title: Cataplexy-related neurons in the amygdala of the narcoleptic dog.
abstract: The amygdala plays an important role in the interpretation of emotionally significant stimuli and has strong projections to brainstem regions regulating muscle tone and sleep. Cataplexy, a symptom of narcolepsy, is a loss of muscle tone usually triggered by sudden, strong emotions. Extracellular single-unit recordings were carried out in the amygdala of narcoleptic dogs to test the hypothesis that abnormal activity of a subpopulation of amygdala neurons is linked to cataplexy. Of the 218 cells recorded, 31 were sleep active, 78 were active in both waking and rapid-eye-movement sleep, 88 were maximally active during waking, and 21 were state independent. Two populations of cells showed a significant change in activity with cataplexy. A population of sleep active cells localized to central and basal nucleus increased discharges prior to and during cataplexy. A population of wake active cells localized to the cortical nucleus decreased activity prior to and during cataplexy. We hypothesize that these cell populations have a role in mediation or modulation of cataplexy through interactions with meso-pontine regions controlling atonia. The anticholinesterase physostigmine, at doses which increased cataplexy, did not alter the activity of the cataplexy-related cells or of other amygdala cells, suggesting that its effect on cataplexy is mediated 'downstream' of the amygdala. The alpha-1 blocker prazosin, at doses which increased cataplexy, increased discharge in a subgroup of the cataplexy active cells and in a number of other amygdala cells, indicating that prazosin may modulate cataplexy by its action on amygdala cells or their afferents.
authors.affiliation: Department of Psychiatry and Brain Research Institute, University of California at Los Angeles, Los Angeles, CA 91020, USA.
authors.forename: S
authors.initials: S
authors.lastname: Gulyani
authors.forename: M-F
authors.initials: MF
authors.lastname: Wu
authors.forename: R
authors.initials: R
authors.lastname: Nienhuis
authors.forename: J
authors.initials: J
authors.lastname: John
authors.forename: J M
authors.initials: JM
authors.lastname: Siegel
mesh_terms: D000200:Action Potentials / Q000187:drug effects; D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D000679:Amygdala / Q000166:cytology / Q000187:drug effects / Q000503:physiopathology*; D000818:Animals; D002385:Cataplexy / Q000503:physiopathology; D002540:Cerebral Cortex / Q000502:physiology / Q000503:physiopathology; D004195:Disease Models, Animal; D004285:Dogs; D004567:Electrodes, Implanted; D004569:Electroencephalography; D004576:Electromyography; D004585:Electrooculography; D006624:Hippocampus / Q000502:physiology / Q000503:physiopathology; D009129:Muscle Tonus; D009290:Narcolepsy / Q000503:physiopathology*; D009474:Neurons / Q000145:classification / Q000187:drug effects / Q000502:physiology; D011224:Prazosin / Q000494:pharmacology; D012894:Sleep Stages / Q000502:physiology; D014851:Wakefulness / Q000502:physiology
chemical_list: D000317:Adrenergic alpha-Antagonists; D011224:Prazosin