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Attention deficit disorders could stem from impaired brain coordination: Researchers uncover link absent between brain regions in attention deficit hyperactivity disorder, schizophrenia -- ScienceDaily

When the researchers attached probes to the mice to measure brain activity, they found mice without ErbB4 had brain regions that were acting independently, rather than together in synchrony. In particular, the researchers studied the prefrontal cortex -- normally associated with decision-making -- and the hippocampus -- a region that supports memory. These two regions coordinate for a variety of brain tasks, including memory and attention. "We found top-down attention, previously thought to be controlled by the prefrontal cortex, also involves the hippocampus in a manner where the two regions are highly synchronized when attention is high," says Mei. "Our findings give importance to synchrony between the prefrontal cortex and hippocampus in top-down attention and open up the possibility that attention deficit disorders, like ADHD, might involve impairments in the synchrony between these two regions." According to the new study, ErbB4 coordinates a cascade of brain signals that "bridge" the two regions. ErbB4 itself encodes a receptor found on the surface of brain cells. The study found that when a protein (neuregulin-1) attaches to the ErbB4 receptor, it triggers a chain reaction that ultimately determines neurotransmitter levels in the prefrontal cortex and hippocampus. Without ErbB4, neurotransmitter levels go awry. The researchers discovered mice lacking ErbB4 have low levels of a particular neurotransmitter -- GABA, or gamma-aminobutyric acid -- in their brain. Low GABA levels can lead to impaired top-down attention in the prefrontal cortex, and impairs how the prefrontal cortex can efficiently coordinate with the hippocampus. The researchers concluded that ErbB4 helps link the two brain regions to maintain attention.

Neuroscientists identify brain circuit necessary for memory formation: New findings challenge standard model of memory consolidation -- ScienceDaily

The researchers labeled memory cells in three parts of the brain: the hippocampus, the prefrontal cortex, and the basolateral amygdala, which stores memories' emotional associations. Just one day after the fear-conditioning event, the researchers found that memories of the event were being stored in engram cells in both the hippocampus and the prefrontal cortex. However, the engram cells in the prefrontal cortex were "silent" -- they could stimulate freezing behavior when artificially activated by light, but they did not fire during natural memory recall. "Already the prefrontal cortex contained the specific memory information," Kitamura says. "This is contrary to the standard theory of memory consolidation, which says that you gradually transfer the memories. The memory is already there." Over the next two weeks, the silent memory cells in the prefrontal cortex gradually matured, as reflected by changes in their anatomy and physiological activity, until the cells became necessary for the animals to naturally recall the event. By the end of the same period, the hippocampal engram cells became silent and were no longer needed for natural recall. However, traces of the memory remained: Reactivating those cells with light still prompted the animals to freeze. In the basolateral amygdala, once memories were formed, the engram cells remained unchanged throughout the course of the experiment. Those cells, which are necessary to evoke the emotions linked with particular memories, communicate with engram cells in both the hippocampus and the prefrontal cortex.