Increase in antidromic excitability in presumed serotonergic dorsal raphe neurons during paradoxical sleep in the cat.
Putative serotonergic dorsal raphe (DRN) neurons display a dramatic state-related change in behaviour, discharging regularly at a high rate during waking and at progressively slower rates during slow-wave sleep (SWS) and ceasing firing during paradoxical sleep (PS). Using the antidromic latency technique and extracellular recording, we have examined the change in neuronal excitability of presumed serotonergic DRN neurons during the wake-sleep cycle in freely moving cats. We found that, under normal conditions, suprathreshold stimulation of the main ascending serotonergic pathway resulted in a marked decrease in both the magnitude and variability of antidromic latency during PS, while subthreshold stimulation led to a marked increase in antidromic responsiveness during PS compared with during other behavioural states. The antidromic latency shift resulted from a change in the delay between the initial segment (IS) and soma-dendritic (SD) spikes, the antidromic latency being inversely related to the interval between the stimulus and the preceding spontaneous action potential. A marked decrease in the magnitude and variability of antidromic latency was also seen following suppression of the spontaneous discharge of DRN neurons by application of 5-HT autoreceptor agonists or muscimol, a potent GABA agonist. A marked IS-SD delay or blockage of SD spikes was, however, seen in association with the PS occurring during recovery from 5-HT autoreceptor agonist or during muscimol application. The present findings are discussed in the light of previous in vitro intracellular recording data and our recent findings of the disfacilitation mechanisms responsible for the cessation of discharge of DRN neurons during PS.
Sakai
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K
INSERM U480, Université Claude Bernard, Lyon 1, Department of Experimental Medicine, 8 Avenue Rockefeller, 69373, Cedex 08, Lyon, France. sakai@univ-lyon1.fr
Crochet
S
S
D017371:8-Hydroxy-2-(di-n-propylamino)tetralin / Q000494:pharmacology; D000818:Animals; D002415:Cats; D005071:Evoked Potentials / Q000187:drug effects / Q000502:physiology*; D005260:Female; D018755:GABA Agonists / Q000494:pharmacology; D008297:Male; D008564:Membrane Potentials / Q000187:drug effects / Q000502:physiology; D008636:Mesencephalon / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D008732:Methoxydimethyltryptamines / Q000494:pharmacology; D009118:Muscimol / Q000494:pharmacology; D009434:Neural Pathways / Q000166:cytology / Q000187:drug effects / Q000502:physiology; D009474:Neurons / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D011903:Raphe Nuclei / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D011930:Reaction Time / Q000187:drug effects / Q000502:physiology; D012701:Serotonin / Q000378:metabolism*; D017366:Serotonin Receptor Agonists / Q000494:pharmacology; D012895:Sleep, REM / Q000187:drug effects / Q000502:physiology*
D018755:GABA Agonists; D008732:Methoxydimethyltryptamines; D017366:Serotonin Receptor Agonists; D009118:Muscimol; D012701:Serotonin; D017371:8-Hydroxy-2-(di-n-propylamino)tetralin