Desipramine treatment differently down-regulates beta-adrenoceptors of freshly isolated neurons and astrocytes.
Article Details
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Sapena R, Morin D, Zini R, Morin C, Tillement JP
Desipramine treatment differently down-regulates beta-adrenoceptors of freshly isolated neurons and astrocytes.
Eur J Pharmacol. 1996 Apr 4;300(1-2):159-62.
- PubMed ID
- 8741184 [ View in PubMed]
- Abstract
Eight days' desipramine administration (16 mg/kg per day i.p.) to rats resulted in a significant decrease in the density of beta-adrenoceptors in neuronal and astroglial cells from rat forebrain and cerebellum without modification of their corresponding affinity. beta-Adrenoceptor subtypes, beta 1 and beta 2, which coexist in neurons and astrocytes, are differently distributed in the brain and differently modified by desipramine administration which down-regulates beta 1-adrenoceptor in forebrain neurons and astrocytes and beta 2-adrenoceptor in cerebellum neurons. This down-regulation affects the predominant subtype, beta 1 or beta 2, of the relevant structure. Astroglial and neuronal beta-adrenoceptors are differently coupled to G-proteins. Only neuronal cells contain the high-affinity conformational state of the beta-adrenoceptors which is sensitive to GTP. The percentage of neuronal receptors in the high-affinity state differs according to brain area. Desipramine treatment decreases the neuronal density of both cerebellar high- and low-affinity sites and only the forebrain high-affinity site. The desipramine effects are thus subtype-dependent and differ between the two brain areas selected.
DrugBank Data that Cites this Article
- Drug Targets
Drug Target Kind Organism Pharmacological Action Actions Desipramine Beta-1 adrenergic receptor Protein Humans UnknownOtherDetails Desipramine Beta-2 adrenergic receptor Protein Humans UnknownAntagonistDetails