t has also shown that cataplexy occurred during vigorous play or when excited. Moreover, it was found that when the medial medulla is stimulated with an electrode muscle tone disappears. This effect appears to occur to prevent muscle movement during REM sleep and some muscle tone regulation while awake. Siegel found that during a cataplectic episode in the narcoleptic dogs this region of the brain became active. Additionally, it was found that in normal individuals this region of the brain is only highly active during REM sleep. A research in Siegels laboratory, Elizabeth Schenkel, demonstrated that normal animals with damaged medial medullas moved during REM sleep. Furthermore, other researchers showed that animals with damage higher on the brain stem, which connected to the medulla raised their heads, walked and appeared to attack imaginary adversaries during REM sleep (78). Another area in the brain has been targeted in playing a role in narcolepsy. This area is called the locus coeruleus. This region releases norepinephrine, which is involved in fight or flight reactions. It has been found that in normal individuals the locus coeruleus is active while awake and inactive during REM sleep. However, narcoleptics have inactive locus coeruleuss before and during cataplexy, just like REM sleep. Since concluding what occurs during these cataplectic attacks research has now focused on why they occur. Researchers have now determined the gene, which causes narcolepsy in dogs, and have concluded that the dogs have a mutation in a receptor for hypocretin or orexin. The dogs receptors lack a part which enables the neurotransmitter to be properly received. Furthermore, mice that have neurons, incapable of sending hypocretin/orexin have symptoms which mimic narcolepsy, including immediate REM sleep. Hypocretin/orexin is produced in the hypothalamus, which has connections to many parts of the brain including the locus coeruleus. However, it is not...
