Distinct pharmacological properties of excitatory amino acid receptors in the rat striatum: study by Na+ efflux assay.

Luini, Alberto; Goldberg, Ora; Teichberg, Vivian I.

doi:10.1073/pnas.78.5.3250

Cited by 64 publications

(12 citation statements)

References 31 publications

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“…Most authors agree that they constitute at least two classes (Watkins & Evans, 1981;Fagg, 1985;Mayer & Westbrook, 1987;Watkins & Olverman, 1987) but some authors have proposed the existence of three classes of 'non-NMDA' receptors (see, e.g. Luini, Goldberg & Teichberg, 1981;Fagni, Baudry & Lynch, 1983;Surtees & Collins, 1985;Davies & Watkins, 1985), while nt the other extreme the very distinction between NMDA and 'non-NMDA' receptors has been questioned (Jahr & Stevens, 1987).…”

Section: Introductionmentioning

confidence: 99%

Quisqualate‐ and kainate‐activated channels in mouse central neurones in culture.

Ascher

Nowak

1988

The Journal of Physiology

187

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SUMMARY1. Quisqualate-and kainate-induced currents were recorded in mouse central neurones in culture, using both 'whole-cell' and 'outside-out' configurations. Experiments were made.at room temperature.2. Both quisqualate-and kainate-induced currents invert at 0 mV when the extracellular and intracellular solutions contain similar concentrations of monovalent cations. The changes of reversal potential produced by changes in the monovalent cation concentrations are consistent with the hypothesis that both agonists activate channels selectively permeable to cations.3. The spectral analysis of the quisqualate-and kainate-induced currents recorded in the whole-cell mode indicates that the main component of the quisqualate noise has a time constant of 10-15 ms while the main component of the kainate noise has a time constant of 2-3 ms.4. In outside-out patches most of the quisqualate-induced current was carried by channels with a conductance of about 8 pS. A small fraction of the quisqualateinduced current appears to be carried by two other channels: the 'NMDA channel' (40-50 pS) (Ascher, Bregestovski & Nowak, 1988) and a 'fast' channel, with a conductance of 15-35 pS, which was not activated by low concentrations of Lglutamate or by NMDA (N-methyl-D-aspartate).5. Most of the kainate-induced current can be attributed to a channel characterized by a conductance of about 4 pS. Here again, outside-out patches revealed the presence of an additional channel, with a conductance of about 20 pS.6. The results are consistent with the notion that there are at least three distinct receptors for excitatory amino acids, each preferentially activated by either NMDA, quisqualate or kainate, each opening channels with multiple conductance states. Other possibilities are discussed.

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Section: Introductionmentioning

confidence: 99%

Quisqualate‐ and kainate‐activated channels in mouse central neurones in culture.

Ascher

Nowak

1988

The Journal of Physiology

187

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“…1) coupled with biochemical processes acting as signal transducers (2)(3)(4)(5)(6)(7). We have recently reported (8) that a specific excitatory amino acid recognition site, sensitive to the inhibitory action of 2-amino-4-phosphonobutanoate (APB), is coupled with phosphatidylinositol (Ptdlns) metabolism in the rat hippocampus.…”

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confidence: 99%

Excitatory amino acid recognition sites coupled with inositol phospholipid metabolism: developmental changes and interaction with alpha 1-adrenoceptors.

Nicoletti¹,

Iadarola²,

Wroblewski³

et al. 1986

Proc. Natl. Acad. Sci. U.S.A.

311

138

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Glutamate, aspartate, ibotenate, and quisqualate activate inositol phospholipid hydrolysis in hippocampal slices prepared from brains of 6-to 8-day-old rats.The stimulation by glutamate and aspartate progressively declines during postnatal development and is negligible after the 24th day of life. In contrast, the stimulation of inositol phospholipid hydrolysis by norepinephrine is low in hippocampal slices from newborn animals and increases during development, reaching mature values after the 35th day of life. In adult hippocampal slices, the stimulation of inositol phospholipid hydrolysis elicited by norepinephrine is inhibited by glutamate in a concentration-dependent fashion. This inhibition can also be brought about by aspartate, 2-amino-4-phosphonobutanoate, and L-phosphoserine, a product ofendogenous phosphatidylserine hydrolysis. ([3H]Ins-1-P) in brain slices treated with Li'. Li' has been found to block the conversion of [3H]Ins-1-P into inositol by inhibiting the enzyme inositol-1-phosphatase (9, 10).Sprague-Dawley rats of various ages (6,8,12,15,19,24, and 35 days) were decapitated. The brains were rapidly removed from the skulls and dissected on ice. Hippocampus, corpus striatum, cerebral cortex, and hypothalamus were sliced (350 x 350 ,m) with a McIlwain tissue chopper, and the slices immediately were suspended in Krebs-Hensleit buffer (118 mM NaCl/4.7 mM KCl/1.3 mM CaCl2/1.2 mM K2HPO4/1.2 mM MgSO4/25 mM NaHCO3/11.7 mM glucose, equilibrated with 95%02/5% CO2 to raise the pH to 7.4) and incubated at 37°C for 30-45 min with three intermediate changes of the buffer. Forty microliters of gravitypacked slices were then transferred to 3-ml vials containing 0.3 ,M myo-[2-3H]inositol (New England Nuclear, specific activity 16.5 Ci/mmol; 1 Ci = 37 GBq) in a final volume of 275 ,ul. After 60 min of incubation, LiCl (7 mM) was added, followed, 20 min later, by transmitter receptor agonists. Antagonists were sometimes added 5 min prior to the agonists. After 60 min, the slices were washed three times with buffer and the reaction (cleavage of inositol phosphates from membrane phospholipids) was stopped by addition of 0.9 ml of chloroform/methanol (1:2). Identical results were obtained when slices were washed free of [3H]inositol before the addition of transmitter receptor agonists. The content of [3H]Ins-1-P was determined according to Berridge et al. (10). Proteins were measured as described by Lowry et al. (11). al-Adrenergic Receptor Binding Assay. The characteristics of a1-adrenergic recognition sites were studied in crude synaptic membranes prepared from rat hippocampus, using [3H]prazosin as a selective ligand, as described (12). RESULTS Age-Dependent Stimulation of PtdIns 1931The publication costs of this article were defrayed in part by page charge payment. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. §1734 solely to indicate this fact.

