A homeostatic conditional reflex (CR) was elaborated to the effect of repeated inhalations in rats of a gas mixture containing 8 percent oxygen. The effect of the conditional response was opposite to that of the unconditional one. After ablation of the frontal cortex, the conditional reaction disappeared. The repeated administration of 40 mg/kg of histamine resulted in a tolerance to the temperature lowering effect of histamine similar to the habituation. An injection of distilled water brought about dishabituation. Tolerance was not influenced by the ablation of the frontal cortex, but the dishabituating effect of distilled water was absent.

Adaptation, Physiological↗

PubMedDate not supplied

Cholecystokinin-octapeptide-induced hypothermia in rats: dose-effect and structure-effect relationships, effect of ambient temperature, pharmacological interactions and tolerance.

Subcutaneous injection of cholecystokinin octapeptide (CCK-8) (0.005-1.25 mg/kg) elicited dose-dependent hypothermia in rats. The threshold of the response was between 0.01 and 0.05 mg/kg and the dose-response curve levelled off at doses larger than 0.2-0.5 mg/kg. Warm and cold ambient temperatures decreased and increased the response, respectively. Pretreatment with capsaicin, morphine, naloxone, atropine, haloperidol or propranolol did not affect the response to CCK-8, whereas pretreatment with phenoxybenzamine and a large dose of proglumide, an antagonist for CCK-receptors, attenuated the hypothermia. It seems that neither capsaicin-sensitive thermal and non-thermal afferents, nor opiate mechanisms are involved in the response, but alpha-adrenoceptors might be of some importance in the hypothermia. Non-sulphated-CCK-8, the C-terminal tetrapeptide and hexapeptide, [D-Ala4]-CCK-8 and [D-Met6]-CCK-8 were ineffective. Chronic treatment with CCK-8 resulted in the development of tolerance to the thermoregulatory effect, while the hypothermic responses to apomorphine and capsaicin were not affected. It seems that the tolerance cannot be attributed to conditioned homeostatic reactions.

Animals↗

PubMedDate not supplied

Brain organization and sleep function.

A view of brain organization and sleep function is presented. Sleep is hypothesized to begin at the neuronal group level. Sleep results in the use and thus maintenance, of synapses that are insufficiently stimulated during wakefulness thereby serving to preserve a constancy of a synaptic superstructure. It is further hypothesized that sleep at the neuronal group level is regulated by the production of substances whose rate of production or catabolism is synaptic use-dependent. If sufficient number of neuronal groups are in a sleep state (also called disjunctive state) then the perception of sleepiness occurs. Coordination of neuronal group sleep results from humoral and neuronal projection systems previously linked to sleep regulation. The theory presented is unique in that it: (a) hypothesizes an organizational level at which sleep occurs; (b) hypothesizes that sleep is neuronal--use-dependent, not wakefulness-dependent; (c) hypothesizes that sleep first occurs in evolution when complex ganglia evolved; and (d) hypothesizes the both non-rapid eye movement sleep (NREMS) and REMS serve the same function of synaptic reorganization. The theory is consistent with past theories of sleep function, yet provides a fundamentally new paradigm for sleep research.

Animals↗

PubMedDate not supplied

Effects of acute and chronic treatment with trazodone, an antidepressant, on the sleep-wake activity in rats.

Rats were treated with trazodone (2.5 or 10 mg kg-1) twice a day (at light and dark onset) for 11 days, after chronic injection of physiological saline. The sleep-wake activity was recorded for 24 h on the baseline day (saline), on trazodone days 1, 5 and 11, and also on day 12, when physiological saline was injected again (withdrawal day). Trazodone administration increased non-REM sleep. The enhancement of non-REM sleep was dose-related and more pronounced during the dark cycle. The promotion of non-REM sleep was enhanced during the chronic treatment. There were no consistent changes in REM sleep. Spectral analysis of the EEG revealed an increase in slow-wave activity after administration of the high dose (10 mg kg-1) of the drug. It is concluded that trazodone, a clinically effective antidepressant, has a non-REM sleep-promoting effect. It is speculated that the promotion of sleep by trazodone may be mediated by serotonergic mechanisms.

