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M Kimura-Takeuchi

Publications and source records attributed to M Kimura-Takeuchi.

8 recordsLinked to original sources

Lateral preoptic lesions void slow-wave sleep enhanced by uridine but not by muramyl dipeptide in rats.

We investigated the site of action of two sleep-inducing substances, viz., muramyl dipeptide (MDP) and uridine. Localized electrolytic lesions were made bilaterally in the lateral preoptic hypothalamus (LPO) in rats and nocturnal 10-h i.c.v. infusions of MDP and uridine were performed before and after the LPO lesions. MDP increased only slow-wave sleep (SWS) in both intact and LPO-lesioned rats. Uridine promoted both SWS and paradoxical sleep (PS) before the LPO lesions whereas it increased only PS after the lesions. These results suggest that the LPO is crucial for SWS-promoting action of uridine but not MDP.

Acetylmuramyl-Alanyl-Isoglutamine↗

Differential sleep modulation by sequentially administered muramyl dipeptide and uridine.

In an attempt to investigate the effects on sleep modulation of order of administration of two substances, sequential intracerebroventricular (ICV) infusions of muramyl dipeptide (MDP, 1.0 nmol) and uridine (5.0 pmol) were conducted in freely behaving rats. To eliminate the influence of intermittent infusions on their behavior, the rats were continuously ICV infused with physiological saline solution, which did not affect their normal sleep-waking dynamics. Under these experimental conditions, uridine infusion (2400-0500 h) attenuated the enhancement of slow-wave sleep (SWS) caused by prior infusion of MDP (1900-2400 h) to the baseline level and, thus, did not exert a sleep-promoting property. In contrast, MDP infusion (2400-0500 h) further potentiated the SWS-enhancing activity of preinfused uridine (1900-2400 h). A single infusion of MDP or uridine (2400-0500 h) similarly enhanced SWS. These results demonstrate that observed differences in the induction and maintenance of sleep are dependent upon the order of exogenously infused uridine and MDP. The time sequence per se of these sleep substances may be responsible for the differential temporal changes in sleep. It is, therefore, assumed that a crucial order of multiple sleep substances may dynamically and differentially regulate sleep in the brain.

Acetylmuramyl-Alanyl-Isoglutamine↗

The role of double-stranded RNA in induction of the acute-phase response in an abortive influenza virus infection model.

The inducer of the acute-phase response in "flu-like" viral infections is not defined. The hypothesis that virus-associated double-stranded (ds) RNA serves this function was investigated by comparison of several acute-phase responses (fever and sleep patterns, white and nucleated red blood cell levels, serum antiviral activity and ceruloplasmin) induced by the synthetic dsRNA polyriboinosinic:polyribocytidylic acid (poly[rI:rC]) with those induced by influenza virus in rabbits. The capacity of either dsRNA or influenza virus to induce hyporesponsiveness with respect to these acute-phase parameters upon rechallenge with the same agent or cross-challenge 24 h later was also examined. Poly(rI:rC) induced only minimal hyporesponsiveness to itself but was a potent inducer of hyporesponsiveness to virus with respect to fever, sleep, leukograms, and antiviral activity. Therefore, poly(rI:rC) can substitute for virus in terms of induction of acute-phase hyporesponsiveness, suggesting that dsRNA of viral origin triggers the acute-phase response in this model of influenza.

Acute-Phase Reaction↗

Influenza virus-induced changes in rabbit sleep and acute phase responses.

Systematic investigations of sleep after viral inoculation have not previously been described. In the present study, rabbits were inoculated intravenously (iv) with control allantoic fluid followed by two sequential inoculations of influenza virus at intervals of 24 h. After each i.v. inoculation, sleep and brain temperature (Tbr), as well as leukocyte distributions and serum levels of antiviral activity and ceruloplasmin, were monitored. The first viral inoculation elicited several acute phase responses, including increased non-rapid-eye-movement sleep (NREMS), Tbr, serum antiviral activity, and serum ceruloplasmin levels, as well as neutrophilia and lymphopenia. In contrast to the effects of the first inoculation, after the second inoculation of virus, all these acute phase parameters were diminished or absent (the hyporesponsive state). Inoculation of naive rabbits with heat-inactivated virus was similarly ineffective; however, inoculation of this group of rabbits with viable virus 24 h later did induce full-scale acute phase responses. The possible role of cytokines in mediating the acute phase response after influenza viral challenge is discussed. Results support the hypothesis that sleep is a facet of the acute phase response involved in host defense mechanisms.

Acute-Phase Reaction↗

Co-circulating sleep substances interactingly modulate sleep and wakefulness in rats.

Putative sleep substances were infused either singly or in combination into the third ventricle of freely behaving male rats for 10 h nocturnal period. The nocturnal amount of slow wave sleep (SWS) and paradoxical sleep (PS), and the number and duration of their episodes were compared to those of the previous night under saline infusion. The single administration revealed that each substance elicited partially differential and partially common sleep-modulatory activity. SWS was enhanced by the d-type of di-1-methylheptyl-2,5-dioxocyclohexane-1,4-dicarboxylate (d-DOC, 2.3 nmol), delta-sleep-inducing peptide (DSIP 2.5 nmol), deoxyuridine (0.1 nmol), muramyl dipeptide (MDP, 2.0 nmol), and prostaglandin D2 (PGD2, 0.36 nmol). Cytidine (10 pmol) increased the number of SWS episodes and reduced their duration, whereas deoxyguanosine (10 pmol) prolonged the duration. Deoxycytidine (10 pmol) and the 1-type of DOC (0.25 nmol) enhanced PS. Uridine (10 pmol) enhanced both SWS and PS. The simultaneous or sequential administration of DSIP, MDP and uridine resulted in a combination-dependent or sequence-dependent change in sleep-waking dynamics, which was quite different from the time-course sleep-modulation induced by the single administration of each substance. The results suggest that co-circulating sleep substances might interact at least in part, either synergistically or antagonistically, on the sleep-regulatory mechanism.

Animals↗

[The hypnogenic effects of delta sleep-inducing peptide (DSIP) analogs: a comparative study in rabbits and rats].

Hypnogenic effects of 3 DSIP analogs with a higher stability against aminopeptidase activity have been studied in rabbits and rats using intraventricular administration (injections and infusions). An analog (D-Ala-2) DSIP augmented slow wave and paradoxical sleep within the 5th, 8th and 11th hours of the recording period. An analog (D-Val-2) DSIP made the same within the 8th and 10th hours, and hexapeptide (D-Ala-2) DSIP (1-6) increased sleep during the 1st, 3rd, and 5th hours. Both nonapeptides augmented sleep in rabbits as well as in rats, though hexapeptide produced this effect in rabbits only, that might be related to some difference in distribution and colocalization of endogenous DSIP-like peptide in the pituitary of two rodent species. It may be suggested that hypnogenic activity of DSIP analogs is determined by the structure of administrated molecule, being mediated by such hormones as GRF and CLIP.

Aminopeptidases↗