Gain Regulation of the Vestibulospinal Reflex following Microinjection of a �-Adrenergic Agonist or Antagonist into the Locus Coeruleus and the Dorsal Pontine Reticular Formation1

2015 ◽  
pp. 134-141 ◽  
Author(s):  
G. Stampacchia ◽  
P. D�Ascanio ◽  
E. Horn ◽  
O. Pompeiano
Keyword(s):  
Locus Coeruleus ◽  
Adrenergic Agonist ◽  
Vestibulospinal Reflex

Perturbation of Ion Channel Conductance Alters the Hypnotic Response to the α2-Adrenergic Agonist Dexmedetomidine in the Locus Coeruleus of the Rat

1994 ◽  
Vol 81 (6) ◽  
pp. 1527-1534 ◽  
Author(s):  
Carla Nacif-Coelho ◽  
Christiane Correa-Sales ◽  
Louise Lenoir Chang ◽  
Mervyn Maze
Keyword(s):  
Ion Channel ◽  
Locus Coeruleus ◽  
Channel Conductance ◽  
Adrenergic Agonist

Reversal of behavioral depression by infusion of an alpha-2 adrenergic agonist into the locus coeruleus

1986 ◽  
Vol 25 (4) ◽  
pp. 385-389 ◽  
Author(s):  
Prudence G. Simson ◽  
Jay M. Weiss ◽  
Laura J. Hoffman ◽  
Monica J. Ambrose
Keyword(s):  
Locus Coeruleus ◽  
Adrenergic Agonist ◽  
Behavioral Depression

Sympatholytic and Minimum Anesthetic Concentration-sparing Responses are Preserved in Rats Rendered Tolerant to the Hypnotic and Analgesic Action of Dexmedetomidine, a Selective α2-adrenergic Agonist

1996 ◽  
Vol 85 (3) ◽  
pp. 565-573. ◽  
Author(s):  
Bradford C. Rabin ◽  
Kristina Reid ◽  
Tian-Zhi Guo ◽  
Eva Gustafsson ◽  
Chousheng Zhang ◽  
...  
Keyword(s):  
Locus Coeruleus ◽  
Chronic Administration ◽  
Adrenergic Agonist ◽  
Receptor Reserve ◽  
Anesthetic Concentration ◽  
Steep Part ◽  
Norepinephrine Turnover ◽  
Sparing Effect ◽  
Sympatholytic Action

Background The development of tolerance to the sympatholytic and anesthetic-reducing effects of alpha(2) agonists after prolonged administration of dexmedetomidine and how the number of available alpha(2) adrenoceptors affects these dexmedetomidine-induced responses was studied. Methods The sympatholytic action of acute and chronic (3 and 10 micrograms.kg-1.h-1 for 7 days) dexmedetomidine, was assessed by the decrease in norepinephrine turnover in the locus coeruleus and hippocampus. The anesthetic-reducing effect of chronic (7 days) dexmedetomidine (5 and 10 micrograms.kg-1.h-1) was studied by determining the minimum alveolar concentration (MAC) for halothane that prevented rats from responding to a supramaximal noxious stimulus of dexmedetomidine (10 or 30 micrograms.kg-1), doses in the steep part of the dose-response curve. The receptor reserve for the norepinephrine turnover and anesthetic-sparing responses to dexmedetomidine was delineated with 0.3-1.0 mg.kg-1 N-ethoxycarbonyl-2-ethoxy-1,2-dihydroquinoline, an irreversible alkylating agent. Results After chronic administration of dexmedetomidine at both doses, acute dexmedetomidine significantly decreased norepinephrine turnover in the hippocampus and locus coeruleus. The baseline minimum anesthetic concentration (MAC) and the MAC-sparing effect to acutely administered dexmedetomidine were preserved after chronic dexmedetomidine treatment. In the N-ethoxycarbonyl-2-ethoxy-1,2-dihydroquinoline experiments, the dexmedetomidine-induced norepinephrine turnover effect required less than 20% and greater than 4% alpha(2) adrenoceptor availability in the locus coeruleus and the dexmedetomidine induced MAC-sparing effect required less than 40% and greater than 20% alpha(2) adrenoceptor availability in the locus coeruleus. Conclusion Tolerance does not develop for either the sympatholytic or MAC-sparing actions of dexmedetomidine, although it is present for the hypnotic response. The durable quality of the sympatholytic and MAC-sparing responses to dexmedetomidine after chronic treatment is explained by a comparatively larger receptor reserve than is needed for the hypnotic and analgesic responses, which are blunted by the same drug treatment regimen.

