Cataplexy-related neurons in the amygdala of the narcoleptic dog
| Autor: | Robert Nienhuis, Ming-Fung Wu, Seema Gulyani, Joshi John, Jerome M. Siegel |
|---|---|
| Rok vydání: | 2002 |
| Předmět: |
Cataplexy
Population Action Potentials Hippocampus Amygdala Article Dogs Basal ganglia medicine Prazosin Animals Premovement neuronal activity Wakefulness education Adrenergic alpha-Antagonists Narcolepsy Cerebral Cortex Neurons Sleep disorder education.field_of_study Electromyography General Neuroscience Electroencephalography medicine.disease Electrodes Implanted Disease Models Animal Electrooculography medicine.anatomical_structure Muscle Tonus Sleep Stages medicine.symptom Psychology Neuroscience medicine.drug |
| Zdroj: | Neuroscience |
| ISSN: | 0306-4522 |
| DOI: | 10.1016/s0306-4522(02)00089-1 |
| Popis: | 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 α-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. Published by Elsevier Science Ltd on behalf of IBRO. |
| Databáze: | OpenAIRE |
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