Neural mechanisms underlying peak-dose dyskinesia induced by levodopa and apomorphine are distinct: Evidence from the effects of the alpha2 adrenoceptor antagonist idazoxan

2001 ◽  
Vol 16 (4) ◽  
pp. 642-650 ◽  
Author(s):  
Susan H. Fox ◽  
Brian Henry ◽  
Micheal P. Hill ◽  
David Peggs ◽  
Alan R. Crossman ◽  
...  
Keyword(s):  
Neural Mechanisms ◽  
Adrenoceptor Antagonist ◽  
Peak Dose ◽  
Alpha2 Adrenoceptor

scholarly journals The selectivity of DG-5128 as a new alpha2-adrenoceptor antagonist

1984 ◽  
Vol 36 ◽  
pp. 243
Author(s):  
Kyozo Yamanaka ◽  
Masafumi Oshita ◽  
Shigeru Kigoshi ◽  
Ikunobu Muramatsu
Keyword(s):  
Adrenoceptor Antagonist ◽  
Alpha2 Adrenoceptor

CGS 7525A, A new, centrally active alpha2 adrenoceptor antagonist

Life Sciences ◽  
1983 ◽  
Vol 32 (4) ◽  
pp. 355-363 ◽  
Author(s):  
Jeffrey M. Liebman ◽  
Richard A. Lovell ◽  
Albert Braunwalder ◽  
George Stone ◽  
Patrick Bernard ◽  
...  
Keyword(s):  
Adrenoceptor Antagonist ◽  
Alpha2 Adrenoceptor

Evidence for activation of both adrenergic and cholinergic nervous pathways by yohimbine, an alpha2-adrenoceptor antagonist

1995 ◽  
Vol 9 (3) ◽  
pp. 248-254 ◽  
Author(s):  
H. Bagheri ◽  
JJ Chale ◽  
LN Guyen ◽  
MA Tran ◽  
M. Berlan ◽  
...  
Keyword(s):  
Adrenoceptor Antagonist ◽  
Alpha2 Adrenoceptor

scholarly journals The Alpha2-Adrenoceptor Antagonist Dexefaroxan Enhances Hippocampal Neurogenesis by Increasing the Survival and Differentiation of New Granule Cells

2005 ◽  
Vol 31 (6) ◽  
pp. 1146-1157 ◽  
Author(s):  
Pamela Rizk ◽  
Julio Salazar ◽  
Rita Raisman-Vozari ◽  
Marc Marien ◽  
Merle Ruberg ◽  
...  
Keyword(s):  
Granule Cells ◽  
Hippocampal Neurogenesis ◽  
Adrenoceptor Antagonist ◽  
Alpha2 Adrenoceptor

The Effect of Imidazoline Receptors and α2-adrenoceptors on the Anesthetic Requirement (MAC) for Halothane in Rats 

1997 ◽  
Vol 87 (4) ◽  
pp. 963-967 ◽  
Author(s):  
Kiyokazu Kagawa ◽  
Tadanori Mammoto ◽  
Yukio Hayashi ◽  
Takahiko Kamibayashi ◽  
Takashi Mashimo ◽  
...  
Keyword(s):  
Minimum Alveolar Concentration ◽  
Inhibitory Effect ◽  
Imidazoline Receptors ◽  
Adrenoceptor Antagonist ◽  
Adrenoceptor Agonist ◽  
Adrenoceptor Agonists ◽  
The Central Nervous System ◽  
Anesthetic Requirement ◽  
Alpha2 Adrenoceptor ◽  
Pharmacologic Actions

Background Recent evidences have documented that several pharmacologic actions of alpha2-adrenoceptor agonists are mediated via activation of not only alpha2-adrenoceptors, but also by imidazoline receptors, which are nonadrenergic receptors in the central nervous system. However, the effect of imidazoline receptors on the anesthesia is not well known, and it is important to clarify the effects of both receptors on anesthesia. Methods Seventy-two rats were anesthetized with halothane, and the anesthetic requirement for halothane was evaluated as minimum alveolar concentration (MAC). The MAC for halothane was determined in the presence of dexmedetomidine (0, 10, 20, and 30 microg/kg, intraperitoneally [IP]), a selective alpha2-adrenoceptor agonist with weak affinity for imidazoline receptors. Then, the authors evaluated the inhibitory effect of rauwolscine (20 mg/kg, IP), an alpha2-adrenoceptor antagonist with little affinity for imidazoline receptors, on the MAC-reducing action of dexmedetomidine (30 microg/kg). Further, the effect of rilmenidine (20, 50, 100, 1000 microg/kg, IP), a selective imidazoline receptor agonist, on the MAC for halothane was also investigated. Results Dexmedetomidine decreased the MAC for halothane dose-dependently, and this MAC-reducing action of dexmedetomidine was completely blocked by rauwolscine. Rilmenidine alone did not change the MAC for halothane. Conclusions The present data indicate that the anesthetic sparing action of dexmedetomidine is most likely mediated through alpha2- adrenoceptors, and the stimulation of imidazoline receptors exerts little effect on the anesthetic requirement for halothane.

