Evidence that peripheral rather than intracranial thermal signals induce thermoregulation.
Numerous effector mechanisms have been discovered, which change body temperature and thus serve to maintain the thermal integrity of homeothermic animals. These mechanisms are driven by thermal signals that are processed by neurons in the hypothalamic preoptic area. To keep a tight control over body temperature, these neurons have to receive accurate thermal information. Although in vitro studies have shown the direct thermosensitive ability of neurons in the preoptic area, other observations suggest the existence of peripheral thermosensation and an ascending thermal pathway to the thermoregulatory center. Direct evidences for either one, or both are still missing. In the present study, brain, rectal, subcutaneous and skin surface temperatures were measured during 15, 30, 60 and 120 min of cold exposure (4 degrees C) in rats and compared with neuronal activation due to cold stress shown by c-fos in situ hybridization histochemistry. Subcutaneous and skin surface temperatures dropped continuously throughout the 120 min of cold exposure by 1.4 degrees C and 6.5 degrees C, respectively. However, during the first 30 min, brain and rectal temperatures increased by 0.3 degrees C and 0.25 degrees C, respectively, and even after 60 min of cold stress, brain temperature did not decrease under the level measured at 0 min. Since the brain temperature did not decrease, it is unlikely that intracranial thermoreceptors are involved in the transmission of "cold" thermal signal to induce thermoregulation. At 30 min of cold exposure, neurons in all known thermoregulatory areas (like the ventrolateral part of the medial preoptic nucleus, the lateral retrochiasmatic area, the lateral parabrachial nucleus and the peritrigeminal nucleus) were already maximally activated. These observations clearly indicate that the activation of neurons in the preoptic and several other thermoregulatory nuclei is induced in vivo by thermal signals originating in the periphery, and not in the CNS.
Bratincsák
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Laboratory of Neuromorphology, Medical Faculty of Semmelweis University and Hungarian Academy of Sciences, Budapest, Hungary. bratiandris@yahoo.com
Palkovits
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M
D000818:Animals; D001345:Autoradiography / Q000379:methods; D001831:Body Temperature / Q000502:physiology*; D001833:Body Temperature Regulation / Q000502:physiology*; D001921:Brain / Q000166:cytology / Q000502:physiology* / Q000528:radiation effects; D003080:Cold Temperature / Q000009:adverse effects; D015870:Gene Expression / Q000528:radiation effects; D017403:In Situ Hybridization / Q000379:methods; D008297:Male; D009474:Neurons / Q000502:physiology*; D016760:Proto-Oncogene Proteins c-fos / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D012867:Skin / Q000294:innervation*; D013315:Stress, Psychological / Q000209:etiology / Q000503:physiopathology; D040521:Subcutaneous Tissue / Q000294:innervation*; D013997:Time Factors
D016760:Proto-Oncogene Proteins c-fos