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Insulin-like growth factor-I (IGF-I) signaling plays a key role in learning and memory processes. While the effects of IGF-I on neurons have been studied extensively, the involvement of astrocytes in IGF-I signaling and the consequences on synaptic plasticity and animal behavior remain unknown. We have found that IGF-I induces long-term potentiation (LTP) of the postsynaptic potentials that is caused by a long-term depression of inhibitory synaptic transmission in mice. We have demonstrated that this long-lasting decrease in the inhibitory synaptic transmission is evoked by astrocytic activation through its IGF-I receptors (IGF-IRs). We show that LTP not only increases the output of pyramidal neurons, but also favors the NMDAR-dependent LTP, resulting in the crucial information processing at the barrel cortex since specific deletion of IGF-IR in cortical astrocytes impairs the whisker discrimination task. Our work reveals a novel mechanism and functional consequences of IGF-I signaling on cortical inhibitory synaptic plasticity and animal behavior, revealing that astrocytes are key elements in these processes. ; This work was supported by Grants BFU2016-80802-P from Agencia Estatal de Investigación Spain/Fondo Europeo de Desarrollo Regional, and from the European Union [Ministerio de Economía y Competitividad (MINECO)] to D.F.d.S.; Grants R01-NS-097312 and R01-DA-048822 from National Institutes of Health/National Institute of Neurological Disorders and Stroke to A.A.; and grants from Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED) and Grant SAF2016-76462-C2-1-P from MINECO to I.T.-A. J.A.Z.-V. was supported by the National Council of Science, Technology and Technological Innovation (CONCYTEC, Perú) through the National Fund for Scientific and Technological Development (FONDECYT, Perú). J.F. received a postdoctoral fellowship from Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP; Grants #2017/14742-0 and #2019/03368-5). We thank the University of Minnesota Viral Vector and Cloning Core for production of some of the viral vectors used in this study; and Dr. G. Perea and Dr. Washington Buño for helpful comments.

Insulin-like growth factor-I (IGF-I) signaling plays a key role in learning and memory processes. While the effects of IGF-I on neurons have been studied extensively, the involvement of astrocytes in IGF-I signaling and the consequences on synaptic plasticity and animal behavior remain unknown. We have found that IGF-I induces long-term potentiation (LTP) of the postsynaptic potentials that is caused by a long-term depression of inhibitory synaptic transmission in mice. We have demonstrated that this long-lasting decrease in the inhibitory synaptic transmission is evoked by astrocytic activation through its IGF-I receptors (IGF-IRs). We show that LTP not only increases the output of pyramidal neurons, but also favors the NMDAR-dependent LTP, resulting in the crucial information processing at the barrel cortex since specific deletion of IGF-IR in cortical astrocytes impairs the whisker discrimination task. Our work reveals a novel mechanism and functional consequences of IGF-I signaling on cortical inhibitory synaptic plasticity and animal behavior, revealing that astrocytes are key elements in these processes. ; This work was supported by Grants BFU2016-80802-P from Agencia Estatal de Investigación Spain/Fondo Europeo de Desarrollo Regional, and from the European Union [Ministerio de Economía y Competitividad (MINECO)] to D.F.d.S.; Grants R01-NS-097312 and R01-DA-048822 from National Institutes of Health/National Institute of Neurological Disorders and Stroke to A.A.; and grants from Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED) and Grant SAF2016-76462-C2-1-P from MINECO to I.T.-A. J.A.Z.-V. was supported by the National Council of Science, Technology and Technological Innovation (CONCYTEC, Perú) through the National Fund for Scientific and Technological Development (FONDECYT, Perú). J.F. received a postdoctoral fellowship from Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP; Grants #2017/14742-0 and #2019/03368-5). We thank the University of Minnesota ...

People who are more avoidant of pathogens are more politically conservative, as are nations with greater parasite stress. In the current research, we test two prominent hypotheses that have been proposed as explanations for these relationships. The first, which is an intragroup account, holds that these relationships between pathogens and politics are based on motivations to adhere to local norms, which are sometimes shaped by cultural evolution to have pathogenneutralizing properties. The second, which is an intergroup account, holds that these same relationships are based on motivations to avoid contact with outgroups, who might pose greater infectious disease threats than ingroup members. Results from a study surveying 11,501 participants across 30 nations are more consistent with the intragroup account than with the intergroup account. National parasite stress relates to traditionalism (an aspect of conservatism especially related to adherence to group norms) but not to social dominance orientation (SDO; an aspect of conservatism especially related to endorsements of intergroup barriers and negativity toward ethnic and racial outgroups). Further, individual differences in pathogen-avoidance motives (i.e., disgust sensitivity) relate more strongly to traditionalism than to SDO within the 30 nations.