Escaping in Twentieth-Century Russia

The article was submitted on 15.06.2017.This article considers the escapees who populated Russia’s twentieth century in astonishingly large numbers. By escapees, the authors mean not only those who had been incarcerated, exiled, and deported, but also others who ignored or willfully violated regulations limiting movement – peasant settlers moving “irregularly” to scarcely-populated or recently depopulated areas; seasonal workers making independent employment arrangements; migrants to the city without the proper papers but desperate to access resources unavailable in the countryside; officials keen to avoid inferior assignments; refugees and evacuees deviating from assigned destinations. These evasive practices are characterized as migrant repertoires, that is, the relationships and networks of contact marked by geographic origin, gender, kinship, friendship, and professional identity that permitted them to adapt to or evade particular migration regimes. State-organized regimes of migration set the terms and resources of movement for all sorts of migrants, from settlers to deportees. The range of migrants surveyed confirms the ambition of Imperial and especially Soviet authorities to manage their peoples, but also the limited capacity of these states to do so. Thus the article suggests that the assumption of people’s powerlessness in the face of overwhelming state power should be reconsidered.Предметом внимания авторов статьи являются самовольные мигранты, которых в России в XX в. было поразительно много. Под самовольными мигрантами подразумеваются не только заключенные в тюрьму, сосланные и депортированные, но и те, кто игнорировал либо умышленно нарушал правила, ограничивающие передвижение, – крестьяне-поселенцы, осуществлявшие «нерегулярные» миграции в малонаселенные или недавно оставленные людьми районы; сезонные работники, самостоятельно вступавшие в трудовые отношения; мигранты в города, не имевшие необходимых документов, но отчаянно нуждавшиеся в доступе к ресурсам, отсутствующим в сельской местности; должностные лица, стремившиеся избежать невыгодных для себя назначений; беженцы и эвакуированные, отклонявшиеся от предписанного маршрута. Эти миграционные практики характеризуются в контексте межличностных взаимоотношений и сетей контактов по признакам географического происхождения, пола, родства, дружбы и профессиональной идентичности, позволяющим им адаптироваться либо уклоняться от определенных миграционных режимов. Организованные государством режимы миграции устанавливают условия и ресурсы передвижения для всех видов мигрантов, от поселенцев до депортированных. Результаты опроса ряда мигрантов подтверждают стремление имперских и особенно советских властей управлять людьми, но в то же время демонстрируют ограниченность их возможностей в этой сфере. Таким образом, авторы статьи полагают, что предположение о бессилии людей перед лицом подавляющей государственной машины преувеличено

Presynaptic BDNF Required for a Presynaptic but Not Postsynaptic Component of LTP at Hippocampal CA1-CA3 Synapses

AbstractBrain-derived neurotrophic factor (BDNF) has been implicated in several forms of long-term potentiation (LTP) at different hippocampal synapses. Using two-photon imaging of FM 1-43, a fluorescent marker of synaptic vesicle cycling, we find that BDNF is selectively required for those forms of LTP at Schaffer collateral synapses that recruit a presynaptic component of expression. BDNF-dependent forms of LTP also require activation of L-type voltage-gated calcium channels. One form of LTP with presynaptic expression, theta burst LTP, is thought to be of particular behavioral importance. Using restricted genetic deletion to selectively disrupt BDNF production in either the entire forebrain (CA3 and CA1) or in only the postsynaptic CA1 neuron, we localize the source of BDNF required for LTP to presynaptic neurons. These results suggest that long-term synaptic plasticity has distinct presynaptic and postsynaptic modules. Release of BDNF from CA3 neurons is required to recruit the presynaptic, but not postsynaptic, module of plasticity

Binding of the auxiliary subunit TRIP8b to HCN channels shifts the mode of action of cAMP

Hyperpolarization-activated cyclic nucleotide-regulated cation (HCN) channels generate the hyperpolarization-activated cation current Ih present in many neurons. These channels are directly regulated by the binding of cAMP, which both shifts the voltage dependence of HCN channel opening to more positive potentials and increases maximal Ih at extreme negative voltages where voltage gating is complete. Here we report that the HCN channel brain-specific auxiliary subunit TRIP8b produces opposing actions on these two effects of cAMP. In the first action, TRIP8b inhibits the effect of cAMP to shift voltage gating, decreasing both the sensitivity of the channel to cAMP (K-1/2) and the efficacy of cAMP (maximal voltage shift); conversely, cAMP binding inhibits these actions of TRIP8b. These mutually antagonistic actions are well described by a cyclic allosteric mechanism in which TRIP8b binding reduces the affinity of the channel for cAMP, with the affinity of the open state for cAMP being reduced to a greater extent than the cAMP affinity of the closed state. In a second apparently independent action, TRIP8b enhances the action of cAMP to increase maximal Ih. This latter effect cannot be explained by the cyclic allosteric model but results from a previously uncharacterized action of TRIP8b to reduce maximal current through the channel in the absence of cAMP. Because the binding of cAMP also antagonizes this second effect of TRIP8b, application of cAMP produces a larger increase in maximal Ih in the presence of TRIP8b than in its absence. These findings may provide a mechanistic explanation for the wide variability in the effects of modulatory transmitters on the voltage gating and maximal amplitude of Ih reported for different neurons in the brain

TRIP8b Regulates HCN1 Channel Trafficking and Gating through Two Distinct C-Terminal Interaction Sites

International audienceHyperpolarization-activated cyclic nucleotide-regulated (HCN) channels in the brain associate with their auxiliary subunit TRIP8b (also known as PEX5R), a cytoplasmic protein expressed as a family of alternatively spliced isoforms. Recent in vitro and in vivo studies have shown that association of TRIP8b with HCN subunits both inhibits channel opening and alters channel membrane trafficking, with some splice variants increasing and others decreasing channel surface expression. Here, we address the structural bases of the regulatory interactions between mouse TRIP8b and HCN1. We find that HCN1 and TRIP8b interact at two distinct sites: an upstream site where the C-linker/cyclic nucleotide-binding domain of HCN1 interacts with an 80 aa domain in the conserved central core of TRIP8b; and a downstream site where the C-terminal SNL (Ser-Asn-Leu) tripeptide of the channel interacts with the tetratricopeptide repeat domain of TRIP8b. These two interaction sites play distinct functional roles in the effects of TRIP8b on HCN1 trafficking and gating. Binding at the upstream site is both necessary and sufficient for TRIP8b to inhibit channel opening. It is also sufficient to mediate the trafficking effects of those TRIP8b isoforms that downregulate channel surface expression, in combination with the trafficking motifs present in the N-terminal region of TRIP8b. In contrast, binding at the downstream interaction site serves to stabilize the C-terminal domain of TRIP8b, allowing for optimal interaction between HCN1 and TRIP8b as well as for proper assembly of the molecular complexes that mediate the effects of TRIP8b on HCN1 channel trafficking