Autoradiographic Localization and Characterization of Adenosine Receptor Subtypes in Mammalian Brain

1991 ◽  
Vol 10 (5) ◽  
pp. 993-1001 ◽  
Author(s):  
Michael F. Jarvis
Keyword(s):  
Adenosine Receptor ◽  
Mammalian Brain ◽  
Receptor Subtypes

Comparative pharmacology of human adenosine receptor subtypes – characterization of stably transfected receptors in CHO cells

1997 ◽  
Vol 357 (1) ◽  
pp. 1-9 ◽  
Author(s):  
K.-N. Klotz ◽  
J. Hessling ◽  
J. Hegler ◽  
C. Owman ◽  
B. Kull ◽  
...  
Keyword(s):  
Adenosine Receptor ◽  
Cho Cells ◽  
Receptor Subtypes

Characterization of adenosine receptor(s) involved in adenosine-induced bronchoconstriction in an allergic mouse model

2003 ◽  
Vol 284 (6) ◽  
pp. L1012-L1019 ◽  
Author(s):  
Ming Fan ◽  
Weixi Qin ◽  
S. Jamal Mustafa
Keyword(s):  
Mouse Model ◽  
Adenosine Receptor ◽  
Receptor Subtypes ◽  
Dependent Manner ◽  
Transcript Levels ◽  
Allergen Sensitization ◽  
Selective Agonist ◽  
Dose Dependent ◽  
Allergic Mouse

We recently reported that adenosine caused bronchoconstriction and enhanced airway inflammation in an allergic mouse model. In this study, we further report the characterization of the subtype of adenosine receptor(s) involved in bronchoconstriction. 5′-( N-ethylcarboxamido)adenosine (NECA), a nonselective adenosine agonist, elicited bronchoconstriction in a dose-dependent manner. Little effects of N 6-cyclopentyladenosine (A1-selective agonist) and 2- p-(2-carboxyethyl)phenethylamino-5′- N-ethylcarboxamidoadenosine (A2A-selective agonist) compared with NECA were observed in this model. 2-Chloro- N 6-(3-iodobenzyl)-9-[5-(methylcarbamoyl)-β-d-ribofuranosyl]adenosine, an A3-selective receptor agonist, produced a dose-dependent bronchoconstrictor response, which was blocked by selective A3 antagonist 2,3-diethyl-4,5-dipropyl-6-phenylpyridine-3-thiocarboxylate-5-carboxylate (MRS1523). However, MRS1523 only partially inhibited NECA-induced bronchoconstriction. Neither selective A1 nor A2A antagonists affected NECA-induced bronchoconstriction. Enprofylline, a relatively selective A2B receptor antagonist, blocked partly NECA-induced bronchoconstriction. Furthermore, a combination of enprofylline and MRS1523 completely abolished NECA-induced bronchoconstrictor response. Using RT-PCR, we found that all four adenosine receptor subtypes are expressed in control lungs. Allergen sensitization and challenge significantly increased transcript levels of the A2B and A3receptors, whereas the A1 receptor message decreased. No change in transcript levels of A2A receptors was observed after allergen sensitization and challenge. These findings suggest that A2B and A3 adenosine receptors play an important role in adenosine-induced bronchoconstriction in our allergic mouse model. Finally, whether the airway effects of the receptor agonists/antagonists are direct or indirect needs further investigations.

Neurochemistry of L-Glutamate Transport in the CNS: A Review of Thirty Years of Progress

2001 ◽  
Vol 66 (9) ◽  
pp. 1315-1340 ◽  
Author(s):  
Vladimir J. Balcar ◽  
Akiko Takamoto ◽  
Yukio Yoneda
Keyword(s):  
Molecular Biology ◽  
Glutamate Transport ◽  
Mammalian Brain ◽  
Activity Data ◽  
System A ◽  
Recent Developments ◽  
The Central Nervous System ◽  
Health And Disease ◽  
Disease Analysis

