Neurotransmitter Surge May Induce Amnesia

Results in rats suggest long-term memory loss may not be due to reduced protein synthesis

THURSDAY, July 19 (HealthDay News) -- Although protein synthesis is thought to play a key role in the formation of long-term memories, a new study suggests this might not be the case. Amnesia in rats caused by the protein-inhibiting chemical anisomycin can be prevented by curbing the surge in neurotransmitters that occurs after injection, according to a report published online July 18 in the Proceedings of the National Academy of Sciences Early Edition.

Paul Gold, Ph.D., from the University of Illinois at Urbana-Champaign, and colleagues measured the levels of norepinephrine, dopamine and serotonin, as well as behavioral responses after intra-amygdala injection of rats with anisomycin, a protein synthesis inhibitor.

The investigators found that levels of the neurotransmitters increased 1,000 to 17,000 percent after injection and then dropped to below baseline within 48 hours. These changes correlated with amnesia-like responses during long-term memory tests. Stabilizing neurotransmitter release by modifying β-adrenergic receptor activity attenuated the anisomycin-induced amnesia while injection of norepinephrine alone before training caused memory deficits.

"The findings described here therefore offer evidence for a substantially different mechanism for the amnesias produced by inhibition of protein synthesis than one of a necessity for de novo protein synthesis for the formation of new long-lasting memories, a conclusion often used as the basis for pursuing changes in gene expression related to memory formation," the authors write.

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