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SH-SY5Y neuroblastoma cells undergo neuronal differentiation and their proliferation is inhibited when they are treated with phorbol 12-myristate 13-acetate (PMA). Insulin and insulin-like growth factor I (IGF-I) are mitogens for the nontreated SH-SY5Y cells, whereas the proliferative response to such factor stimulation is lost upon differentiation, in(More)
N-ethylmaleimide (NEM) treatment has been shown to inactivate regulatory GTP-binding N (G)-proteins in many preparations, including slices of rat hippocampus. NEM-treatment (100 microM for 15 min) has been used to examine the possible involvement of a N-protein in the prejunctional inhibitory effect of an adenosine analogue, R-PIA acting on A1-receptors,(More)
In the transversely cut rat hippocampus, adenosine caused a dose-dependent increase in the accumulation of [3H]cyclic AMP from [3H]ATP. Adenosine breakdown products were inactive. AMP was somewhat less effective than adenosine, and its effect could be partially, but not completely, abolished by alpha, beta-methylene-ADP and GMP, which inhibited its(More)
In the present experiments we have examined the effect of N-ethylmaleimide (NEM) on the release of [3H]glutamate from rat hippocampal slices. Pretreatment of slices with NEM in a concentration between 50 microM and 200 microM, can inhibit the GTP-binding protein (Ni) that transmits receptor signals into inhibitions of adenylate cyclase, without affecting(More)
CONTEXT Multiple endocrine neoplasia type 1 (MEN1) is a tumor syndrome of the parathyroid, endocrine pancreas, and anterior pituitary caused by mutations in the MEN1 gene on 11q13. OBJECTIVE The goal of this study was to determine the MEN1 mutation spectrum and detection rate among Swedish patients and identify which patient categories should be tested(More)
The effect of three stable adenosine analogues, L-phenylisopropyl-adenosine (L-PIA), 2-chloroadenosine, and adenosine 5'-ethylcarboxamide (NECA), on cyclic AMP accumulation was studied in five different cell lines derived from the nervous system. In N18-neuroblastoma cells, with cholinergic properties, all three analogues caused an increased accumulation of(More)
The administration of a stable adenosine analogue, L-N6-phenylisopropyladenosine (L-PIA, 0.3 mg/kg i. p.), caused a decrease in the accumulation of L-DOPA in the rat hippocampus after blockade of aromatic amino acid decarboxylase by NSD 1015 (150 mg/kg). Conversely, the adenosine receptor antagonist theophylline (15 mg/kg) increased the L-DOPA accumulation.(More)