Sensory selection and movement locally and globally modulate neural responses in seemingly similar ways. For example, locomotion enhances visual responses in mouse primary visual cortex (V1), resembling the effects of spatial attention on primate visual cortical activity. However, interactions between these local and global mechanisms and the resulting effects on perceptual behavior remain largely unknown. Here, we describe a novel mouse visual spatial selection task in which animals either monitor one of two locations for a contrast change (''selective mice'') or monitor both (''non-selective mice'') and can run at will. Selective mice perform well only when their selected stimulus changes, giving rise to local electrophysiological changes in the corresponding hemisphere of V1 including decreased noise correlations and increased visual information. Non-selective mice perform well when either stimulus changes, giving rise to global changes across both hemispheres of V1. During locomotion, selective mice have worse behavioral performance, increased noise correlations in V1, and decreased visual information, while non-selective mice have decreased noise correlations in V1 but no change in performance or visual information. Our findings demonstrate that mice can locally or globally enhance visual information, but the interaction of the global effect of locomotion with local selection impairs behavioral performance. Moving forward, this mouse model will facilitate future studies of local and global sensory modulatory mechanisms and their effects on behavior.

No abstract

The relationships between protein synthesis and neuronal survival are poorly understood. In chicken nucleus magnocellularis (NM), significant alterations in overall protein synthesis precede neuronal death induced by deprivation of excitatory afferent activity. Previously we demonstrated an initial reduction in the overall rate of protein synthesis in all deprived NM neurons, followed by quick recovery (starting at 6h) in some, but not all, neurons. Neurons with recovered protein synthesis ultimately survive while others become “ghost” cells (no detectable Nissl substance) at 12–24h and die within 48h. To explore the mechanisms underlying this differential influence of afferent input on protein synthesis and cell survival, the current study investigates the involvement of eukaryotic translation elongation factor 2 (eEF2), the phosphorylation of which reduces overall protein synthesis. Using immunocytochemistry for either total or phosphorylated eEF2 (p-eEF2), we find significant reductions in the level of phosphorylated, but not total, eEF2 in NM neurons as early as 0.5h to 1h following cochlea removal. Unexpectedly, neurons with low levels of p-eEF2 show reduced protein synthesis at 6h indicated by a marker for active ribosomes. At 12h, all “ghost” cells exhibited little or no p-eEF2 staining although not every neuron with a comparable low level of p-eEF2 was a “ghost” cell. These observations demonstrate that a reduced level of p-eEF2 is not responsible for immediate responses (including reduced overall protein synthesis) of a neuron to compromised afferent input, but may impair the neuron’s ability to initiate recovery signaling for survival and make the neuron more vulnerable to death.

The claustrum is a small subcortical structure with widespread connections with disparate regions of the cortex. These far-reaching projections have led to many hypotheses concerning its function. However, we know little about how claustrum input affects neural activity in cortex, particularly beyond frontal areas. Here, using optogenetics and multi-regional Neuropixels recordings from over 15,000 neurons in awake mice, we demonstrate that the effect of claustrum input differs depending on brain area, layer, and cell type. Brief claustrum stimulation produces approximately 1 spike per claustrum neuron, which affects many fast-spiking (FS; putative inhibitory) but very few regular-spiking (RS; putative excitatory) cortical neurons. Prolonged claustrum stimulation affects many more cortical FS and RS neurons. More inhibition occurs in frontal regions and deeper layers, while more excitation occurs in posterior regions and superficial layers. These differences imply that the function of claustrum input to cortex depends on the area, supporting the idea that claustro-cortical circuits are organized into functional modules.