Subchronic treatment with prazosin improves passive avoidance learning in aged mice: possible relationships to α 1 -receptor up-regulation

Knauber, Jens; Müller, Wernér E.G.

doi:10.1007/s007020070005

Cited by 25 publications

(18 citation statements)

References 44 publications

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“…Prazosin (Sigma) was dissolved in sterile water and administered at 1.0 or 3.0 mg/kg IP in a volume of 10 ml/kg. These doses were based on previous studies in mice examining the effects of prazosin on memory (Galeotti et al, 2004; Introini-Collison, Saghafi, Novack, & McGaugh, 1992; Knauber & Muller, 2000). …”

Section: Methodsmentioning

confidence: 99%

A role for α₁-adrenergic receptors in extinction of conditioned fear and cocaine conditioned place preference.

Bernardi¹,

Lattal²

2010

Behavioral Neuroscience

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Previous work has demonstrated an important role for adrenergic receptors in memory processes in fear and drug conditioning paradigms. Recent studies have also demonstrated alterations in extinction in these paradigms using drug treatments targeting β-and α 2 -adrenergic receptors, but little is known about the role of α 1 -adrenergic receptors in extinction. The current study examined whether antagonism of α 1 -adrenergic receptors would impair the consolidation of extinction in fear and cocaine conditioned place preference (CPP) paradigms. After contextual fear conditioning, injections of prazosin (1.0 or 3.0 mg/kg) following nonreinforced context exposures slowed the loss of conditioned freezing over the course of five extinction sessions (Experiment 1). After cocaine place conditioning, prazosin had no effect on the rate of extinction over eight nonreinforced test sessions. Following post-extinction reconditioning, however, prazosin-treated mice showed a robust place preference, but vehicle-treated mice did not, suggesting that prazosin reduced the persistent effects of extinction (Experiment 2). These results confirm the involvement of the α 1 -adrenergic receptor in extinction processes in both appetitive and aversive preparations.

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Section: Methodsmentioning

confidence: 99%

A role for α₁-adrenergic receptors in extinction of conditioned fear and cocaine conditioned place preference.

Bernardi¹,

Lattal²

2010

Behavioral Neuroscience

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“…Prazosin hydrochloride and propranolol hydrochloride were obtained from SigmaAldrich (Saint Quentin, France) and used at doses (prazosin 1.5 mg/kg and propranolol 10 mg/kg) that were found effective after acute i.p. injection in the mouse (Sallaz and Jourdan 1996;Knauber and Muller 2000). All drugs were dissolved in 0.9% sterile saline (vehicle) and injected i.p.…”

Section: Drugsmentioning

confidence: 99%

Noradrenergic control of odor recognition in a nonassociative olfactory learning task in the mouse

Veyrac

Nguyen²,

Marien³

et al. 2007

Learn. Mem.

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The present study examined the influence of pharmacological modulations of the locus coeruleus noradrenergic system on odor recognition in the mouse. Mice exposed to a nonrewarded olfactory stimulation (training) were able to memorize this odor and to discriminate it from a new odor in a recall test performed 15 min later. At longer delays (30 or 60 min), the familiar odor was no longer retained, and both stimuli were perceived as new ones. Following a post-training injection of the ␣ 2 -adrenoceptor antagonist dexefaroxan, the familiar odor was still remembered 30 min after training. In contrast, both the ␣ 2 -adrenoceptor agonist UK 14304 and the noradrenergic neurotoxin DSP-4 prevented the recognition of the familiar odor 15 min after the first exposure. Noradrenaline release in the olfactory bulb, assessed by measurement of the extracellular noradrenaline metabolite normetanephrine, was increased by 62% following dexefaroxan injection, and was decreased by 38%-44% after treatment with UK 14304 and DSP-4. Performance of mice in the recall test was reduced by a post-training injection of the ␤-adrenoceptor antagonist propranolol or the ␣ 1 -antagonist prazosin, thus implicating a role for ␤-and ␣ 1 -adrenoceptors in the facilitating effects of noradrenaline on short-term olfactory recognition in this model.

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“…For determination of the time course of central α 1 -adrenoceptor occupation after oral treatment with prazosin or anseculin, a modified ex vivo binding assay with highly concentrated tissue homogenates was used [Müller and Stillbauer, 1983;Knauber and Müller, 2000a]. Animals were killed in different time intervals (t = 2, 15, 30, 45, 60, 90, and 120 min) after administration of a single dose of the compound with stomach tube (anseculin or prazosin; 1 mg/kg, p.o.).…”

Section: Ex Vivo Assay Of a 1 -Adrenoceptor Membrane Preparation And mentioning

confidence: 99%

“…Animals were killed by cervical dislocation and the brains were rapidly removed and immediately frozen at -20°C until used for binding studies. The preparations of total brain homogenates (without cerebellum) and the assay procedure were performed according to Knauber and Müller [2000a]. Forebrain were weighed and homogenized in ice-cold buffer containing 50 mM Tris-HCl (pH 7.0) at 4°C using a teflon/glass homogenizer.…”

Section: Compound Administrationmentioning

confidence: 99%

Biochemical profile of anseculin (KA‐672) at different brain receptors

Knauber

Müller

2002

Drug Development Research

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Anseculin (KA-672) is a multifunctional antidementia agent under development that may be of therapeutic value in the treatment of progressive neuronal and cognitive decline, which are common in Alzheimer disease. In vitro and ex vivo experiments have characterized anseculin as a potent functional antagonist of central α 1 -adrenoceptors. In comparison to prazosin, the in vitro potency of anseculin for α 1 -adrenoceptors is about 8 times less. Like prazosin, anseculin shows an inhibition of phenylephrine-(norepinephrine-) induced accumulation of inositol phosphates. Oral treatment with 1 mg/kg anseculin or 1 mg/ kg prazosin show similar effects on α 1 -adrenergic receptor binding ex vivo, indicating a greater ex vivo potency of anseculin on central α 1 -adrenergic receptors. Anseculin has only weak affinity for central muscarinic cholinergic receptors. Anseculin inhibited adenylate cyclase and reduced intracelluar cAMP levels of about 30%, similar to the 5-HT 1A agonist, 8-OH-DPAT. Together with its high affinity for 5-HT 1A receptors (IC 50 for 3 H-8-OH-DPAT binding is about 8 nM), these data suggest that anseculin also exhibits 5-HT 1A agonistic properties. Drug Dev.

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Subchronic treatment with prazosin improves passive avoidance learning in aged mice: possible relationships to α 1 -receptor up-regulation

Cited by 25 publications

References 44 publications

A role for α₁-adrenergic receptors in extinction of conditioned fear and cocaine conditioned place preference.

A role for α₁-adrenergic receptors in extinction of conditioned fear and cocaine conditioned place preference.

Noradrenergic control of odor recognition in a nonassociative olfactory learning task in the mouse

Biochemical profile of anseculin (KA‐672) at different brain receptors

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