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takyon writes:

Well? Are you ready?

Imagine if doctors could precisely insert a tiny amount of a custom drug into a specific circuit in your brain and improve your depression (or other mood problems) — instead of treating the entire brain. That's exactly what Duke University researchers have explored in mice. Stress-susceptible animals that appeared depressed or anxious were restored to relatively normal behavior this way, according to a study appearing in the forthcoming July 20 issue of Neuron. The plan was to define specific glitches in the neural circuits and then use a drug to fix them. The ambitious goal: go from a protein, to a signaling activity, to a cell, to a circuit, to activity that happens across the whole brain, to actual behavior.

The team started by precisely placing arrays of 32 electrodes in four brain areas of the mice [...] Then they recorded brain activity as these mice were subjected to a stressful situation called chronic social defeat.* This allowed the researchers to observe the activity between the prefrontal cortex and three areas of the limbic system that are implicated in major depression. To interpret the complicated data coming from the electrodes, the team used machine learning algorithms — identifying which parts of the data seemed to be the timing control signal between the prefrontal cortex and the limbic system— and then zeroed in on the individual neurons involved in that cortical signal and its corresponding circuit.

They then applied engineered molecules called DREADD (Designer Receptors Exclusively Activated by Designer Drug), developed by University of North Carolina at Chapel Hill pharmacologist Bryan Roth, in very tiny amounts (0.5 microliter). A drug that attaches only to that DREADD is then administered to give the researchers control over the circuit. They found that direct stimulation of PFC-amygdala neural circuitry with DREADDs normalized PFC-dependent limbic synchrony in stress-susceptible animals and restored normal behavior. The researchers suggest that their findings also demonstrate an interdisciplinary approach that can be used to identify the large-scale network changes that underlie complex emotional pathologies and the specific network nodes that can be used to develop targeted interventions.

Dysregulation of Prefrontal Cortex-Mediated Slow-Evolving Limbic Dynamics Drives Stress-Induced Emotional Pathology (DOI: 10.1016/j.neuron.2016.05.038)

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