Table 1.

Pathophysiological role of phospho-nNOS at Ser847 in neurons.

Tissue/Cell Type	Method	Outcome	Reference
Mouse neostriatal slices	Treatment with calyculin A or okadaic ocid	Inhibition of glutamate/NO signal	[47]
Rat hippocampal neurons	Treatment with glutamate (low/high concentration)	Inhibition of NO production	[49]
Mouse hippocampal HT22 cells	Treatment of cells exposed CoCl2 with propofol	Neuroprotective effects	[48]
CGCs1 cells, PC12 cells (nNOS expressed)	Treatment with nicotine	Neuroprotective effects	[28]
Rat hippocampus	Ischemia/reperfusion	Neuroprotective effects	[54]
Rat hippocampus	SAH (increasing ICP2)	Neuroprotective effects	[55]
Rat hippocampus	Treatment of GABA3 agonists	Neuroprotective effects	[56]
Rat hippocampus	Transient ischemic preconditionning	Neuroprotective effects	[57]
Rat hippocampus	Ischemia/reperfusion	Neuroprotective effects	[58]
Rat hippocampus	Ischemia/reperfusion	Neuroprotective effects	[59]
Mouse hippocampus	Hypothermia	Neuroprotective effects	[60]
Hamster suprachiasmatic nuclei	Diumal circadian	Photic circadian entrainment	[61]
Mouse spinal cords	Peripheral nerve injury	Neuroprotective effects	[62]
Rat supraoptic/paraventricular nuclei	Treatment of prolactin	Inhibition of vasopressin/oxytocin secretion	[63]
Mouse nucleus intermediolateralis	Spinal cord injury	Autonomic failure	[64]
Mouse periaqueductal grey matter	Treatment of morphine	Analgesic tolerance	[65]
Rat cerebellum	Hyperammonemia	Inhibition of NO production	[66]

¹ CGCs, cerebellar granule cells; ² ICP, intracranial pressure; ³ GABA, γ-aminobutyric acid.