Top-down attention increases coding abilities by altering firing rates and rate variability. In the frontal eye field (FEF), a key area enabling top-down attention, attention induced firing rate changes are profound, but its effect on different cell types is unknown. Moreover, FEF is the only cortical area investigated in which attention does not affect rate variability, as assessed by the Fano factor, suggesting that task engagement affects cortical state nonuniformly. We show that putative interneurons in FEF of Macaca mulatta show stronger attentional rate modulation than putative pyramidal cells. Partitioning rate variability reveals that both cell types reduce rate variability with attention, but more strongly so in narrow-spiking cells. The effects are captured by a model in which attention stabilizes neuronal excitability, thereby reducing the expansive nonlinearity that links firing rate and variance. These results show that the effect of attention on different cell classes and different coding properties are consistent across the cortical hierarchy, acting through increased and stabilized neuronal excitability.
Attention is critical to high-level cognition, and attentional deficits are a hallmark of cognitive dysfunction. A key transmitter for attentional control is acetylcholine, but its cellular actions in attention-controlling areas remain poorly understood. Here we delineate how muscarinic and nicotinic receptors affect basic neuronal excitability and attentional control signals in different cell types in macaque frontal eye field. We found that broad spiking and narrow spiking cells both require muscarinic and nicotinic receptors for normal excitability, thereby affecting ongoing or stimulus-driven activity. Attentional control signals depended on muscarinic, not nicotinic receptors in broad spiking cells, while they depended on both muscarinic and nicotinic receptors in narrow spiking cells. Cluster analysis revealed that muscarinic and nicotinic effects on attentional control signals were highly selective even for different subclasses of narrow spiking cells and of broad spiking cells. These results demonstrate that cholinergic receptors are critical to establish attentional control signals in the frontal eye field in a cell type-specific manner.
Our data support a role for CB1 at the level of the thalamus acting as a dynamic modulator of visual information being sent to the cortex, apparently maintaining the salience of the signal within upper and lower boundaries. This may account for some of the behavioral effects of cannabis.
Cortical slow oscillations (≲1 Hz) are an emergent property of the cortical network that integrate connectivity and physiological features. This rhythm, highly revealing of the characteristics of the underlying dynamics, is a hallmark of low complexity brain states like sleep, and represents a default activity pattern. Here, we present a methodological approach for quantifying the spatial and temporal properties of this emergent activity. We improved and enriched a robust analysis procedure that has already been successfully applied to both in vitro and in vivo data acquisitions. We tested the new tools of the methodology by analyzing the electrocorticography (ECoG) traces recorded from a custom 32-channel multi-electrode array in wild-type isoflurane-anesthetized mice. The enhanced analysis pipeline, named SWAP (Slow Wave Analysis Pipeline), detects Up and Down states, enables the characterization of the spatial dependency of their statistical properties, and supports the comparison of different subjects. The SWAP is implemented in a data-independent way, allowing its application to other data sets (acquired from different subjects, or with different recording tools), as well as to the outcome of numerical simulations. By using the SWAP, we report statistically significant differences in the observed slow oscillations (SO) across cortical areas and cortical sites. Computing cortical maps by interpolating the features of SO acquired at the electrode positions, we give evidence of gradients at the global scale along an oblique axis directed from fronto-lateral toward occipito-medial regions, further highlighting some heterogeneity within cortical areas. The results obtained using the SWAP will be essential for producing data-driven brain simulations. A spatial characterization of slow oscillations will also trigger a discussion on the role of, and the interplay between, the different regions in the cortex, improving our understanding of the mechanisms of generation and propagation of delta rhythms and, more generally, of cortical properties.
The development and maturation of cortical circuits relies on the coordinated actions of long and short range axonal guidance cues. In this regard, the class 3 semaphorins and their receptors have been seen to be involved in the development and maturation of the hippocampal connections. However, although the role of most of their family members have been described, very few data about the participation of Semaphorin 3E (Sema3E) and its receptor PlexinD1 during the development and maturation of the entorhino-hippocampal (EH) connection are available. In the present study, we focused on determining their roles both during development and in adulthood. We determined a relevant role for Sema3E/PlexinD1 in the layer-specific development of the EH connection. Indeed, mice lacking Sema3E/PlexinD1 signalling showed aberrant layering of entorhinal axons in the hippocampus during embryonic and perinatal stages. In addition, absence of Sema3E/PlexinD1 signalling results in further changes in postnatal and adult hippocampal formation, such as numerous misrouted ectopic mossy fibers. More relevantly, we describe how subgranular cells express PlexinD1 and how the absence of Sema3E induces a dysregulation of the proliferation of dentate gyrus progenitors leading to the presence of ectopic cells in the molecular layer. Lastly, Sema3E mutant mice displayed increased network excitability both in the dentate gyrus and the hippocampus proper.
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