These are the findings of Dr. Tallie Z. Baram and her collaborators at the UC Irvine College of Medicine, Neurocrine Biosciences, Inc., and the Max Planck Institute of Psychiatry. For the first time, the researchers have identified how increased amounts of a key messenger for stress, the neuropeptide CRH, can inhibit the normal growth of dendrites, which are branch-like protrusions of neurons that send and receive messages from other brain cells.
The researchers believe CRH ultimately may be responsible for these poorly developed zones in brain cells. Results of their study appear in the current online early edition of the Proceedings of the National Academy of Sciences.
"These findings may prove to be highly relevant for understanding the origins of several human brain disorders, and they also point to some potential preventive treatments," said Baram, the Danette Shepard Chair in Neurological Studies. "The activation of stress hormones and molecules seems to initiate a complex cascade of brain effects that is related to depression and dementia. This study reveals a novel role of CRH in this cascade."
Communication among brain cells is the foundation of cognitive processes such as learning and memory. In several human brain disorders where learning and similar thought processes are abnormal, dendrites in the hippocampus where learning and memory occurs - have been found to be small or poorly developed. Normally, CRH is found in the hippocampus, and small amounts that are released during stress may improve cellular communication.
But when the investigators in this study grew the hippocampus of baby rats in a dish and administered higher doses of CRH to the cultured hippoca
Contact: Tom Vasich
University of California - Irvine