This year, an old concept introduced by Nathaniel Kleitman (see Kleitman N., Basic Rest-activity cycle - 22 years later. Sleep 5(4), 311-317 for the most recent review) was brought back to life by two very interesting paper by Bill Blessing. The original Kleitman's idea has been revisited and incorporated into a behavioral theoretical frame in which the thermogenic activity of the brown adipose tissue acts as a key determinant in the setting the level of activity of the animal. The final concept that William Blessing is try to endorse is that the appearance of long period of active behavior are conditioned by the correct functioning of the thermogenetic autonomic system. In other words, if the brain does not get warm up, it will not function well enough to consent a long period of activity.
I can't help but being supportive of research lines like this, that are leaded by a coherent integrative view of the organism functions, therefore inviting everyone to read the two discussed papers.
Physiol Behav. 2011 Nov 15;
Authors: Blessing W, Mohammed M, Ootsuka Y
Laboratory rats, throughout the 24hour day, alternate between behaviorally active and non active episodes that Kleitman called the basic rest-activity cycle (BRAC). We previously demonstrated that brown adipose tissue (BAT), body and brain temperatures and arterial pressure and heart rate increase in an integrated manner during behaviorally active phases. Studies show that eating is preceded by increases in body and brain temperature, but whether eating is integrated into the BRAC has not been investigated. In the present study of chronically instrumented, unrestrained Sprague-Dawley rats, peaks in BAT temperature occurred every 96±7 and 162±16min (mean±SE, n=14 rats) in dark and light periods respectively, with no apparent underlying regularity. With food available ad libitum, eating was integrated into the BRAC in a temporally precise manner. Eating occurred only after an increase in BAT temperature, commencing 15±1min (mean±SE) after the onset of an increase, with no difference between dark and light phases. There was no preprandial or postprandial relation between intermeal interval and amount eaten during a given meal. Remarkably, with no food available the rat still disturbed the empty food container 16±1min (p>0.05 versus ad libitum food) after the onset of increases in BAT temperature, and not at other times. Rather than being triggered by changes in levels of body fuels or other meal-associated factors, in sedentary laboratory rats with ad libitum access to food eating commences as part of the ultradian BRAC, a manifestation of intrinsic brain activity.
PMID: 22115948 [PubMed - as supplied by publisher]
SR59230A, a beta-3 adrenoceptor antagonist, inhibits ultradian brown adipose tissue thermogenesis and interrupts associated episodic brain and body heating:
Am J Physiol Regul Integr Comp Physiol. 2011 Oct;301(4):R987-94
Authors: Ootsuka Y, Kulasekara K, de Menezes RC, Blessing WW
Brown adipose tissue (BAT) thermogenesis occurs episodically in an ultradian manner approximately every 80-100 min during the waking phase of the circadian cycle, together with highly correlated increases in brain and body temperatures, suggesting that BAT thermogenesis contributes to brain and body temperature increases. We investigated this in conscious Sprague-Dawley rats by determining whether inhibition of BAT thermogenesis via blockade of beta-3 adrenoceptors with SR59230A interrupts ultradian episodic increases in brain and body temperatures and whether SR59230A acts on BAT itself or via sympathetic neural control of BAT. Interscapular BAT (iBAT), brain, and body temperatures, tail artery blood flow, and heart rate were measured in unrestrained rats. SR59230A (1, 5, or 10 mg/kg ip), but not vehicle, decreased iBAT, body, and brain temperatures in a dose-dependent fashion (log-linear regression P < 0.01, R(2) = 0.3, 0.4, and 0.4, respectively, n = 10). Ultradian increases in BAT, brain, and body temperature were interrupted by administration of SR59230A (10 mg/kg ip) compared with vehicle, resuming after 162 ± 24 min (means ± SE, n = 10). SR59230A (10 mg/kg ip) caused a transient bradycardia without any increase in tail artery blood flow. In anesthetized rats, SR59230A reduced cooling-induced increases in iBAT temperature without affecting cooling-induced increases in iBAT sympathetic nerve discharge. Inhibition of BAT thermogenesis by SR59230A, thus, reflects direct blockade of beta-3 adrenoceptors in BAT. Interruption of episodic ultradian increases in body and brain temperature by SR59230A suggests that BAT thermogenesis makes a substantial contribution to these increases.
PMID: 21813867 [PubMed - indexed for MEDLINE]