Biology subjects

Ito, W.

Publications and source records attributed to Ito, W..

7 recordsLinked to original sources

bioRxiv2026

Affiliation in mice induced by an auditory-conditioned stimulus

Social affiliation is a vital survival strategy that promotes well-being across species. While innate threats consistently trigger affiliation, it remains unclear whether learned threats engage the same affiliative systems. Here, we report that an auditory conditioned stimulus induced affiliation in mice. In same-sex dyads, mice subjected to auditory fear conditioning increased proximity during presentation of the conditioned stimulus (CS). This CS-evoked affiliation was independent of freezing levels, required familiarity between partners, and depended on intact basolateral amygdala-to-ventral hippocampus inputs and oxytocin signaling. These findings suggest that neural pathways activated by learned and innate threats converge on shared social-affiliation circuitry.

neuroscience↗

bioRxiv2024

Sex and stress interactions in fear synchrony of mouse dyads

Socially coordinated threat responses support the survival of animal groups. Given their distinct social roles, males and females must differ in such coordination. Here, we report such differences during the synchronization of auditory-conditioned freezing in mouse dyads. To study the interaction of emotional states with social cues underlying synchronization, we modulated emotional states with prior stress or modified the social cues by pairing unfamiliar or opposite-sex mice. In same-sex dyads, males exhibited more robust synchrony than females. Stress disrupted male synchrony in a prefrontal cortex-dependent manner but enhanced it in females. Unfamiliarity moderately reduced synchrony in males but not in females. In dyads with opposite-sex partners, fear synchrony was resilient to both stress and unfamiliarity. Decomposing the synchronization process in the same-sex dyads revealed sex-specific behavioral strategies correlated with synchrony magnitude: following partners state transitions in males and retroacting synchrony-breaking actions in females. Those were altered by stress and unfamiliarity. The opposite-sex dyads exhibited no synchrony-correlated strategy. These findings reveal sex-specific adaptations of socio-emotional integration defining coordinated behavior and suggest that sex-recognition circuits confer resilience to stress and unfamiliarity in opposite-sex dyads.

neuroscience↗

bioRxiv2022

Sex differences in social synchronization of conditioned fear.

Socially coordinated threat responses support the survival of social groups, and the distinct social roles of males and females predict sex differences in such coordination. However, this study area remains unexplored in mice, the most commonly used laboratory species. Here, we examined two behaviors: a recently reported fear synchrony, where paired mice synchronize auditory-conditioned freezing more strongly in males, and a newly identified CS-induced affiliation, where mice increase proximity upon a conditioned stimulus. These behaviors necessitate the integration of social cues with emotional CS. To understand how sex influences that process, we manipulated social cues through partner familiarity and emotional states via prior stress. Unfamiliarity moderately reduced synchrony in male dyads but not in females. Whereas stress disrupted male synchrony and contrarily enhanced female synchrony. Unfamiliarity eliminated CS-induced affiliation in both sexes, while stress caused males to distance each other but had no effects in females. Interestingly, heterosexual dyads showed resilience in both coordinated behaviors unaffected by stress or unfamiliarity. These findings reveal sex-specific adaptations in socio-emotional integration when orchestrating socially coordinated behaviors and suggest that the sex-recognition circuits confer stress- and unfamiliarity-resilience, in particular, in heterosexual dyads.

neuroscience↗

bioRxiv2019

Disinhibition-assisted LTP in the prefrontal-amygdala pathway via suppression of somatostatin-expressing interneurons

Natural brain adaptations often involve changes in synaptic strength. The artificial manipulations can help investigate the role of synaptic strength in a specific brain circuit not only in various physiological phenomena like correlated neuronal firing and oscillations but also in behaviors. High and low-frequency stimulation at presynaptic sites has been used widely to induce long-term potentiation (LTP) and depression (LTD), respectively. This approach is effective in many brain areas, but not in the basolateral amygdala (BLA), because the robust local GABAergic tone inside the BLA restricts synaptic plasticity. Here, we identified the subclass of GABAergic neurons that gate LTP in the BLA afferents from the dorsomedial prefrontal cortex (dmPFC). Chemogenetic suppression of somatostatin-positive interneurons (Sst-INs) enabled the ex vivo LTP by high-frequency stimulation of the afferent, but the suppression of parvalbumin-positive interneurons (PV-INs) did not. Moreover, optogenetic suppression of Sst-INs with Arch also enabled LTP of the dmPFC-BLA synapses both ex vivo and in vivo. These findings reveal that Sst-INs but not PV-INs gate LTP in the dmPFC-BLA pathway and provide a method for artificial synaptic facilitation in BLA.

neuroscience↗

bioRxiv2018

Observing fear enables plasticity of the dmPFC-BLA pathway during subsequent learning of inhibitory avoidance

Observing fear in others is a form of social distress. In mice, it leads to the formation of silent synapses in the prefrontal-amygdala pathway and enhances inhibitory avoidance learning at a later time. Here, we report that observing fear enabled ex vivo LTP. The unsilencing of silent synapses was the prevailing mechanism and the plasticity was occluded by inhibitory avoidance training. In free moving mice with OF experience, the inhibitory avoidance training transiently facilitated local field potentials evoked in BLA by stimulating the prefrontal afferents. The facilitation persisted during the first 4 hours after IA training, which is the time when IA memories consolidate. Thus, the OF-generated silent synapses enable plasticity that may enhance consolidation of IA memories.

neuroscience↗

bioRxiv2017

Impaired social contacts with familiar anesthetized conspecific in CA3-restricted BDNF knockout mice

Familiarity is the vital characteristic conveyed by social cues to determine behaviors towards conspecific. Here we characterize social contacts to familiar vs unfamiliar male conspecific, anesthetized to eliminate inter-male aggression. During initial 10 min (phase-1), subjects contacted demonstrators vigorously regardless of familiarity. During subsequent 80 min (phase-2), however, they contacted more with familiar than unfamiliar conspecifics. Then, this test was applied on highly aggressive mice with hippocampal CA3-restricted BDNF knockout (KO), in which aggression may mask other behaviors. KO showed less preference to contacting familiar conspecific than wild type (WT) during phase-2 but no differences during phase-1. Among non-social behaviors, eating duration was shorter in the presence of familiar than unfamiliar conspecific in WT, but same in KO. Additionally, KO exhibited reduced pain sensitization. Altogether, these findings suggest that KO has deficits in circuits that process social cues from familiar conspecifics and pain and, possibly, underlie empathy-like behaviors.

animal behavior and cognition↗

bioRxiv2017

Overexpression of Channelrhodopsin 2 interferes with the GABAb receptor-mediated depression of GABA release from the somatostatin-containing interneurons of the prefrontal cortex

Region and cell-type restricted expression of light activated ion channels is the indispensable tool to study properties of synapses in specific circuits and to monitor synaptic alterations by various stimuli including neuromodulators and behaviors, both ex vivo and in vivo. These analyses require the light-activated proteins or viral vectors for their delivery that do not interfere with the phenomenon under study. Here, we report a case of such interference in which the high-level expression of Channelrhodopsin-2 (ChR2) introduced in the somatostatin-positive GABAergic neurons (SOM-INs) of the dorsomedial prefrontal cortex (dmPFC) by an adeno-associated virus vector (AAV) weakens the presynaptic GABAb receptor-mediated suppression of GABA release.

neuroscience↗