Analysis of Variance↗

PubMedDate not supplied

Sleep, microbes and cytokines.

Dynamic changes in sleep in response to infectious challenge are a facet of the acute phase response. Changes in sleep induced by infection seem to be of recuperative value to the host. Furthermore, loss of sleep is associated with changes in immune function. Specific components of microbes such as muramyl peptides or endotoxin from bacteria or double-stranded RNA from virus induce sleep responses. These microbial-induced responses are mediated via enhanced cytokine and hormone production. Interleukin-1, tumor necrosis factor and interferon-alpha are somnogenic. Interleukin-1-enhanced sleep involves growth hormone-releasing hormone. Microbial-cytokine-altered sleep results from an amplification of physiological sleep mechanisms.

Acetylmuramyl-Alanyl-Isoglutamine↗

PubMedDate not supplied

Diurnal variations of tumor necrosis factor alpha mRNA and alpha-tubulin mRNA in rat brain.

The experiments described herein were designed to determine whether tumor necrosis factor alpha (TNF-alpha) displays a diurnal variation in various areas of the normal rat brain. TNF-alpha mRNA transcripts were detected by reverse-transcriptase polymerase chain reaction. To monitor diurnal changes in TNF-alpha and alpha-tubulin expression, rats were sacrificed every 4 h for 24 h starting 1 h after light onset; relative mRNA levels were determined for the cerebellum, cortex, hippocampus, hypothalamus and brainstem. TNF-alpha mRNA was higher during the light than in the dark phase in the hypothalamus and hippocampus. alpha-Tubulin mRNA exhibited a similar diurnal variation in the hypothalamus, hippocampus and cortex. In contrast, beta-actin mRNA was lower during the light phase than the dark phase in the hippocampus and cortex. The observed diurnal variations in TNF-alpha mRNA are consistent with the hypothesis that TNF has a physiological role in the brain.

Animals↗

PubMedDate not supplied

[Peptidergic modulation of sleep: a comparative study of analogs of the peptide DSIP].

Effects of intracerebroventricular administration of 3 DSIP analogues with higher stability against proteolysis, on subsequent sleep were studied in rabbits and rats previously implanted with electrodes and cannulas. Significant increase of total sleep time (mainly due to slow wave sleep) after administration of the peptides (D-Trp1) DSIP and (D-Tyr1) DSIP as compared with the control injections to the same animals was found during the first 3-5 hours in rabbits and 12 hours in rats. Shortened analogue (D-Trp1) DSIP1-6 had no effect on rabbit sleep and significantly reduced slow wave sleep in rats during the first 3 hours. It is concluded that some DSIP-like peptides which are more stable against aminopeptidases, can modulate rodent sleep.

Animals↗

PubMedDate not supplied

Effects of elevated ambient temperatures on the sleep-waking activity of rats with impaired warm reception.

The sleep-waking activities of intact and of capsaicin-desensitized rats (animals with damaged peripheral and central warm receptors) were studied at room temperature and at the warm ambient temperatures of 32 and 34 degrees C. At 32 degrees C, the time spent in sleep increased significantly in the desensitized animals, while a decrease in the amount of deep slow wave sleep was found in the controls. At 34 degrees C, the amount of the sleep-waking stages returned to the levels observed at room temperature in the desensitized rats. A further decrease in sleep and a significantly increased wakefulness was found in the controls. At both warm ambient temperatures, the body temperature of the desensitized rats was significantly higher than that of the controls. We suggest that warm environments exert a dual effect on the sleep-waking activity. The activating effect abolished by desensitization seems to be in connection with capsaicin-sensitive thermoreceptors, while the deactivation brought about by heat is not influenced by capsaicin.

Animals↗