The review highlights the landmark studies leading from the discovery and initial characterization of the Na+-dependent "high affinity" uptake in the mammalian brain to the cloning of individual transporters and the subsequent expansion of the field into the realm of molecular biology. When the data and hypotheses from 1970's are confronted with the recent developments in the field, we can conclude that the suggestions made nearly thirty years ago were essentially correct: the uptake, mediated by an active transport into neurons and glial cells, serves to control the extracellular concentrations of L-glutamate and prevents the neurotoxicity. The modern techniques of molecular biology may have provided additional data on the nature and location of the transporters but the classical neurochemical approach, using structural analogues of glutamate designed as specific inhibitors or substrates for glutamate transport, has been crucial for the investigations of particular roles that glutamate transport might play in health and disease. Analysis of recent structure/activity data presented in this review has yielded a novel insight into the pharmacological characteristics of L-glutamate transport, suggesting existence of additional heterogeneity in the system, beyond that so far discovered by molecular genetics. More compounds that specifically interact with individual glutamate transporters are urgently needed for more detailed investigations of neurochemical characteristics of glutamatergic transport and its integration into the glutamatergic synapses in the central nervous system. A review with 162 references.

In Vivo Characterization of Muscarinic Receptor Subtypes That Mediate Vasodilatation in Patients With Essential Hypertension

Hypertension ◽  
1995 ◽  
Vol 26 (1) ◽  
pp. 70-77 ◽  
Author(s):  
Tobias A. Bruning ◽  
Peter C. Chang ◽  
Maarten G.C. Hendriks ◽  
Pieter Vermeij ◽  
Martin Pfaffendorf ◽  
...  
Keyword(s):  
Essential Hypertension ◽  
Muscarinic Receptor ◽  
Receptor Subtypes ◽  
Muscarinic Receptor Subtypes ◽  
In Vivo Characterization

Functional Characterization of GABAA Receptors in Neonatal Hypothalamic Brain Slice

2002 ◽  
Vol 88 (4) ◽  
pp. 1655-1663 ◽  
Author(s):  
Ren-Qi Huang ◽  
Glenn H. Dillon
Keyword(s):  
Functional Characterization ◽  
Minor Component ◽  
Dehydroepiandrosterone Sulfate ◽  
Receptor Subtypes ◽  
Hypothalamic Neurons ◽  
Inhibitory Neurotransmitter ◽  
Old Rats ◽  
A Minor ◽  
Whole Cell Recordings

The hypothalamus influences a number of autonomic functions. The activity of hypothalamic neurons is modulated in part by release of the inhibitory neurotransmitter GABA onto these neurons. GABAA receptors are formed from a number of distinct subunits, designated α, β, γ, δ, ε, and θ, many of which have multiple isoforms. Little data exist, however, on the functional characteristics of the GABAA receptors present on hypothalamic neurons. To gain insight into which GABAA receptor subunits are functionally expressed in the hypothalamus, we used an array of pharmacologic assessments. Whole cell recordings were made from thin hypothalamic slices obtained from 1- to 14-day-old rats. GABAA receptor-mediated currents were detected in all neurons tested and had an average EC50 of 20 ± 1.6 μM. Hypothalamic GABAA receptors were modulated by diazepam (EC50 = 0.060 μM), zolpidem (EC50 = 0.19 μM), loreclezole (EC50 = 4.4 μM), methyl-6,7-dimethoxy-4-ethyl-β-carboline (EC50= 7.7 μM), and 5α-pregnan-3α-hydroxy-20-one (3α-OH-DHP). Conversely, these receptors were inhibited by Zn2+ (IC50 = 70.5 μM), dehydroepiandrosterone sulfate (IC50 = 16.7 μM), and picrotoxin (IC50 = 2.6 μM). The α4/6-selective antagonist furosemide (10–1,000 μM) was ineffective in all hypothalamic neurons tested. The results of our pharmacological analysis suggest that hypothalamic neurons express functional GABAA receptor subtypes that incorporate α1 and/or α2 subunits, β2 and/or β3 subunits, and the γ2 subunit. Our results suggest receptors expressing α3–α6, β1, γ1, and δ, if present, represent a minor component of functional hypothalamic GABAA receptors.

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