Short-term propofol anaesthesia down-regulates clock genes expression in the master clock.

Background: Propofol anesthesia triggers phase-advances of circadian rhythms controlled by the suprachiasmatic nuclei (SCN), the master clock. Besides, inhalational anesthesia has been associated with a subsequent reduction of Per2 mRNA levels in the whole brain of rodents. The acute effects of propofol anesthesia per se on the SCN molecular clockwork remain unclear.

Disruption of the circadian system by environmental factors: Effects of hypoxia, magnetic fields and general anesthetics agents.

The biological clock of mammals is under the control of external factors, social life and the environment, and of internal genetic factors. When the biological clock of an individual is no longer in phase with its environment, either because there is no longer any harmony (desynchronization) between the two systems (shift work, night work, and transmeridian flights..

Propofol anesthesia significantly alters plasma blood levels of melatonin in rats.

Background: General anesthesia combined with surgery has been shown to decrease the nocturnal peak of melatonin in patients. However, the role of anesthesia itself on melatonin secretion remains unknown. We previously showed that anesthesia induced by propofol modifies the circadian time structure in both rats and humans and phase advances the circadian rest-activity rhythm in rats.

[Postanesthesia cognitive dysfunction].

The cognitive dysfunctions observed in patients after anesthesia are due not only to the effects of but also to the surgery, the disease requiring surgery, and post-operative treatment. Initial cognitive recovery from anesthetic agents is usually fast, from several hours to several days, but can be delayed by postoperative treatment (analgesia, for example) that have deleterious cognitive effects. During the initial period after surgery, acute impairment of cognitive functions is seen in some patients at risk (major surgery, aged patients, brain sensitivity, or sepsis), specifically transitory (1-3 days in most cases) postoperative delirium.

Plasma corticosterone in rats is specifically increased at recovery from propofol anesthesia without concomitant rise of plasma ACTH.

General anesthesia combined with surgery is commonly associated with post-operative stress-response in humans. Effects on the hypothalamic-pituitary-adrenal axis (HPA) during and after anesthesia are correlated with the magnitude of surgery and choice of anesthetics. The aim of our study in rats was to characterize the effects of general anesthesia without any surgery on HPA regulation of corticosterone and adrenocorticotropic hormone (ACTH) secretions.

Circadian disruption of body core temperature and rest-activity rhythms after general (propofol) anesthesia in rats.

Background: General anesthesia is commonly associated with sleep disorders, fatigue, drowsiness, and mood alterations in patients. The authors examined whether general (propofol) anesthesia can impact the circadian temporal structure by disturbing circadian rest-activity and body temperature rhythms under normal light-dark conditions (light-dark 12:12 h) in rats.

Methods: A group of rats was anesthetized with propofol, and another was injected with 10% Intralipid, which was used as a control lipidic solution.

General anesthetics effects on circadian temporal structure: an update.

Disruptions of circadian and biological rhythms as well as general anesthesia can induce sleep disorders, resulting in an increase in sleepiness and drowsiness and a decrease in vigilance. It has been previously shown that circadian time can influence the pharmacologic sensitivity and the duration of action of general anesthetics. Studies on interactions between general anesthesia and circadian rhythms are few, but all of them suggest an important role of general anesthetics on circadian rhythms.

Involvement of the basal cholinergic forebrain in the mediation of general (propofol) anesthesia.

Background: Recent studies have pointed out the involvement of the basal forebrain gamma-aminobutyric acid-mediated system in mediating the effects of general anesthesia. In this study, the authors asked whether the basal forebrain cholinergic system is also involved in mediating the effects of general anesthetics such as propofol.

Methods: Cholinergic lesions were produced by administration of the selective immunotoxin 192 immunoglobulin G-saporin into the lateral ventricles, the medial septum, or the nucleus basalis magnocellularis.

Delayed aversive effects of high-dose fentanyl. Prevention by a polyamine-deficient diet.

The present study aimed to examine the effects of an acute administration of the mu-opioid receptor fentanyl on affect as assessed by place-conditioning procedure in rats. We determined the affective properties of fentanyl not only immediately following its administration, but also 24h later. Experiments were performed using the dose of fentanyl (240 gamma/kg; four injections of 60 gamma/(ml kg) every 15 min, subcutaneously) for which secondary hyperalgesia has been previously described.

Texture analysis of brain MRI evidences the amygdala activation by nociceptive stimuli under deep anesthesia in the propofol-formalin rat model.

Magnetic resonance images of rat brain were analyzed by texture analysis in order to study the effects of a nociceptive stimulation (formalin test) under propofol deep anesthesia. Changes of the texture in different cerebral brain areas acquired before and after stimulation were checked. Our statistical analysis of texture shows that these changes were present only in the amygdala, in agreement with the facts already known about the unconscious memorization of nociceptive stimuli.

Fos immunolabelling evidence for brain regions involved in the Pavlovian degraded contingency effect and in its disruption by atropine.

Using a fear conditioning preparation, [Carnicella, S., Pain, L., Oberling, P.

Reciprocal relationships between general (Propofol) anesthesia and circadian time in rats.

Several common postdischarge symptoms, such as sleep disorders, headache, drowsiness or general malaise, evoke disturbances of circadian rhythms due to jet lag (ie crossing time zones) or shift work rotation. Considering that general anesthesia is associated with numerous effects on the central nervous system, we hypothesized that it may also act on the circadian timing system. We first determined the effects of the circadian timing on general anesthesia.

Cholinergic effects on fear conditioning I: the degraded contingency effect is disrupted by atropine but reinstated by physostigmine.

Rationale: The cholinergic system has been shown to modulate contextual fear conditioning. However, with the exception of trace conditioning studies, most of the available data have focussed on independent context, i.e.

In vivo dopamine measurements in the nucleus accumbens after nonanesthetic and anesthetic doses of propofol in rats.

Unlabelled: There is growing evidence that propofol acts on affective and reward processes. We designed this study to assess the effect of propofol on the concentration of dopamine in the nucleus accumbens, a main component of the mesolimbic system. The concentration of dopamine in the nucleus accumbens was assessed by using in vivo brain microdialysis in freely moving rats.

The anesthetics propofol and ketamine inhibit cocaine-induced egr-1 gene expression in rat forebrain.

Acute cocaine injection to rats is known to induce the expression of immediate early genes in the forebrain, the effect being primarily mediated by the dopaminergic system. We examined the effect of the anesthetics ketamine and propofol on cocaine-induced egr-1 mRNA expression. Using in situ hybridization, we show that both compounds did not induce egr-1 gene by themselves, but were able to dose-dependently reduce cocaine-induced egr-1 mRNA synthesis in the nucleus accumbens, caudate-putamen and cingulate cortex.

Effect of a nonsedative dose of propofol on memory for aversively loaded information in rats.

Background: The effects of propofol on memory for aversive information are not well determined. The authors evaluated the effects of a minimal nonsedative dose of propofol or midazolam on memory in rats, using an apparatus composed of two compartments: a large bright anxiogenic one and a small dark neutral one.

Methods: Groups of rat received propofol (9 mg/kg, intraperitoneally) or midazolam (3 mg/kg).

Fentanyl enhancement of carrageenan-induced long-lasting hyperalgesia in rats: prevention by the N-methyl-D-aspartate receptor antagonist ketamine.

Background: Tissue damage may produce hyperalgesia, allodynia, and persistent pain. The authors recently reported that fentanyl elicits analgesia but also activates N-methyl-D-aspartate-dependent pain facilitatory processes opposing analgesia. In nonsuffering rats, this leads to a long-lasting enhancement in pain sensitivity.