LSD1 is an environmental stress-sensitive negative modulator of the glutamatergic synapse.

Along with neuronal mechanisms devoted to memory consolidation -including long term potentiation of synaptic strength as prominent electrophysiological correlate, and inherent dendritic spines stabilization as structural counterpart- negative control of memory formation and synaptic plasticity has been described at the molecular and behavioral level. Within this work, we report a role for the epigenetic corepressor Lysine Specific Demethylase 1 (LSD1) as a negative neuroplastic factor whose stress-enhanced activity may participate in coping with adverse experiences. Constitutively increasing LSD1 activity via knocking out its dominant negative splicing isoform neuroLSD1 (neuroLSD1KO mice), we observed extensive structural, functional and behavioral signs of excitatory decay, including disrupted memory consolidation. A similar LSD1 increase, obtained with acute antisense oligonucleotide-mediated neuroLSD1 splicing knock down in primary neuronal cultures, dampens spontaneous glutamatergic transmission, reducing mEPSCs. Remarkably, LSD1 physiological increase occurs in response to psychosocial stress-induced glutamatergic signaling. Since this mechanism entails neuroLSD1 splicing downregulation, we conclude that LSD1/neuroLSD1 ratio modulation in the hippocampus is instrumental to a negative homeostatic feedback, restraining glutamatergic neuroplasticity in response to glutamate. The active process of forgetting provides memories with salience. With our work, we propose that softening memory traces of adversities could further represent a stress-coping process in which LSD1/neuroLSD1 ratio modulation may help preserving healthy emotional references.

Ex novo episodes of acute glomerulonephritis and Guillain-Barré syndrome: a case report.

A nine-year-old girl had several ex novo episodes of acute glomerulonephritis with clinical evidence of rapid progression in two of them. Guillain-Barré syndrome was diagnosed 10 days after the second episode of acute glomerulonephritis. Two renal biopsies (performed at about a four-year interval) gave morphological evidence of new episodes of acute glomerulonephritis. To our knowledge this is the first report of an association between ex novo episodes of acute glomerulonephritis and Guillain-Barré syndrome.

Growth evaluation in children with acute renal failure of unknown etiology.

We performed a retrospective study on 47 children over 1 year of age with severe acute renal failure (ARF) treated with hemodialysis (HD) at our Center from 1978 to 1986 in order to evaluate the diagnostic and prognostic value of growth indexes at hospital admission as a criterion to distinguish cases of ARF without previous chronic renal failure (CRF) from cases in which CRF was not previously diagnosed. The age of the patients ranged from 17 months to 13 years. The cause of ARF was identified in 41 children; 5 of them remained on HD for different reasons (hemolytic uremic syndrome with arteriolar involvement in 3 cases; renal vein thrombosis in 1; endoextracapillary glomerulonephritis in 1). No apparent cause of ARF was found in the other 6 children who remained on chronic HD. A careful history showed that these 6 children had had uremic symptoms for many years. When height was expressed as height standard deviation score (HSDS), the 6 children with ARF of unknown etiology showed significantly lower HSDS values compared with the other 41 children in whom a cause of ARF was diagnosed (p less than 0.001). In conclusion, growth failure in children requiring HD for ARF of unknown etiology is an important criterion that suggests a previously undiagnosed CRF and thus consequently a negative long-term prognosis.