Disease relevance of Nme2

• Positive hybridization signal was observed in the ganglion cells throughout the postnatal days (P) examined, whereas strong signals were detected in the photoreceptor inner segments and the inner nuclear layer exclusively at P16 and P18 [1].

High impact information on Nme2

• This approach has also shown that triosephosphate isomerase, aconitate hydratase, M-protein, nucleoside diphosphate kinase B, and myoglobin are S-thiolated during post-ischemic reperfusion [2].
• This was followed by a period of rapid maturation (from approximately P12 to approximately P18), consisting of changes in Na(+)-spike discharge, emergence of repetitive bursts of Na(+) spikes terminated by Ca(2+) spikes (Ca(2+)-Na(+) bursts), generation of the trimodal pattern, and a significant expansion of the dendritic tree [3].
• Finally, in both Ammon's horn and the dentate gyrus, cells resembling reactive microglia are also observed and, in particular, in the perforant path projections from P9 to P18, suggesting their participation not only in phagocytosis of dead cells but also in axonal elimination and/or fiber reorganization [4].
• By P18 the GABA reversal potential was shifted close to the resting potential and GGABA produced a shunting inhibition [5].
• RGS4 expression was temporarily confined to the CA pyramidal cell layer and not detectable in the dentate gyrus at P10 and P18 [6].

Biological context of Nme2

• The normal developmental increase in GABA(A) receptor currents occurred on schedule (P18) in sham-treated sSC, but NMDA treatment caused premature up-regulation (P12) [7].
• At P18, the rats were killed, and the brains were processed for histology and immunohistochemistry [8].
• Auditory evoked potentials (AEPs) were recorded epidurally at vertex in the freely moving rat, yielding the prominent components P18 and N40 from the average waveform [9].
• After a decline on day 1 of lactation (L1), PR mRNA levels had increased again on L3 and L14 compared with P15, P18, P20, P21 and P21pm (at 2200-2300 h on P21) [10].

Anatomical context of Nme2

• During development, CSPG expression became visible at postnatal day (P) 4 in the superior olivary complex, at P8 in the midbrain, and at P18 in the cortex [11].
• In the cerebral cortex, the expression of rgpr85 was gradually decreased postnatally and became undetectable by P18 [12].
• The E levels of the diencephalon are very low in comparison to the NE and DA concentrations, but present a gradual increase from E17 to P18 [13].
• At P25 rhodopsin levels were higher than at P18, while photoreceptor cell DNA was essentially the same as in the younger rats [14].
• NAPDH-d-positive neurons are detected as early as postnatal day (P)5, especially in the peripheral retina; intense labeling of somata and long lengths of dendrites is obtained between P10 and P18, after which only the somata exhibit NADPH-d activity [15].

Associations of Nme2 with chemical compounds

• It is unclear why younger infants (P12) consume more 10 and 20% ethanol than older (P18) infants [16].
• The data show a biphasic pattern in NE changes of the three brain areas, with a first increase in the late prenatal period, followed by a further development from P0 to P18, thus reaching the adult levels [13].
• Furthermore, the light-enhanced startle observed in P18 rats was prevented by a systemic injection of the noradrenergic beta-receptor antagonist propranolol [17].
• We report here experiments in which the competitive NMDA receptor antagonist CGP 39551 was administered to rat pups from postnatal day 7 (P7) to P18 [18].
• Prenatal cocaine exposure resulted in increased Fos in males in response to AMPH (2 mg/kg) at P18 and cocaine (10 mg/kg) at 1-2 months [19].

Analytical, diagnostic and therapeutic context of Nme2

• In situ hybridization at P18 showed that expression of Na+ channel alpha II and beta I mRNA was dramatically downregulated in tufted cells, while signals in mitral cells showed no detectable changes [20].

References