Flexible spatial learning requires both the dorsal and ventral hippocampus and their functional interactions with the prefrontal cortex.

When faced with changing contingencies, animals can use memory to flexibly guide actions, engaging both frontal and temporal lobe brain structures. Damage to the hippocampus (HPC) impairs episodic memory, and damage to the prefrontal cortex (PFC) impairs cognitive flexibility, but the circuit mechanisms by which these areas support flexible memory processing remain unclear. The present study investigated these mechanisms by temporarily inactivating the medial PFC (mPFC), the dorsal HPC (dHPC), and the ventral HPC (vHPC), individually and in combination, as rats learned spatial discriminations and reversals in a plus maze. Bilateral inactivation of either the dHPC or vHPC profoundly impaired spatial learning and memory, whereas bilateral mPFC inactivation primarily impaired reversal versus discrimination learning. Inactivation of unilateral mPFC together with the contralateral dHPC or vHPC impaired spatial discrimination and reversal learning, whereas ipsilateral inactivation did not. Flexible spatial learning thus depends on both the dHPC and vHPC and their functional interactions with the mPFC.

Saliency affects feedforward more than feedback processing in early visual cortex.

Early visual cortex activity is influenced by both bottom-up and top-down factors. To investigate the influences of bottom-up (saliency) and top-down (task) factors on different stages of visual processing, we used transcranial magnetic stimulation (TMS) of areas V1/V2 to induce visual suppression at varying temporal intervals. Subjects were asked to detect and discriminate the color or the orientation of briefly-presented small lines that varied on color saliency based on color contrast with the surround. Regardless of task, color saliency modulated the magnitude of TMS-induced visual suppression, especially at earlier temporal processing intervals that reflect the feedforward stage of visual processing in V1/V2. In a second experiment we found that our color saliency effects were also influenced by an inherent advantage of the color red relative to other hues and that color discrimination difficulty did not affect visual suppression. These results support the notion that early visual processing is stimulus driven and that feedforward and feedback processing encode different types of information about visual scenes. They further suggest that certain hues can be prioritized over others within our visual systems by being more robustly represented during early temporal processing intervals.

Force generated by actomyosin contraction builds bridges between adhesive contacts.

Extracellular matrices in vivo are heterogeneous structures containing gaps that cells bridge with an actomyosin network. To understand the basis of bridging, we plated cells on surfaces patterned with fibronectin (FN)-coated stripes separated by non-adhesive regions. Bridges developed large tensions where concave cell edges were anchored to FN by adhesion sites. Actomyosin complexes assembled near those sites (both actin and myosin filaments) and moved towards the centre of the non-adhesive regions in a treadmilling network. Inhibition of myosin-II (MII) or Rho-kinase collapsed bridges, whereas extension continued over adhesive areas. Inhibition of actin polymerization (latrunculin-A, jasplakinolide) also collapsed the actomyosin network. We suggest that MII has distinct functions at different bridge regions: (1) at the concave edges of bridges, MIIA force stimulates actin filament assembly at adhesions and (2) in the body of bridges, myosin cross-links actin filaments and stimulates actomyosin network healing when breaks occur. Both activities ensure turnover of actin networks needed to maintain stable bridges from one adhesive region to another.