Cytochemical Evidence for Presynatic β-Adrenergic Regulation of Secretion in the Developing Rat Submandibular Gland

1977 ◽  
Vol 35 ◽  
pp. 430-431
Author(s):  
L.S. Cutler
Keyword(s):  
Cyclic Amp ◽  
Adenylate Cyclase ◽  
Submandibular Gland ◽  
Neonatal Rat ◽  
Cyclase Activity ◽  
Adenylate Cyclase Activity ◽  
Parotid Glands ◽  
Adrenergic Agonist ◽  
Rat Submandibular Gland

Many studies previously have shown that the B-adrenergic agonist isoproterenol and the a-adrenergic agonist norepinephrine will stimulate secretion by the adult rat submandibular (SMG) and parotid glands. Recent data from several laboratories indicates that adrenergic agonists bind to specific receptors on the secretory cell surface and stimulate membrane associated adenylate cyclase activity which generates cyclic AMP. The production of cyclic AMP apparently initiates a cascade of events which culminates in exocytosis. During recent studies in our laboratory it was observed that the adenylate cyclase activity in plasma membrane fractions derived from the prenatal and early neonatal rat submandibular gland was retractile to stimulation by isoproterenol but was stimulated by norepinephrine. In addition, in vitro secretion studies indicated that these prenatal and neonatal glands would not secrete peroxidase in response to isoproterenol but would secrete in response to norepinephrine. In contrast to these in vitro observations, it has been shown that the injection of isoproterenol into the living newborn rat results in secretion of peroxidase by the SMG (1).

In vivo evidence for dopaminergic regulation of the canine pituitary intermediate lobe

1986 ◽  
Vol 113 (4) ◽  
pp. 471-478 ◽  
Author(s):  
R. J. Kemppainen ◽  
J. L. Sartin
Keyword(s):  
Dopamine Antagonist ◽  
Test Substance ◽  
Intermediate Lobe ◽  
Adrenergic Agonist ◽  
Serotonin Agonist ◽  
Dopaminergic Pathway ◽  
Pre Treatment ◽  
Pituitary Intermediate Lobe ◽  
Dopaminergic Regulation

Abstract. In order to examine regulation of pituitary intermediate lobe secretion, plasma immunoreactive (i)ACTH, cortisol, and α-MSH responses to iv bolus injections of CRF, quipazine maleate (serotonin agonist), isoproterenol (β-adrenergic agonist) or haloperidol (dopamine antagonist) were determined in conscious, unrestrained dogs. Endocrine responses to these test substances were also determined in dogs pre-treated with dexamethasone. Administration of one or more doses of each test substance resulted in significant elevations in plasma iACTH and cortisol concentrations. Only haloperidol injection caused significant increases in plasma iα-MSH. Following dexamethasone pre-treatment, plasma iACTH and cortisol increases in response to all test substances were considerably reduced or abolished. Dexamethasone did not alter baseline or haloperidol-stimulated plasma ia-MSH concentrations. However, infusion of bromocriptine mesylate (dopamine agonist) in combination with dexamethasone pre-treatment reduced the plasma iα-MSH response to haloperidol. We conclude that a dopaminergic pathway is important in the in vivo regulation of pituitary intermediate lobe activity in dogs.

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