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Mikulovic, S.

Publications and source records attributed to Mikulovic, S..

4 recordsLinked to original sources

Dorsal ocelli set the luminance-dependent operating state of the bumblebee visual system

Despite long-standing hypotheses that insect dorsal ocelli modulate compound-eye processing to support flight stabilization, dim-light navigation, and locomotor speed, the neurophysiological basis of these functions remains unclear. Combining behavioural assays with multi-site local field potential recordings in bumblebees, we tested how ocellar input affects compound-eye processing. Ocellar occlusion impaired orientation precision at dusk, supporting a role for ocelli in dim-light navigation. Under bright daytime skies, occlusion did not affect orientation but reduced flight speed, consistent with a role in locomotor control under high illumination. Neurophysiologically, ocellar occlusion disrupted luminance-dependent scaling across the visual system, most prominently in the medulla. In intact bees, broadband neural power scaled inversely with luminance, decreasing under bright and increasing under dim conditions. When ocellar input was blocked, this relationship reversed, leaving visual-system activity in a high-power, dark-like state even under bright illumination. Ocellar modulation was particularly evident in the green-sensitive pathway, implicated in optic-flow processing and flight-speed regulation, providing a neural correlate of the behavioural speed reduction while UV-sensitive responses remained largely invariant following ocellar occlusion. These findings reconcile disparate views of ocellar function and identify ocelli as regulators of the neural dynamic range supporting orientation in low light and movement control in bright conditions.

neuroscience↗

Autism-like behavior induced by conditional ablation of the Bassoon gene in GABAergic interneurons

Synaptic dysfunction and resulting imbalance of excitatory vs. inhibitory transmission are fundamental aspects of autism spectrum disorders (ASD). Here we addressed the role of inhibitory synapse disturbances in ASD employing mice with a conditional ablation in inhibitory forebrain interneurons of the presynaptic active zone scaffolding protein Bassoon (Bsn), a key factor in synaptic development, activity and maintenance. The conditional Bsn gene knock out resulted in a reduction of synaptic vesicles and reduced synaptic efficacy of affected inhibitory synapses as well as diminished GABAergic inhibition in hippocampal pyramidal neurons. Bsn mutants further displayed a reconfiguration of the hippocampal synaptic network in vivo, as seen in subfield-specific changes of inhibitory synaptic markers and reduced numbers of parvalbumin interneurons, culminating in disturbance of hippocampal network activity patterns and profound mitochondrial and metabolic dysregulation. Importantly, the mutant mice developed behavioral abnormalities reminiscent of ASD including widespread social behavioral deficits and novelty-induced hyperarousal with altered motor behavior, increased anxiety and epileptiform activity. Bsn conditional knock out mice thus provide strong evidence for a causal involvement of GABAergic synapses in the emergence of ASD-related behavioral and physiological phenotypes.

neuroscience↗

Neuronal networks in the dorsal hippocampus causally regulate rescue behavior in mice

Prosocial behaviors, such as rescuing individuals in need, are crucial for social cohesion across species. While key brain regions involved in rescue behavior have been identified, the underlying neural mechanisms remain unclear. The hippocampus (HPC), known for its role in memory and spatial navigation, also contributes to emotional and social processing. However, its specific involvement in prosocial behavior is not well understood. Here, we investigate the causal role of the HPC in learning and executing rescue behavior in mice. Using chemogenetics, we show that the dorsal HPC (dHPC), but not the ventral HPC (vHPC), is essential for acquiring rescue behavior. Calcium imaging of the dHPC reveals network consolidation during successful rescues, with distinct synchronized ensembles and activity patterns linked to liberations of an individual in need. These findings establish a novel role for the dHPC in prosocial behavior, providing insights into the neural mechanisms underlying empathy-driven actions.

neuroscience↗

Locomotion induced by medial septal glutamatergic neurons is linked to intrinsically generated persistent firing

The medial septum and diagonal band of Broca (MSDB) serve as a central hub in an ascending brainstem pathway that conveys sensory and motor signals to the limbic system. However, the cellular and circuit mechanisms underlying these functions remain unclear. Here, we show that transient optogenetic activation of MSDB VGluT2 neurons initiates a structured arousal sequence - beginning with facial movements, followed by pupil dilation and locomotion. Neuropixels recordings reveal persistent MSDB neuronal activity that strongly correlates with arousal-related behaviors. We demonstrate that persistent firing (PF) is an intrinsic property of a subset of MSDB neurons, independent of ongoing synaptic input. PF neurons and putative GABAergic theta-bursting neurons predicted movement initiation, with population activity scaling with initiation magnitude, unlike other MSDB populations. These findings identify PF in the MSDB as a central neural mechanism that orchestrates the transition from preparatory movements to full behavioral engagement, bridging sensory input with locomotor arousal and supporting state transitions within the limbic system.

neuroscience↗