Scientists in Portugal Use Neurolucida Explorer to Analyze Neuroplasticity in Depression

Nucleus Accumbens

Nucleus Accumbens

Life’s little pleasures often elude those suffering from depression, including rats, who show little interest in sugar water after experiencing stress. This behavior leads scientists to speculate that the illness might be characterized by a defect in the brain’s neural reward circuit.

Recent research focuses on a key element of this circuit – the nucleus accumbens (NAc), part of the brain region known as the ventral striatum, which is thought to regulate motivation and reward processing. In a new study of stress-induced depression in rats, researchers at the University of Minho in Braga, Portugal saw morphological changes in the dendrites of medium spiny neurons in the NAc, alongside disturbances in gene expression in this region. They also saw these changes reversed after administering antidepressants.

By using Neurolucida Explorer to analyze 3D reconstructions of medium spiny neurons generated with Neurolucida, the researchers observed longer than normal dendrites and greater spine density in the depressed rats. According to the paper, these findings contrast with studies of the hippocampus and prefrontal cortex, where chronic stress leads to shorter dendrites.

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Researchers Control Rodent Depression With Optogenetics

Imagine if you could switch your depression off like a light. Researchers did it in mice. They used optogenetics to gain more insight into how brain circuits work in cases of depression, and discovered that different types of stress trigger different activity patterns in the same brain circuit.

Two papers published recently in the journal Nature describe how neuronal activity in specific brain circuits in mice can be turned on and off to control depression-like behavior. Both studies used optogenetics, a research method pioneered by one of our customers, Dr. Karl Deisseroth that combines fiber optics and genetic engineering to control the activity of specific neurons. Dr. Deisseroth, a neuroscientist and psychiatrist at Stanford University contributed to both papers. Continue reading “Researchers Control Rodent Depression With Optogenetics” »

Yale Researchers Make Breakthrough in Possible Depression Treatment

Commonly used as a human anaesthetic and animal tranquilizer, the experimental drug ketamine became famous in the last two decades as a hallucinatory club drug known as “Special K.” Now, researchers at Yale University say the drug is beneficial in treating depression by increasing synaptic connections in parts of the brain that regulate mood and cognition.

Dr. Ronald Duman, who uses Stereo Investigator and Neurolucida at his lab at the Yale School of Medicine was a co-author of the study. He and Dr. George Aghajanian studied rats exposed to stressful situations that produce symptoms similar to those found in human depression.

It appears that depression lowers the number of neuronal synaptic connections in the prefrontal cortex and hippocampus. Current antidepressants reverse these effects, but may take a long time to work, and aren’t successful in all cases. According to Drs. Duman and Aghajanian, ketamine “produces rapid (within hours) antidepressant responses in patients who are resistant to typical antidepressants,” by promoting new synaptic connections and reversing synaptic loss from stress.

“Ketamine works on an entirely different type of neurotransmitter system than current antidepressants, which can take months to improve symptoms of depression and do not work at all for one out of every three patients. Understanding how ketamine works in the brain could lead to the development of an entirely new class of antidepressants, offering relief for tens of millions of people suffering from chronic depression,” according to the Yale School of Medicine press release.

Learn more about the study on, and read the free abstract or full paper (by subscription) at

R. S. Duman, G. K. Aghajanian. Synaptic Dysfunction in Depression: Potential Therapeutic Targets. Science, 2012; 338 (6103): 68 DOI: 10.1126/science.1222939