This contribution increases by a factor of two the total number o

This contribution increases by a factor of two the total number of alpha-neurotoxins sequenced

from the Micrurus genus in currently available literature.”
“Chromatin structure has a crucial role in processes of metabolism, including transcription, DNA replication and DNA damage repair. An evolutionarily conserved variant of histone H2A, called H2AX, is one of the key components of chromatin. H2AX becomes rapidly phosphorylated on chromatin surrounding DNA double-strand breaks (DSBs). Recent studies have shown that H2AX and other components of damaged chromatin also become modified by acetylation and ubiquitylation. This review discusses how specific combinations of histone modifications affect the accumulation and function of DNA repair factors (MDC1, RNF8, click here RNF168, 53BP1, BRCA1) and chromatin remodeling complexes (INO80, SWR1, TIP60-p400) at DSBs. These collectively regulate DSB repair and checkpoint arrest, avoiding

genomic instability and oncogenic transformation in higher eukaryotes.”
“Mammalian neurokinin-3 (NK3) receptors of the tachykinin family of neuropeptides have been shown to activate dopaminergic neurons of the ventral tegmental area (VTA), a midbrain area displaying dopaminergic dysfunctional activity in schizophrenia. The recent finding of NK3, receptors in VTA neuronal nucleus highlights a new level of neuromodulation, in addition to the traditional tachykinin-induced NK3 receptor internalization and activation of second messenger signaling pathways. The function of nuclear NK3 receptors is still unknown. TCL SAHA HDAC manufacturer It is also unclear how dopaminergic activation is affecting the NK3 receptor distribution in the VTA. In the present study, trafficking of the NK3 receptor in somatodendritic profiles of dopaminergic and non-dopaminergic neurons

of the rat VTA was investigated following acute systemic administration of the dopamine D-1/D-2 receptor agonist apomorphine. VTA sections were dual immunolabeled for the NK3 receptor (immunogold) and the dopamine synthesizing enzyme tyrosine hydroxylase (TH, immunoperoxidase). Electron microscopic quantifications of somatic and dendritic densities of NK3 immunogold particles with or without TH immunolabeling were compared in vehicle-injected or apomorphine-injected rats. In dopaminergic (TH) neurons, apomorphine evoked a significant increase in NK3 receptor densities in cytoplasmic and nuclear portions of the soma. These changes were accompanied by a respective decrease and increase in plasmalemmal and cytoplamic NK3 receptor densities in dopaminergic dendrites. In non-TH neurons, presumably GABAergic neurons of the VTA, the NK3 receptor densities in somata and dendrites were not significantly altered by apomorphine. The results suggest that dopaminergic receptor activation is inducing a rapid mobilization of NK3 receptors in VTA dopaminergic neurons.

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