13 research outputs found
The neurotoxicant PCB-95 by increasing the neuronal transcriptional repressor REST down-regulates caspase-8 and increases Ripk1, Ripk3 and MLKL expression determining necroptotic neuronal death
GADOLINIUM AND NEOMYCIN BLOCK VOLTAGE-SENSITIVE CA2+ CHANNELS WITHOUT INTERFERING WITH THE NA+-CA2+ ANTIPORTER IN BRAIN NERVE-ENDINGS
NA+-CA-2+ EXCHANGE ACTIVITY IN CENTRAL NERVE-ENDINGS .2. RELATIONSHIP BETWEEN PHARMACOLOGICAL BLOCKADE BY AMILORIDE ANALOGS AND DOPAMINE RELEASE FROM TUBEROINFUNDIBULAR HYPOTHALAMIC NEURONS
MEMBRANE EVENTS AND IONIC PROCESSES INVOLVED IN DOPAMINE RELEASE FROM TUBEROINFUNDIBULAR NEURONS .2. EFFECT OF THE INHIBITION OF THE NA+-CA++ EXCHANGE BY AMILORIDE
POSSIBLE INVOLVEMENT OF CA++ IONS, PROTEIN KINASE-C AND NA+-H+ ANTIPORTER IN INSULIN-INDUCED ENDOGENOUS DOPAMINE RELEASE FROM TUBEROINFUNDIBULAR NEURONS
Intracellular and plasma membrane-initiated pathways involved in the [Ca2+] i elevations induced by iodothyronines (T3 and T2) in pituitary GH3 cells
The role of 3, 5, 3′-triiodo-l-thyronine (T3) and its metabolite 3, 5-diiodo-l-thyronine
(T2) in modulating the intracellular Ca 2+ concentration ([Ca 2+] i) and endogenous nitric
oxide (NO) synthesis was evaluated in pituitary GH 3 cells in the absence or presence of
extracellular Ca 2+. When applied in Ca 2+-free solution, T2 and T3 increased [Ca 2+] i, in a
dose-dependent way, and NO levels
THE NA+-CA2+ EXCHANGER ACTIVITY IN CEREBROCORTICAL NERVE-ENDINGS IS REDUCED IN OLD COMPARED TO YOUNG AND MATURE RATS WHEN IT OPERATES AS A CA2+ INFLUX OR EFFLUX PATHWAY
EFFECT OF MAITOTOXIN ON CYTOSOLIC CA-2+ LEVELS AND MEMBRANE-POTENTIAL IN PURIFIED RAT-BRAIN SYNAPTOSOMES
PURE UPTAKE BLOCKERS OF DOPAMINE CAN REDUCE PROLACTIN SECRETION - STUDIES WITH DICLOFENSINE
Neuronal NOS activation during oxygen and glucose deprivation triggers cerebellar granule cell death in the later reoxygenation phase
The present study investigated the temporal relationship between neuronal nitric oxide synthase (nNOS) activity and expression and the development of neuronal damage occurring during anoxia and anoxia followed by reoxygenation. For this purpose, cerebellar granule cells were exposed to 2 hr of oxygen and glucose deprivation (OGD) and 24 hr of reoxygenation. To clarify the consequences of nNOS activity inhibition on neuronal survival, cerebellar granule cells were exposed to OGD, both in the absence of extracellular Na(+) ([Na(+)](e)), a condition that by reducing intracellular Ca(2+) ([Ca(2+)](I)) prevents Ca(2+)-dependent nNOS activation, and in the presence of selective and nonselective nNOS inhibitors, such as N(omega)-L-allyl-L-arginine (L-ALA), N(omega)-propyl-L-arginine (NPLA), and L-nitro-arginine-methyl-ester (L-NAME), respectively. The results demonstrated that the removal of [Na(+)](e) hampered the [Ca(2+)](i) increase and decreased expression and activity of nNOS. Similarly, the increase of free radical production present in cerebellar neurons, exposed previously to OGD and OGD/reoxygenation, was abolished completely in the absence of [Na(+)](e). Furthermore, the absence of [Na(+)](e) in cerebellar neurons exposed to 2 hr of OGD led to the improvement of mitochondrial activity and neuronal survival, both after the OGD phase and after 24 hr of reoxygenation. Finally, the exposure of cerebellar neurons to L-ALA (200 nM), and L-NAME (500 microM) was able to effectively reduce NO(*) production and caused an increase in mitochondrial oxidative activity and an improvement of neuronal survival not only during OGD, but also during reoxygenation. Similar results during OGD were obtained also with NPLA (5 nM), another selective nNOS inhibitor. These data suggest that the activation of nNOS is highly accountable for the neuronal damage occurring during the OGD and reoxygenation phases