Perinatal hypoxic-ischemic brain injury affects the glutamatergic signal transduction coupled with neuronal ADP-ribosyl cyclase activity.

Agonists of glutamate ionotropic (NMDA) and metabotropic receptors (mGluRI and mGluRIII) had the regulatory effect on ADP-ribosyl cyclase/CD38 activity in cerebellar granular cells of newborn rats. Perinatal hypoxic-ischemic brain injury was followed by dysregulation of this mechanism.

Perinatal hypoxic and ischemic damage to the central nervous system causes changes in the expression of connexin 43 and CD38 and ADP-ribosyl cyclase activity in brain cells.

The expression of connexin 43 and CD38 and ADP ribosyl cyclase activity in brain cells were studied in rats with experimental hypoxic and ischemic damage to the CNS. Changes in the expression and activity of the enzyme were detected over the course of ischemic injury indicating a possible contribution of NAD(+)-converting activity and NAD(+)-transporting processes to the pathogenesis of acute cerebral ischemic injury.

[The role of P2X7 receptors in modulation of the functional activity of peritoneal macrophages in mice with peritonitis].

The role of P2X7 receptors in modulation of the functional activity of macrophages in mice with model peritonitis has been studied. It is established that the functional activity of murine macrophages under such conditions is increased, which is accompanied by the growth of P2X7(+) macrophages and a bidirectional change of the their functional activity under the action of P2X7 modulators. The role of P2X7-associated mechanisms in regulation of the macrophage activity during inflammation is discussed.