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A Constanti

Publications and source records attributed to A Constanti.

87 records · Page 5Linked to original sources
PubMed1978

A study of the interactions between glutamate and aspartate at the lobster neuromuscular junction.

The depolarization produced by bath-applied or iontophoretically applied glutamate and aspartate were recorded from lobster muscle fibres by means of intracellular microelectrodes. 2 Bath-applied glutamate or aspartate evoked reversible, membrane depolarizations; however, responses to repeated applications of aspartate decreased progressively in amplitude until a plateau level was attained. Repeated applications of glutamate, kainate, domoate or quisqualate did not produce a similar effect. 3 After a dose of glutamate, responses to bath-applied aspartate were enhanced. Responses to other depolarizing agonists were little affected by previous administration of glutamate. Aspartate dose-depolarization curves were therefore constructed after initial aspartate responses had stabilized. The log-log transforms of the aspartate and glutamate curves had limiting slopes of 0.8 and 2.1 respectively. 4 Iontophoretic application of aspartate to single glutamate-sensitive sites produced small depolarizations with slow time course, compared with the glutamate potentials. When aspartate and glutamate were pulsed simultaneously from a twin-barrelled pipette, the resultant glutamate potential was enhanced. It is suggested that this potentiation was due to summation of agonist concentrations in the receptor region interacting with a second-order dose-response relationship. 5 Bath-applied aspartate increased the amplitude and prolonged the half-decay time of the glutamate potential. This effect was particularly noticeable when the glutamate potential was of slow time course. 6 It is proposed that bath-applied aspartate has an agonist effect whose magnitude is possibly exaggerated by concomitant release of glutamate and/or inhibition by glutamate of aspartate uptake. This agonist action of aspartate is thought to be exerted mainly on extrajunctional areas of the glutamate-sensitive sites.

Animals↗
PubMed1978

Interaction of pentobarbitone and gamma-aminobutyric acid on mammalian sympathetic ganglion cells.

1. Interactions of bath-applied pentobarbitone and gamma-aminobutyric acid (GABA) on neurones in isolated superior cervical ganglia of the rat have been examined with intracellular microelectrodes. 2. Pentobarbitone itself (30 micrometer-1 mM) showed no clear or consistent GABA-like effects: changes in resting input conductance and membrane potential were small and variable. 3. Pentobarbitone (100 micrometer) strikingly enhanced the conductance increases produced by GABA and 3-aminopropanesulphonic acid, and reversed the depression of GABA-evoked responses by bicuculline. 4. It is concluded that reversal of bicuculline action at the membrane conductance level might be explained by augmentation of GABA-action. This augmentation cannot be attributed to 'partial agonist' properties of pentobarbitone or to interference with glial transport processes.

Aminobutyrates↗
PubMed1976

A comparative study of the action of gamma-aminobutyric acid and piperazine on the lobster muscle fibre and the frog spinal cord.

1 The effects of gamma-aminobutyric acid (GABA) and piperazine were compared on two in vitro preparations, the lobster muscle fibre and the frog spinal cord. 2 Both GABA and piperazine increased the membrane conductance of single lobster muscle fibres without changing the membrane potential; sigmoidal log dose-conductance curves for these agents were obtained and a similar model expressed the receptor interaction of both substances. 3 The actions of GABA and piperazine on lobster muscle were antagonized by picrotoxin and were Cl-dependent. 4 In the frog spinal cord GABA depolarized the dorsal roots presumably by mimicking the activity of the transmitter depolarizing the primary afferents; sigmoidal log dose-response curves for GABA were obtained. 5 On the dorsal roots piperazine produced either depolarizations or biphasic responses; these were mainly indirect effects as was shown by experiments in the presence of tetrodotoxin (TTX). 6 The effects of GABA on the dorsal root (in TTX-treated cords) were antagonized by picrotoxin whereas those of piperazine were more resistant to this alkaloid. The GABA-induced responses appeared to be largely Na+-dependent while both Na+ and Cl- seemed to mediate the effects of piperazine. 7 It is proposed that piperazine has GABA-agonist activity on lobster muscle but little GABA-like activity on the frog spinal cord.

Aminobutyrates↗
PubMed1976

A comparative study of the effects of glutamate and kainate on the lobster muscle fibre and the frog spinal cord.

