Recurrent interactions in local cortical circuits

Local microcircuits within neocortical columns form key determinants of sensory processing. Here, we investigate the excitatory synaptic neuronal network of an anatomically defined cortical column, the C2 barrel column of mouse primary somatosensory cortex. This cortical column is known to process tactile information related to the C2 whisker. Through multiple simultaneous whole-cell recordings, we quantify connectivity maps between individual excitatory neurons located across all cortical layers of the C2 barrel column. Synaptic connectivity depended strongly upon somatic laminar location of both presynaptic and postsynaptic neurons, providing definitive evidence for layer-specific signaling pathways. The strongest excitatory influence upon the cortical column was provided by presynaptic layer 4 neurons. In all layers we found rare large-amplitude synaptic connections, which are likely to contribute strongly to reliable information processing. Our data set provides the first functional description of the excitatory synaptic wiring diagram of a physiologically relevant and anatomically well-defined cortical column at single-cell resolution.

Anatomical studies demonstrate that excitatory connections in cortex are not uniformly distributed across a network but instead exhibit clustering into groups of highly connected neurons. The implications of clustering for cortical activity are unclear. We studied the effect of clustered excitatory connections on the dynamics of neuronal networks that exhibited high spike time variability owing to a balance between excitation and inhibition. Even modest clustering substantially changed the behavior of these networks, introducing slow dynamics during which clusters of neurons transiently increased or decreased their firing rate. Consequently, neurons exhibited both fast spiking variability and slow firing rate fluctuations. A simplified model shows how stimuli bias networks toward particular activity states, thereby reducing firing rate variability as observed experimentally in many cortical areas. Our model thus relates cortical architecture to the reported variability in spontaneous and evoked spiking activity.

By homologous recombination of an internal ribosome entry site and Cre recombinase coding region into the 3′-untranslated region of the mouse Emx1 gene, we have generated a strain of mice, Emx1 IRES cre , that expresses the Cre recombinase in a spatial and temporal pattern like that observed for Emx1. When mated to reporter strains, these mice are a sensitive means to fate-map the Emx1-expressing cells of the developing forebrain. Our results demonstrate that radial glia, Cajal-Retzius cells, glutamatergic neurons, astrocytes, and oligodendrocytes of most pallial structures originate from an Emx1-expressing lineage. On the other hand, most of the pallial GABAergic neurons arise outside the Emx1-expressing lineage. Structures that are located near the basal ganglia (e.g., the amygdala and endopiriform nuclei) are not uniformly derived from Emx1-expressing cells.