Regional Features of the Expression of Genes Involved in Neurogenesis and Apoptosis in the Brain of Adult Rats

Kolobov, V. V.; Сторожева, З. И.; Gruden, M. A.; Шерстнев, В. В.

doi:10.1007/s10517-012-1816-3

Cited by 5 publications

(6 citation statements)

References 14 publications

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“…In comparison with the prefrontal cortex, hippocampal Apaf1 expression was significantly reduced in contrast with higher expression levels of Ascl1, Pura, S100a6 and Tnf genes. These data were further validated by disclosed correlations between gene regional expression rates [27]. It was particularly striking that the expression of three genes (Ascl1, Casp3 and S100a6) was most consistent in the brain structures studied, and this finding prompted their selection as archetypical in terms of neurogenesis and/or apoptosis in the hippocampus, prefrontal cortex and cerebellum.…”

Section: Introductionmentioning

confidence: 74%

“…In order to compensate this issue and disclose adolescent gene potency, we have recently assessed the concurrent expression of a range of genes involved in neurogenesis and apoptosis (Apaf1, Ascl1, Bax, Bcl2, Casp3, Casp8, Casp9, Dffb, Myh10, Naip2, Napa, Notch2, Numb, Pura, S100a6, Tnf) in the hippocampus, prefrontal cortex and cerebellum of naïve adult rats [27]. The results concurred with the concept that because the hippocampus and cortex are both forebrain structures, they have many cellular and structural features in common, whereas the cerebellum has a distinct developmental origin and therefore a unique cellular composition.…”

Section: Discussionmentioning

confidence: 99%

“…In accordance with a previously reported protocol [27], the total RNA fraction from samples of rat hippocampus, prefrontal cortex and cerebellum (median horizontal fragment including both hemispheres and the vermis) was isolated using TRIzol (Invitrogen, USA), the RNA preparations were then purified from genome DNA admixture by DNase previously [32]. The R values determined by the 2 -ΔΔCt method could not be used to detect the correlations between the genes in the prefrontal cortex, as the R values for all test genes were fixed and equal to 1.…”

Section: Real-time Pcr Analysismentioning

confidence: 99%

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Distinct functional brain regional integration of Casp3, Ascl1 and S100a6 gene expression in spatial memory

Gruden

Сторожева

Sewell

et al. 2013

Behavioural Brain Research

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Evaluating the brain structural expression of defined genes involved in basic biological processes of neurogenesis, apoptosis or neural plasticity may facilitate the understanding of genetic mechanisms underlying spatial memory. The aim of the present study was to compare Ascl1, Casp3 and S100a6 gene expression in the hippocampus, prefrontal cortex and cerebellum of adult rats in water maze spatial memory performance. After four days training, the mean platform time (<10s) was evidence of stable long-term spatial memory formation. Real time PCR analysis revealed a positive inter-structural correlation for S100a6/Casp gene expression between the prefrontal cortex and the cerebellum but a negative correlation for S100a6/Ascl1 transcribed genes between the prefrontal cortex and hippocampus during swimming in the active controls. However, during spatial memory performance there was only one inter-structural correlation between the prefrontal cortex and cerebellum with respect to Casp3 expression, though there were intra-structural correlations between Casp3/Ascl1 transcriptions within the prefrontal cortex and hippocampus as well as between Ascl1/S100a6 in the cerebellum. In active learners versus naive controls, the transcrption of all genes was augmented in the prefrontal cortex but Casp3 and Ascl1 were also elevated in hippocampus whilst only S100a6 increased in the cerebellum. The findings endorsed the role of the hippocampus in memory acquisition in addition to an integrative relationship with the prefrontal cortex and cerebellum. This structural and molecular configuration is important for creation of novel neural circuitry for consolidation and reconsolidation of memory trace with an involvement of coupled processes of neurogenesis, apoptosis or neural plasticity.

