title: Striatal hyperthermia associated with arousal: intracranial thermorecordings in behaving rats.
abstract: Humans and experimental animals show strong increases in body temperature in response to a variety of stimuli presumed to have stress as their common denominator. To assess the brain's role in this 'emotional' hyperthermia, temperatures were continuously recorded in dorsal and ventral striatum and in deep temporal muscle of freely moving rats exposed to different arousing and mild stress stimuli (placement in the test cage, 20-s sound stimulation, i.v. saline injection, 3-min social interaction with conspecific, and 3-min tail-pinch). The stimuli caused brain hyperthermia of differing degrees but similar pattern, in both the dorsal and ventral striatum. Ventral striatum had approximately 0.4 degrees C higher basal temperature than dorsal striatum, each of these brain temperatures was higher than that in deep temporal muscle. Maximal increases in brain temperature ( approximately 0.8-1.2 degrees C for 20-40 min) occurred upon placement in the test cages, during tail-pinch and during social interaction, all of which were accompanied by behavioral activation. These increases developed with short onset latencies (up to 5-15 s) and always preceded increases in muscle temperature. Significant but smaller increases in brain temperature ( approximately 0.2 degrees C for 4-6 min) were detected after sound stimulation and i.v. saline injection that induced minimal changes in behavior and no change in muscle temperature. Thus, it appears that brain hyperthermia can be triggered by quite different arousing or stressful stimuli that disturb an organism's homeostasis and demand adaptive responding. Although the exact mechanisms of local heat production in brain tissue remain to be confirmed, neuronal activation appears to be the primary triggering force behind changes in brain temperature that are sufficient to affect body temperature. Because most neural processes are temperature-dependent, change in local temperature may result in dramatic modulation of the efficiency of neural processes in situations critical for life-support and during adaptive behavior.
authors.affiliation: Behavioral Neuroscience Branch, National Institute on Drug Abuse -- Intramural Research Program, 5500 Nathan Shock Drive, Baltimore, MD 21224, USA. ekiyatki@intra.nida.nih.gov
authors.forename: E A
authors.initials: EA
authors.lastname: Kiyatkin
authors.forename: R A
authors.initials: RA
authors.lastname: Wise
mesh_terms: D000161:Acoustic Stimulation / Q000009:adverse effects; D000818:Animals; D001143:Arousal / Q000502:physiology*; D001522:Behavior, Animal / Q000502:physiology*; D001831:Body Temperature / Q000502:physiology*; D003342:Corpus Striatum / Q000502:physiology*; D004780:Environment, Controlled; D005334:Fever / Q000503:physiopathology*; D008297:Male; D009474:Neurons / Q000502:physiology; D010146:Pain / Q000503:physiopathology; D010812:Physical Stimulation / Q000009:adverse effects; D051381:Rats; D020318:Rats, Long-Evans; D012919:Social Behavior; D013312:Stress, Physiological / Q000503:physiopathology*; D013703:Temporal Muscle / Q000502:physiology; D013821:Thermometers