title: Adenosine modulation of [Ca2+]i in cerebellar granular cells: multiple adenosine receptors involved.
abstract: Elimination of adenosine by addition of adenosine deaminase (ADA) to the media leads to alterations in intracellular free calcium concentration ([Ca(2+)](i)) in cerebellar granular cells. Adenosine deaminase brings about increases or decreases in [Ca(2+)](i) depending on the previous activation state of the cell. These effects are dependent on the catalytic activity of adenosine deaminase, since its previous catalytic inactivation with Hg(2+) prevents the above-mentioned changes in intracellular calcium. Extracellular calcium is required for the increase in [Ca(2+)](i) promoted by ADA. This rise is insensitive to thapsigargin, but sensitive to micromolar concentrations of Ni(2+). Toxins specific for L, N and P/Q calcium channels do not overtly reduce this effect. N(6)-Cyclopentyl adenosine (CPA), an A(1) receptor agonist, produces a partial reversion of ADA effects, while CGS21680, A(2A)/A(2B) receptor agonist, slightly enhances them. Expression of A(1), A(2A), A(2B) and A(3) adenosine receptor mRNAs was detected in cerebellar granular cell cultures. These results suggest that adenosine modulate [Ca(2+)](i) in cerebellar granule cells through different adenosine receptor subtypes which, at least in part, seem to act through R-type calcium channels.
authors: Area de Bioquímica-C.R.I.B., Facultad de Químicas, Universidad de Castilla-La Mancha, Camilo Jose Cela, 10, Ciudad Real, 13071, Spain.
authors: Javier
authors: J
authors: Vacas
authors: Mercedes
authors: M
authors: Fernández
authors: Manuel
authors: M
authors: Ros
authors: Pablo
authors: P
authors: Blanco
mesh_terms: D000241:Adenosine / Q000031:analogs & derivatives* / Q000172:deficiency* / Q000378:metabolism / Q000494:pharmacology; D058907:Adenosine A1 Receptor Agonists; D000243:Adenosine Deaminase / Q000494:pharmacology; D000818:Animals; D000831:Animals, Newborn; D002118:Calcium / Q000378:metabolism; D020908:Calcium Channels, R-Type / Q000187:drug effects / Q000378:metabolism; D020013:Calcium Signaling / Q000187:drug effects / Q000502:physiology*; D002478:Cells, Cultured; D002525:Cerebellar Cortex / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D007424:Intracellular Fluid / Q000187:drug effects / Q000378:metabolism; D009474:Neurons / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D009532:Nickel / Q000494:pharmacology; D010627:Phenethylamines / Q000494:pharmacology; D012333:RNA, Messenger / Q000187:drug effects / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D043682:Receptor, Adenosine A1 / Q000378:metabolism; D018047:Receptors, Purinergic P1 / Q000187:drug effects / Q000235:genetics / Q000378:metabolism*
chemical_list: D058907:Adenosine A1 Receptor Agonists; D020908:Calcium Channels, R-Type; D010627:Phenethylamines; D012333:RNA, Messenger; D043682:Receptor, Adenosine A1; D018047:Receptors, Purinergic P1; C061282:2-(4-(2-carboxyethyl)phenethylamino)-5'-N-ethylcarboxamidoadenosine; C048599:N(6)-cyclopentyladenosine; D009532:Nickel; D000243:Adenosine Deaminase; D000241:Adenosine; D002118:Calcium