Receptor types mediating the excitatory actions of exogenousl-aspartate andl-glutamate in rat olfactory cortex

4 Similar amino acid-induced depolarizations were observed in slices of just the CA1 region or in whole slices bathed in tetrodotoxin. Isolated alvear fibres, however, were insensitive to the excitatory amino acids. 5 D-2-Amino-5-phosphonovalerate (APV, 50pM) selectively and reversibly antagonized responses induced by NMDA (apparent pA2 = 5.21). 6 Kynurenic acid (1 mM) reversibly depressed responses to the three agonists tested. The doseratios for antagonism of AMPA, kainate and quisqualate were 6.9, 5.6 and 4.6 respectively. 7 This preparation has a different sensitivity profile to agonists from those of previously reported preparations of spinal cord, neocortex and cerebellum. The greater sensitivity to NMDA may be due to the higher density of NMDA receptors in the hippocampus. The effects of the antagonists, APV and kynurenate, are similar to those found in other brain areas.

“…Quantitative pharmacological data of a similar type have also been obtained from olfactory cortex by use of a wick electrode technique (e.g. Surtees & Collins, 1985).…”

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

A quantitative study of the actions of excitatory amino acids and antagonists in rat hippocampal slices

Blake

Brown

Collingridge

1988

“…Second, although there is controversy regarding the identity of the LOT transmitter(s) (ffrench-Mullen et al, 1985;Collins, 1986), APB Amplitude of conditioning response (mV) Figure 6 Drug effects on the increase in synaptic facilitation produced by 2-amino-4-phosphonobutyrate (APB) (1 mM). Each point is the mean % facilitation (n between 3 and 6) measured at fixed amplitudes of the conditioning response in slices stimulated at a constant conditioning interval of 100 ms. For clarity, the s. (Surtees & Collins, 1985;Collins & Brown, 1986). Even if the identities of the LOT transmitters are at fault, antagonism of postsynaptic receptors by APB would seem unlikely for it has been reported that at the perforant-path-dentate gyrus of the hippocampus, a site which also exhibits synaptic facilitation, postsynaptic receptor blockers reduce conditioning and test responses equally (Harris & Cotman, 1985).…”

Section: Discussionmentioning

confidence: 99%

“…When applied to olfactory cortex slices, APB depresses transmission at the lateral olfactory tract (LOT)-superficial pyramidal cell synapse (Collins, 1982;Hon et al, 1982;Hearn et al, 1986), a site at which glutamate and/or aspartate are neurotransmitter candidates (Collins, 1986). Although a potent antagonist of synaptic transmission in the olfactory cortex, APB does not block the postsynaptic actions of glutamate and aspartate (Hori et al, 1982;Surtees & Collins, 1985;Collins & Brown, 1986) suggesting that either the identification of the LOT transmitter is at fault or, perhaps, that APB has a presynaptic site of action (Harris & Cotman, 1983).…”

Section: Introductionmentioning

confidence: 99%

Possible presynaptic actions of 2‐amino‐4‐phosphonobutyrate in rat olfactory cortex

Anson

Collins

1987

Self Cite

1 The effect of 2-amino-4-phosphonobutyrate (APB) on facilitation at the lateral olfactory tract (LOT)-superficial pyramidal cell synapse of the olfactory cortex has been studied by recording the relative changes in amplitude of the N-waves evoked on stimulation of the LOT by pairs of stimuli. 2 Although APB (0.01 to 5 mM) reduced the amplitude of the conditioning response there was an overall increase in facilitation over conditioning intervals of up to 1700 ms which was concentrationdependent and inversely related to the concentration of extracellular calcium (1.25 to 5 mM). 3 The L-(+ )-isomer ofAPB was more potent than the D-(-)-form in increasing synaptic facilitation. 4 The potassium channel blockers 4-aminopyridine (0.25mM), 3,4-diaminopyridine (0.1mM), tetraethylammonium (10 mM) and catechol (1 mM) all reduced facilitation but failed to antagonize the increase in facilitation produced by APB (I mM). In contrast, all 4 drugs antagonized APB-induced reductions in the amplitude of the conditioning response. 5 APB (1 mM) significantly reduced the K+-evoked release of endogenous aspartate and glutamate but not of y-aminobutryic acid from slices of olfactory cortex. 6 It is suggested that APB reduces the amplitude of the conditioning response and increases synaptic facilitation by reducing transmitter release from the LOT terminals. The mechanism is unlikely to involve activation of terminal potassium currents.

“…In some experiments, agonist-evoked changes in the d.c. potential across slices were monitored using the technique described by Brown & Galvan (1979) as modified by Surtees & Collins (1985). In principle, extracellular electrodes measure the potential difference across 500pm thick slices; when an excitant drug is applied to one surface of the slice it will l depolarize neurones adjacent to that surface which will therefore become negative with respect to the other surface.…”

Section: Measurement Of Agonist-evoked Depolarizationsmentioning

confidence: 99%

Sites and mechanisms of action of catechol (1,2‐dihydroxybenzene) in the rat olfactory cortex slice

Collins

Dewhurst

1986

1 Synaptic transmission in the isolated olfactory cortex slice from the rat was monitored by recording the surface field potentials evoked on lateral olfactory tract (LOT) stimulation. Catechol (approximately 0.05 to 2 mM) caused a concentration-dependent, partially reversible increase in the amplitudes of all field potentials. 2 In a series of conditioning experiments, catechol (1 mM) potentiated postsynaptic inhibition by a mechanism which was at least partially picrotoxin-insensitive. 3 When the relationship between the stimulus input and evoked output was investigated in picrotoxin-treated slices, for a given tract action potential amplitude, catechol (0.25 and 0.5 mM) increased the amplitude of the field potential known as the N-wave; in contrast, for a given N-wave amplitude, the latency of the population spike was increased. 4 Catechol (1 mM) increased the K+-evoked release of endogenous aspartate by a tetrodotoxininsensitive mechanism whereas the release of glutamate and 'y-aminobutyric acid (GABA) was unaffected. 5Catechol (1 mM) had no effect on submaximal depolarizations evoked by L-aspartate, L-glutamate or GABA. 6 It is concluded that catechol potentiates excitatory transmission at the LOT-superficial pyramidal cell synapse, possibly by increasing evoked transmitter release. Other synaptic actions of catechol may be consequent upon this increased excitatory input but the results do not exclude the possibility of separate and distinct actions on polysynaptic transmission.