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  • Title: An investigation into the effect of the type IV phosphodiesterase inhibitor rolipram in the modulation of glutamate release from rat prefrontocortical nerve terminals.
    Author: Wang SJ.
    Journal: Synapse; 2006 Jan; 59(1):41-50. PubMed ID: 16247764.
    Abstract:
    The present study was conducted to explore the influence of rolipram, a specific inhibitor of the phosphodiesterase type 4 (PDE4) isoform, on glutamate release in the rat prefrontal cortex, using isolated nerve terminal (synaptosome) preparation. In prefrontocortical nerve terminals, rolipram potentiated the Ca(2+)-dependent release of glutamate evoked by 4-aminopyridine (4AP) in a concentration-dependent manner. This potentiation of release was occluded by the activation of PKA by Sp-cAMP or beta-adrenergic receptor agonist and prevented by the inhibition of PKA by Rp-cAMP or KT5720, indicating a PKA-mediated mechanism. The rolipram-mediated potentiation of glutamate release is associated with an increase both in the 4AP-evoked depolarization of the synaptosomal plasma membrane potential and in 4AP-evoked Ca(2+) influx into synaptosomes. Moreover, Ca(2+) ionophore ionomycin-induced glutamate release was also facilitated by rolipram. These results concluded that phosphodiesterase 4 inhibited by rolipram produces an increase in PKA activation, which subsequently enhances the voltage-dependent Ca(2+) influx by increasing terminal excitability as well as the vesicular release machinery to cause an increase in evoked glutamate release from rat prefrontocortical nerve terminals.
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