scholarly journals Effects of the alpha2-adrenoceptor antagonist yohimbine on maternal behavior in lactating rats

1990 ◽  
Vol 52 ◽  
pp. 169
Author(s):  
Akiko Dohbutsu ◽  
Hakubun Inoue ◽  
Nobuyoshi Hayashi ◽  
Toru R. Saito ◽  
Kunie Kamata ◽  
...  
Keyword(s):  
Maternal Behavior ◽  
Adrenoceptor Antagonist ◽  
Alpha2 Adrenoceptor

scholarly journals Effects of Anesthesia and Species on the Uptake or Binding of Radioligands In Vivo in the Göttingen Minipig

2013 ◽  
Vol 2013 ◽  
pp. 1-9 ◽  
Author(s):  
Aage K. O. Alstrup ◽  
Anne M. Landau ◽  
James E. Holden ◽  
Steen Jakobsen ◽  
Anna C. Schacht ◽  
...  
Keyword(s):  
Blood Flow ◽  
Tracer Uptake ◽  
Adrenoceptor Antagonist ◽  
Positron Emission ◽  
Neuroscience Research ◽  
Initial Clearance ◽  
Alpha2 Adrenoceptor ◽  
Kinetics Of ◽  
Volumes Of Distribution

Progress in neuroscience research often involves animals, as no adequate alternatives exist to animal models of living systems. However, both the physiological characteristics of the species used and the effects of anesthesia raise questions of common concern. Here, we demonstrate the confounding influences of these effects on tracer binding in positron emission tomography (PET). We determined the effects of two routinely used anesthetics (isoflurane and propofol) on the binding of two tracers of monoamine function, [C11]SCH23390, a tracer of the dopamine D1 and D5 receptors, and the alpha2-adrenoceptor antagonist, [C11]yohimbine, in Göttingen minipigs. The kinetics of SCH23390 in the pigs differed from those of our earlier studies in primates. With two different graphical analyses of uptake of SCH23390, the initial clearance values of this tracer were higher with isoflurane than with propofol anesthesia, indicative of differences in blood flow, whereas no significant differences were observed for the volumes of distribution of yohimbine. The study underscores the importance of differences of anesthesia and species when the properties of radioligands are evaluated under different circumstances that may affect blood flow and tracer uptake. These differences must be considered in the choice of a particular animal species and mode of anesthesia for a particular application.

Isoflurane and Nociception

2002 ◽  
Vol 96 (2) ◽  
pp. 367-374 ◽  
Author(s):  
Wade S. Kingery ◽  
Geeta S. Agashe ◽  
Tian Z. Guo ◽  
Shigehito Sawamura ◽  
M. Frances Davies ◽  
...  
Keyword(s):  
Antinociceptive Effect ◽  
Spinal Pathways ◽  
Alpha Adrenoceptors ◽  
Adrenoceptor Antagonist ◽  
Dopamine Beta Hydroxylase ◽  
Inhalation Anesthetic ◽  
Antinociceptive Effects ◽  
Site Of Action ◽  
Mitochondrial Toxin ◽  
Alpha2 Adrenoceptor

Background The authors recently established that the analgesic actions of the inhalation anesthetic nitrous oxide were mediated by noradrenergic bulbospinal neurons and spinal alpha2B adrenoceptors. They now determined whether noradrenergic brainstem nuclei and descending spinal pathways are responsible for the antinociceptive actions of the inhalation anesthetic isoflurane, and which alpha adrenoceptors mediate this effect. Methods After selective lesioning of noradrenergic nuclei by intracerebroventricular application of the mitochondrial toxin saporin coupled to the antibody directed against dopamine beta hydroxylase (DbetaH-saporin), the antinociceptive action of isoflurane was determined. Antagonists for the alpha1 and alpha2 adrenoceptors were injected at spinal and supraspinal sites in intact and spinally transected rats to identify the noradrenergic pathways mediating isoflurane antinociception. Null mice for each of the three alpha2-adrenoceptor subtypes (alpha2A, alpha2B, and alpha2C) and their wild-type cohorts were tested for their antinociceptive response to isoflurane. Results Both DbetaH-saporin treatment and chronic spinal transection enhanced the antinociceptive effects of isoflurane. The alpha1-adrenoceptor antagonist prazosin also enhanced isoflurane antinociception at a supraspinal site of action. The alpha2-adrenoceptor antagonist yohimbine inhibited isoflurane antinociception, and this effect was mediated by spinal alpha2 adrenoceptors. Null mice for the alpha2A-adrenoceptor subtype showed a reduced antinociceptive response to isoflurane. Conclusions The authors suggest that, at clinically effective concentrations, isoflurane can modulate nociception via three different mechanisms: (1) a pronociceptive effect requiring descending spinal pathways, brainstem noradrenergic nuclei, and supraspinal alpha1 adrenoceptors; (2) an antinociceptive effect requiring descending noradrenergic neurons and spinal alpha2A adrenoceptors; and (3) an antinociceptive effect mediated within the spinal cord for which no role for adrenergic mechanism has been found.

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