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Objective: Despite the number of studies on the contribution of pelvic floor muscles (PFM) to the penile erection process, their significance is still underestimated. The goal of this study was to investigate the role of PFM in the erection process in non-human primates., Materials and Methods: First, we performed an anatomical study of the penile structures in 12 baboon cadavers. Next, we created chronic electrophysiological models of normal erectile function in 25 olive baboons. We implanted electrodes on the cavernous nerves to control penile blood filling and placed other electrodes on the pudendal nerve to stimulate the ischiocavernosus muscles (ICM) contractions after sufficient blood filling, thus simulating both vascular and muscular phases of penile erection. We controlled the intracavernous pressure (ICP) during nerve stimulations and further performed a mathematical analysis of the collected data., Results: We described the main pro-erectile muscle anatomy and its relationship with penile structures in monkeys. During neurostimulation studies, we showed the key role of ICM in achieving full penile rigidity with suprasystolic ICP up to 120-300 mm Hg. We also developed a math model for calculating the pro-erectile muscle's contraction force with high accuracy., Conclusion: In this study, we demonstrated the crucial role of PFM in the penile erection process using the monkey model, supporting the previous studies' data. We consider these results essential for a better, more complex understanding of the penile erection process and the participating structures in each stage. This is essential for further improving and designing novel erectile dysfunction diagnostics and treatment techniques.

Previous studies of the alpha-synuclein null mutant mice on the C57Bl6 genetic background have revealed reduced number of dopaminergic neurons in their substantia nigra pars compacta (SNpc). However, the presence in genomes of the studied mouse lines of additional genetic modifications that affect expression of genes located in a close proximity to the alpha-synuclein-encoding Snca gene makes these data open to various interpretations. To unambiguously demonstrate that the absence of alpha-synuclein is the primary cause of the observed deficit of dopaminergic neurons, we employed a recently produced constituent alpha-synuclein knockout mouse line B6(Cg)-Snca tm1.2Vlb /J. The only modification introduced to the genome of these mice is a substitution of the first coding exon and adjusted short intronic fragments of the Snca gene by a single loxP site. We compared the number of dopaminergic neurons in the SNpc of this line, previously studied B6(Cg)-Snca tm1Rosl /J line and wild type littermate mice. A similar decrease was observed in both knockout lines when compared with wild type mice. In a recently published study we revealed no loss of dopaminergic neurons following conditional inactivation of the Snca gene in neurons of adult mice. Taken together, these results strongly suggest that alpha-synuclein is required for efficient survival or maturation of dopaminergic neurons in the developing SNpc but is dispensable for survival of mature SNpc dopaminergic neurons.

Unlabelled: BACKGROUND AND ОBJECTIVE: Loss of conformation and function of sufficient number of proteins with high aggregation capacity plays an important role in the pathogenesis of many neurodegenerative disorders (NDD). Due to a recent discovery of new array of proteins with the capacity to form aggregates of nonamyloid type, new NDD models as well as a new level of understanding in vivo models which are already exist is needed. DNA/RN A binding proteins - FUS and TDP-43 play a crucial role in the pathogenesis of some forms of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia. The objective of the study was to develop a new ALS transgenic model., Material and Methods: In cell culture experiments, we studied mutant FUS proteins capable to form intracellular deposits morphologically similar to those observed in the autopsy material of ALS patients., Results and Conclusion: We created a transgenic mice line, in which a pathogenic form of human FUS protein was expressed in the nervous system. That led to the aggregation of FUS protein in spinal cord and motor neurons with the following degeneration and development of a phenotype, similar to the human ALS disease phenotype, in young grown-up animals. This neurodegenerative phenotype corresponds to a great number of clinical manifestations of human ALS and is an adequate transgenic model of the disease.