Scholfield, 1979;Collins, 1979;Scholfield, 1980;Scholfield, 1982); therefore the former explanation (Collins et al, 1982) or cerebral cortex (Potashner, 1978) suggesting that baclofen acts before the…”

Section: Effect Ofbaclofen On Synaptic Responsesmentioning

confidence: 99%

Baclofen blocks postsynaptic inhibition but not the effect of muscimol in the olfactory cortex

Scholfield

1983

British J Pharmacology

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1The olfactory cortex slice preparation from the guinea-pig brain was used to study the effects of baclofen on inhibition using intracellular recording. Stimulation of the lateral olfactory tract activates sequentially excitatory and inhibitory pathways. Inhibition is manifest as a period of increased membrane conductance (termed postsynaptic inhibitory conductance, IPSC).2 Bath application of baclofen (0.2-50011M) reversibly blocked the IPSC. Baclofen also produced a secondary increase in the amplitude and duration of the initial excitatory postsynaptic potential.3 Baclofen (0.5-500 tM) slightly augmented the ability of bath-applied muscimol to increase the resting membrane conductance. Baclofen had no effect on cell excitability and membrane potential and no effect on the action of 'y-aminobutyric acid (GABA), noradrenaline, glycine, taurine or 5-hydroxytrypamine. 4 These results confirm previous suggestions that baclofen at low concentrations acts outside the GABA receptor mediating the IPSC perhaps by reducing the release of the excitatory transmitter activating the inhibitory interneurones.

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“…terminals (Pickles, 1979), and that it is released from the olfactory cortex during l.o.t. stimulation (Collins, 1979).…”

Section: Discussionmentioning

confidence: 99%

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

Cain¹,

Simmonds²

1982

The Journal of Physiology

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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.

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Evidence of a neurotransmitter role for aspartate and γ‐aminobutyric acid in the rat olfactory cortex

Cited by 98 publications

References 17 publications

NMDA antagonists increase recovery of evoked potentials from slices of rat olfactory cortex after anoxia

NMDA antagonists increase recovery of evoked potentials from slices of rat olfactory cortex after anoxia

Baclofen blocks postsynaptic inhibition but not the effect of muscimol in the olfactory cortex

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

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