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“…It was hypothesized that glutamate depolarizes the neuronal membrane via an increase in Na + conductance [78,187,277]. The glutamate effect on neuronal activity can be antagonized by many varieties of dipeptide, such as γ-Dglutamyglycine (DGG) and L -glutamic acid diethyl ester (GDEE).…”

Section: Classification Of Glutamate Agonistsmentioning

confidence: 99%

Sensory-Motor Integration in the Medial Medulla

Lai¹,

Siegel²

2005

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The rostromedial medulla, including the nucleus gigantocellularis (NGC) and magnocellularis (NMC), plays a role as a relay nucleus for both the sensory and motor systems. The NGC/NMC is important in the modulation of somatic and visceral activities. Electrophysiological and pharmacological studies have shown that the NGC/NMC is involved in nociception, locomotion, regulation of basal muscle tone, sleep, as well as cardiovascular and pulmonary activities. Pharmacological and electrical stimulation of the NGC/NMC can produce opposite effects on physiological functions: analgesia or hyperalgesia, and suppression or facilitation of motor activity, depending on the subgroups of neurons activated and the states of the sleep-wake cycle at the time of stimulation. Sensory inputs including noxious and innocuous stimuli converge on the NGC/NMC. The NGC/NMC also plays a role as a relay nucleus, which sends sensory information to the higher centers. The NGC/NMC receives projections from the supra-bulbar motor facilitatory and inhibitory areas, and plays an important role in the regulation of motor activity. Pharmacologically, neurons in the NGC/NMC contribute to opioid, glutamate, GABA, acetylcholine, dopamine, substance P, neurotensin, hypocretin (orexin), and cannabinoid mediated sensory and motor activities, as well as cardiovascular and pulmonary functions. In this review, we will discuss the neuronal morphology, physiological functions and pharmacological characterization of the rostromedial medulla. We will consider the evidence that dysfunction of the NGC/NMC is a factor in a number of neurological diseases, including Parkinson's disease, restless legs syndrome, periodic leg movement, REM sleep behavior disorder, amyotrophic lateral sclerosis and narcolepsy. INTRODUNTIONThe medullary reticular formation is traditionally segregated into the medial somatic-and lateral visceralrelated areas. However, somatic and autonomic activities are well coordinated. For example, cardiovascular-respiratory changes are correlated with somatic sensory-motor activity during exercise. Coordination of somatic and autonomic activity can result from interconnections between somatic and autonomic control structures, as well as interactions within nuclei, which are involved in both somatic and autonomic activities. The rostromedial medulla (RMM) is one of the areas of the central nervous system (CNS) that is involved in both somatic and autonomic regulation. However, the RMM has traditionally been considered as a somatic nociceptive and a motor control area. The autonomic role of the RMM has received little attention, although Bach [22] demonstrated that the activation of RMM causes changes in cardiovascular and respiratory activity, as well as the facilitation and inhibition of somatic motor activity in 1952. Therefore, we will discuss the functional aspects of RMM in the modulation of both somatic and autonomic systems in this review. Section 1 will focus on the morphology of the RMM, and the anatomical link between RMM and the other areas...

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Distinct pharmacological properties of excitatory amino acid receptors in the rat striatum: study by Na+ efflux assay.

Abstract: Specific 22Na' efflux rates from preloaded rat striatal slices are increased in a dose-dependent manner by L-glutamate and other excitatory amino acids displaying the following order of efficiency:

Cited by 64 publications

References 31 publications

Quisqualate‐ and kainate‐activated channels in mouse central neurones in culture.

Quisqualate‐ and kainate‐activated channels in mouse central neurones in culture.

Excitatory amino acid recognition sites coupled with inositol phospholipid metabolism: developmental changes and interaction with alpha 1-adrenoceptors.

Sensory-Motor Integration in the Medial Medulla

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