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Section: Introductionmentioning

confidence: 74%

Section: Discussionmentioning

confidence: 99%

Section: Real-time Pcr Analysismentioning

confidence: 99%

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Distinct functional brain regional integration of Casp3, Ascl1 and S100a6 gene expression in spatial memory

Gruden

Сторожева

Sewell

et al. 2013

Behavioural Brain Research

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“…Three other exclusive proteins of high intensity appear with FU‐CJD particles. First, MYH10 (#7, Table ) is involved in neurogenesis and apoptosis in rat brain and may contribute to the neurodegenerative cascade. Second, CH60 (Hsp60, chaperonin, #16), could be a non‐specific mitochondrial contaminant.…”

Section: Resultsmentioning

confidence: 99%

Proteomic analysis of host brain components that bind to infectious particles in Creutzfeldt‐Jakob disease

2015

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Transmissible encephalopathies (TSEs), such as CJD and scrapie, are caused by infectious agents that provoke strain-specific patterns of disease. Misfolded host prion protein (PrP-res amyloid) is believed to be the causal infectious agent. However, particles that are stripped of PrP retain both high infectivity and viral proteins not detectable in uninfected mouse controls. We here detail host proteins bound with FU-CJD infectious brain particles by proteomic analysis. More than 98 proteins were differentially regulated, and 56 FU-CJD exclusive proteins were revealed after PrP, GFAP, C1q, ApoE and other late pathologic response proteins were removed. Stripped FU-CJD particles revealed HSC70 (144× the uninfected control), cyclophilin B, an FU-CJD exclusive protein required by many viruses, and early endosome-membrane pathways known to facilitate viral processing, replication, and spread. Synaptosomal elements including synapsin-2 (at 33×) and AP180 (a major FU-CJD exclusive protein) paralleled the known ultrastructural location of 25nm virus-like TSE particles and infectivity in synapses. Proteins without apparent viral or neurodegenerative links (copine-3), and others involved in viral-induced protein misfolding and aggregation, were also identified. Human sCJD brain particles contained 146 exclusive proteins, and heat shock, synaptic and viral pathways were again prominent, in addition to Alzheimer (AD), Parkinson, and Huntington aggregation proteins. Host proteins that bind TSE infectious particles can prevent host immune recognition and contribute to prolonged cross-species transmissions (the species barrier). Our infectious particle strategy, which reduces background sequences by >99%, emphasizes host targets for new therapeutic initiatives. Such therapies can simultaneously subvert common pathways of neurodegeneration.

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“…From what was said in the previous sections (again see ‘Regression I’), it is clear that mismatch, both under stress and during learning, is followed by adaptation, which is associated in many cases with the formation of models of new interactions with the environment – new systems. An important component of the formation is a common mechanism: the specialization of neurons newly emerging in the mature brain (adult neurogenesis) (for more details, see Alexandrov 2006; Kolobov et al 2012; Frankland et al 2013). With regard to acute stress, it has been shown that adult neurogenesis, which might be up‐regulated under stress condition (Kirby et al 2013; Egeland et al 2015), dampens its negative effects (including depression), on the one hand, and improves the development of adaptation to stress (including the formation of new behaviour in a stressful situation, an increase in the ‘plasticity of the brain', ‘improving memory’), on the other (Roozendaal et al 2009; Snyder et al 2011; Kirby et al 2013; Egeland et al 2015).…”

Section: Similarities Between Learning and Stressmentioning

confidence: 99%

Regression II. Development through regression

Alexandrov¹,

Svarnik²,

Znamenskaya³

et al. 2020

J Analytical Psychology

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As shown in our previous paper ('Regression I. Experimental approaches to regression', JAP, 65, 2, 345-65), the common mechanism of regression can be described as reversible dedifferentiation, which is understood as a relative increase of the proportion of low-differentiated (older) systems in actualized experience. Experimental data show that regression following disease (chronic tension headache) is followed by adaptation and an increase in system differentiation in that experience domain which contains systems responsible for that adaptation. The results of mathematical modelling support the idea that reversible dedifferentiation can be one of the mechanisms for increasing the effectiveness of adaptation through learning. Reversible dedifferentiation, which is phenomenologically described as regression, is a general mechanism for restructuring the organism-environment interactions in situations where behaviours that were effective in the past become ineffective. Reversible dedifferentiation has evolved as a component of adaptation when new behaviours are formed and large-scale modifications in the existing behaviours are required in the face of changes in the external and/or internal environment. Thus, the authors believe that this article provides evidence for Jung's view that regression is not only a 'return' to past forms of thinking, affects and behaviour, but that regressive processes provide a significant impetus for psychological growth and development.

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Regional Features of the Expression of Genes Involved in Neurogenesis and Apoptosis in the Brain of Adult Rats

Cited by 5 publications

References 14 publications

Distinct functional brain regional integration of Casp3, Ascl1 and S100a6 gene expression in spatial memory

Distinct functional brain regional integration of Casp3, Ascl1 and S100a6 gene expression in spatial memory

Proteomic analysis of host brain components that bind to infectious particles in Creutzfeldt‐Jakob disease

Regression II. Development through regression

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