An unexpected discovery by UCLA life scientists holds promise for the future development of treatments for post-traumatic stress disorder and other anxiety disorders, and potentially for Alzheimer’s disease and other memory-impairment diseases.
The researchers, led by UCLA professor of psychology Michael Fanselow, have discovered what may be a completely unexplored drug target for the treatment of anxiety disorders. The research is published Jan. 7 in the journal Science.
Normally, when people or animals experience a frightening event, they learn to fear the place of the event and any signals that were present at the time. This occurs because the nerve cells in certain brain regions increase their ability to excite or stimulate one another, said Fanselow, a member of
UCLA’s Brain Research Institute.
Most neuroscience research has emphasized how this phenomenon occurs through chemical communication among neurotransmitters flowing across synapses — the space between neurons. However, there are also small, inhibitory neurons in these regions as well, which have direct electrical contact with one another through connecting channels known as “gap junctions,” Fanselow said. Gap junctions are very common in invertebrates but rare in mammals, where they are found on only certain inhibitory interneurons.
“Because of this, no one has looked at the importance of these gap junctions for learning, memory and emotion,” Fanselow said. “We hypothesized that these gap junctions may be very important. Because the gap junctions cause the inhibitory neurons to fire together, they may cause these inhibitory neurons to act as a pacemaker for the excitatory neurons, making them fire at the same time so they are better able to make fear memories.”
More here:‘Long-shot’ discovery may lead to advances in treating anxiety, memory disorders
