Cutaneous sympathetic motor rhythms during a fever-like response induced by prostaglandin E(1).
Neuronal population discharges within the CNS and in somatic and sympathetic motor nerves often display oscillations. Peripheral oscillations may provide a window into central mechanisms, as they often show coherence with population activity of subsets of central neurones. The reduction in heat loss through the cutaneous circulation during fever may be mediated via sympathetic premotor neurones not utilised during normal temperature regulation. Consequently, here we assessed, in anaesthetised rats, whether the frequency signature of population sympathetic discharge observed in neurones innervating the tail (thermoregulatory) circulation changed during a fever-like response induced by intracerebroventricular injection of prostaglandin E(1). We found that when core temperature was raised to 38.8-40.5 degrees C sympathetic activity was abolished. Following administration of prostaglandin (400 ng or 1 microg per rat), activity was restored to levels seen prior to heating (154+/-53.5%; n=10). Injection of vehicle had no effect (n=7). Prior to heating when most animals were in central apnoea (14/18) two peaks were observed in autospectra of sympathetic activity: one at 0.68-0.93 Hz (T-peak) and another at the frequency of ventilation (2 Hz). Central respiratory drive was recruited during hyperthermia where it was 1:2 locked to the frequency of ventilation and following prostaglandin administration, an additional peak in sympathetic autospectra was seen at this frequency. Time-evolving spectra indicated that this peak resulted from the dynamic locking of the 'T-peak' to central respiratory drive. Our data show that during a fever-like response the dominant oscillations in sympathetic activity controlling a thermoregulatory circulation and their dynamic coupling to respiratory-related inputs are similar to those seen under normal conditions. Therefore, during this fever-like response, the neural substrate(s) underlying the oscillations is not reconfigured and remains capable of sculpturing the pattern of sympathetic neuronal discharge that may be regulated by several descending pathways.
Collins
D R
DR
Department of Physiology, Royal Free and University College Medical School, University College London, Royal Free Campus, London NW3 2PF, UK.
Korsak
A
A
Gilbey
M P
MP
D000200:Action Potentials / Q000187:drug effects / Q000502:physiology*; D000527:Alprostadil / Q000378:metabolism / Q000494:pharmacology*; D000818:Animals; D001158:Arteries / Q000187:drug effects / Q000294:innervation* / Q000502:physiology; D001683:Biological Clocks / Q000187:drug effects / Q000502:physiology*; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D001833:Body Temperature Regulation / Q000187:drug effects / Q000502:physiology; D001921:Brain / Q000502:physiology; D004525:Efferent Pathways / Q000502:physiology; D005334:Fever / Q000378:metabolism* / Q000503:physiopathology; D006339:Heart Rate / Q000187:drug effects / Q000502:physiology; D006979:Hyperthermia, Induced; D008297:Male; D010507:Periodicity; D051381:Rats; D017207:Rats, Sprague-Dawley; D012143:Respiratory Physiological Phenomena / Q000187:drug effects; D017779:Sympathetic Fibers, Postganglionic / Q000187:drug effects / Q000502:physiology*; D013623:Tail / Q000098:blood supply / Q000294:innervation / Q000502:physiology; D014661:Vasoconstriction / Q000187:drug effects / Q000502:physiology*
D000527:Alprostadil