1 The depolarizing actions of glutamate and its conformationally restricted analogue kainate were investigated on the lobster muscle fibre and the frog spinal cord using intracellular and extracellular recordings, respectively. 2 Bath-applied kainate was less potent than glutamate on the lobster fibre but more potent on the frog cord. From the log-log transformation of dose-response curves it was proposed that more than one glutamate molecule was necessary to activate both the lobster and the frog receptor sites. In the frog, at least three kainate molecules were thought to be required for receptor activation. 3 The ionic dependence of glutamate and kainate responses appeared different for the two tissues. 4 Some possible explanations of the differential tissue sensitivity to kainate are discussed.

Animals↗
PubMed1976

Antagonism by some antihistamines of the amino acid-evoked responses recorded from the lobster muscle fibre and the frog spinal cord.

1 The effects of some antihistamines on the lobster muscle fibre and the frog spinal cord were investigated using intracellular and extracellular recordings, respectively. 2. On lobster muscle, histamine H1-blockers reversibly antagonized responses to bath-applied glutamate, aspartate and quisqualate but not responses to gamma-aminobutyric acid (GABA). Iontophoretic glutamate potentials were also reduced. Histamine (up to 1 mM) had no effect on this preparation. 3 The H1-antagonists produced a small increase in muscle membrane conductance and a slight hyperpolarization. These effects were largely unchanged in a low C1- bathing solution. Procaine (1 mM) decreased membrane conductance and did not affect responses to GABA or glutamate. 4 The H2-antagonist burimamide blocked both glutamate and GABA-evoked responses on the lobster muscle without affecting resting potential or conductance. 5 In the frog cord, bath-applied histamine produced ventral root depolarizations and dorsal root hyperpolarizations (sometimes biphasic responses). These effects were reduced by tetrodotoxin (TTX) but not by antazoline (H1-blocker) or burimamide; the latter reversibly antagonized responses to both glutamate and GABA on TTX-treated cords while antazoline was ineffective. 6 It is suggested that antihistamines can act as non-specific amino acid antagonists by interacting at the level of the receptor-coupled ionophores.

Amino Acids↗
PubMed1975

Effects of glutamate and glutamic acid diethyl ester on the lobster muscle fibre and the frog spinal cord.

The effect of bath applications of glutamic acid diethyl ester (GDE) and glutamate on the lobster muscle fibre and the from spinal cord were examined. In the lobster muscle fibre GDE (2 X 10(-3) M) did not antagonize the depolarizing action of glutamate (10(-4) M). In the frog spinal cord a small reduction in the excitatory effects of glutamate (10(-4)-10(-3) M) after GDE pretreatment was found only if the latter was given in very high doses (over 2 X 10(-3) M) which stimulated the neuronal firing. These observations show that GDE is not a specific antagonist of glutamate in these tissues.

Action Potentials↗
PubMedDate not supplied

Expression of functional GABA, glycine and glutamate receptors in Xenopus oocytes injected with rat brain mRNA.

The use of Gurdon's Xenopus oocyte translation system has allowed the production of neurotransmitter receptors in a foreign cell membrane, following the translation of microinjected mRNA isolated from various sources. This very accessible and relatively simple preparation permits the study of the requirements for receptor-ionophore function, assembly and membrane integration. This analysis is presently feasible for the peripheral nicotinic acetylcholine receptor, the chick brain gamma-aminobutyrate (GABA) receptor and the rat brain serotonin receptor. We now report the novel and successful expression of the GABA, glycine, glutamate and related acidic amino acid receptors of mammalian brain, and show that they exhibit pharmacologically separate identities when their mRNAs are processed in the amphibian oocyte.

Animals↗
PubMedDate not supplied

Carbachol-evoked suppression of excitatory neurotransmission in guinea-pig olfactory cortex slices is unlikely to involve an M4-muscarinic receptor subtype.

Depression of the electrically-evoked surface-negative field potential (N-Wave) by bath-superfusion of carbachol was measured in guinea-pig olfactory cortex slices maintained in vitro. The possibility that this response, previously proposed to be mediated via a presynaptic M1: muscarinic receptor, might in fact be due to M4 receptor activation, was investigated by testing the effectiveness of himbacine (a proposed M4-selective antagonist) on our cortical preparation. Himbacine (100 nM-1 microM) had no effect on the N-wave potential alone, but it induced a clear competitive-type inhibition of carbachol effects. Schild plot analysis (regression slope constrained to unity) of pooled data yielded a pA2 value of 7.2 for this antagonist (n = 7 slices). This value accords more with that expected for the interaction of himbacine with M1 receptors (approximately 7.2) than with functionally expressed M4 receptors (approximately 8.5-8.5). We therefore conclude that M4-type muscarinic receptors are unlikely to be involved in mediating this presynaptic carbachol response.

Alkaloids↗