Description
This study investigates the role of vasoactive intestinal peptide (VIP) interneurons in adult ocular dominance plasticity, focusing on how different components of VIP signalling contribute to cortical network reorganisation following monocular deprivation (MD). While plasticity is most prominent during the critical period, the adult visual cortex retains a limited but functionally relevant capacity for experience-dependent change. Locomotion has been shown to enhance this plasticity via a VIP→SST disinhibitory circuit, yet the specific contributions of VIP peptide signalling versus GABAergic output remain unclear.
To address this, two transgenic mouse models were used: VIP knockout (VIPKO) mice, lacking VIP peptide signalling, and VIP-cre;Vgat fl/fl (VIPVGAT) mice, in which GABA release from VIP interneurons is impaired. In vivo two-photon calcium imaging was performed in awake mice to record neuronal activity in layer 2/3 of primary visual cortex across baseline, MD and recovery timepoints. Functional connectivity was assessed using pairwise correlations and then multilayer community analysis. Noise and signal correlations, population coupling was also assessed to help explain potential network configuration.
At the network level, VIPVGAT mice showed trends towards increased modularity, greater community number, and reduced flexibility, consistent with a more segregated and less adaptable network, although these effects were not statistically significant. The most robust finding was a significant change in similarity to baseline community structure, indicating sustained network reorganisation across all groups.
Across all groups, MD induced a reduction in correlations and population coupling, consistent with network reorganisation. Control mice showed partial recovery, particularly during locomotion, suggesting stabilisation of a reorganised network. VIPKO mice exhibited broadly similar network organisation but showed an ipsilateral bias in recovery, indicating asymmetric restoration of connectivity. In contrast, VIPVGAT mice showed weaker recovery overall, with noise correlations and population coupling failing to return towards baseline, especially during running.
Overall, these findings suggest that GABAergic output from VIP interneurons plays a role in coordinating activity-dependent recovery and network restructuring in the adult visual cortex.
Lay Abstract
The adult brain retains some capacity for plasticity, allowing it to adapt to changes in sensory input, although this is more limited than during early development. This study investigates how neuronal circuits in the visual cortex reorganise following monocular deprivation (MD), where one eye is temporarily closed, and how this process is influenced by vasoactive intestinal peptide (VIP) interneurons.
VIP interneurons form part of a disinhibitory circuit that increases cortical responsiveness, particularly during locomotion. However, it is unclear whether their role in plasticity depends on VIP signalling itself or their GABAergic output. To address this, two mouse models were studied: VIP knockout (VIPKO) mice and VIP-cre;Vgat fl/fl (VIPVGAT) mice with impaired GABA release.
Neuronal activity was recorded using in vivo two-photon calcium imaging across baseline, deprivation and recovery. Functional connectivity and network organisation were analysed using multilayer community analysis and correlation measures.
MD reduced neuronal correlations and altered network organisation in all groups. Control mice showed partial recovery, especially during locomotion. VIPKO mice showed similar patterns but with a bias towards the non-deprived eye, whereas VIPVGAT mice showed weaker recovery overall.
These findings suggest that GABAergic output from VIP interneurons contributes to network-level plasticity in the adult visual cortex.
| Lay Title | The role of VIP interneurons in ocular dominance plasticity |
|---|---|
| Role | Other |