Pharmacological and molecular evidence for dopamine D-1 receptor expression by striatal astrocytes in culture

Citation
P. Zanassi et al., Pharmacological and molecular evidence for dopamine D-1 receptor expression by striatal astrocytes in culture, J NEUROSC R, 58(4), 1999, pp. 544-552
Citations number
20
Categorie Soggetti
Neurosciences & Behavoir
Journal title
JOURNAL OF NEUROSCIENCE RESEARCH
ISSN journal
03604012 → ACNP
Volume
58
Issue
4
Year of publication
1999
Pages
544 - 552
Database
ISI
SICI code
0360-4012(19991115)58:4<544:PAMEFD>2.0.ZU;2-O
Abstract
The neurotransmitter dopamine (DA) at a 10 mu M concentration elicited a st imulation of intracellular cyclic AMP (cAMP) accumulation in cultured astro cytes derived from embryonic rat striatum. This accumulation was partially blocked by the beta-adrenergic receptors antagonist propranolol, mimicked b y the D-1 agonist SKF 38393 and by the mixed D-1/D-2 agonist apomorphine. A regional heterogeneity in the magnitude of dopamine-induced cAMP accumulat ion was observed in cultured astrocytes obtained from different brain areas . The maximum effect was observed in striatal astrocytes, a lower effect in cortical astrocytes, and no increase was detected in cerebellar astrocytes , Reverse transcription-polymerase chain reaction (RT-PCR) coupled to South ern blot hybridization demonstrated that striatal astrocytes express only D -1 receptor mRNA and Western blot analysis confirmed the expression of the D-1 receptor protein in striatal astrocytes, In contrast to what found in n eurons, the D-1-dependent cAMP formation ia striatal astrocytes is partiall y reduced by pertussis toxin (PTX) treatment, The stimulation of D-1 recept ors or the activation of adenylyl cyclase by forskolin led to an increase o f cytosolic and nuclear protein kinase A (PKA) catalytic activity. The pres ence of dopamine D-1 receptors in cultured striatal astrocytes suggests a r ole of dopamine in the regulation of cellular processes in striatal astrocy tes. J. Neurosci. Res. 58:544-552, 1999. (C) 1999 Wiley-Liss, Inc.