May 28, 1999 -- Snake venoms produce devastating effects on the nervous system, so it comes as somewhat of a surprise that the brain of a mouse would harbor a molecule similar to a major component of the deadly toxins. Howard Hughes Medical Institute (HHMI) researchers at The Rockefeller University have found that this is indeed the case and they believe that the molecule they discovered, called lynx1, may be involved in pathways that are linked to memory and muscle function.
Nathaniel Heintz, an HHMI investigator at The Rockefeller University, emphasized that at this time the discovery by his group, which is reported in the May 28, 1999, issue of the journal Neuron, pertains only to cultured mouse cells. "The presence of lynx1 in the brain is really provocative because parts of the protein bear a striking resemblance to certain snake toxins," said Heintz.
When a poisonous snake bites a person, alpha-neurotoxins in the venom block acetylcholine receptors on the tips of muscle nerves. Acetylcholine is a neurotransmitter that helps to activate muscles and causes them to contract. Most who are killed by venomous snakes die of respiratory failure because the alpha-neurotoxins shut down the diaphragm muscles, causing suffocation.
While searching for genes that regulate brain development, Heintz and postdoctoral associate Julie Miwa found lynx1. The investigators decided to continue studying lynx1 when experiments indicated that the gene is expressed in the mouse brain two to three weeks after birth -- a time during which the wiring of the mouse's nervous system is fine-tuned. Further experiments showed that expression of the newly found gene was restricted to certain classes of neurons in the brain, suggesting a specialized and perhaps unique role for the protein.
Heintz and Miwa, however, did not realize the full impact of their discovery
until they identified the fam
Contact: Jim Keeley
Howard Hughes Medical Institute