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N Itowi

Publications and source records attributed to N Itowi.

10 recordsLinked to original sources

Effects of intracerebroventricular histamine injection on circadian activity phase entrainment during rapid illumination changes.

Histamine is reported to have different effects on shifting the circadian activity phase depending on its circadian administration time (CT). The delay-sensitive period is CT 12-15, and the advance-sensitive period is CT 0-3. The activity phase of rats was entrained by a new light-dark cycle within a week in groups treated with either saline or i.c.v. histamine at CT 12-15. However, on treatment at CT 0-3 the activity phase of the group treated with histamine was entrained by the new light-dark cycle in half the period required for entrainment in the control group.

Activity Cycles

Histaminergic neuron system: morphological features and possible functions.

The histaminergic neuron systems in rat brain have been identified by immunocytochemical techniques using antibodies against histidine decarboxylase or histamine itself. Here, the details of the distribution of the histaminergic neuron networks are presented. Judging from the widespread distribution of the nervous system, it is postulated that the histaminergic neuron system is involved in various brain functions. Some functions, including the circadian rhythms, sleep-arousal cycles, drinking, feeding, thermoregulation, and neuroendocrine controls which were elucidated by administration of alpha-fluoromethylhistidine, a suicide substrate for histidine decarboxylase, are discussed here, although the true functions are still under investigations.

Animals

Effect of histamine depletion on the circadian amplitude of the sleep-wakefulness cycle.

Behavioral states of rats were automatically classified with a newly developed computer program into three sleep stages (awake, slow-wave sleep and REM sleep) from continuous long-term EEG and EMG recordings for several circadian cycles under entrained circumstances (L:D = 12:12). Histamine was depleted by 100 mg/kg intraperitoneal administration of a specific inhibitor of its synthesis, alpha-fluoromethylhistidine, in the mid-light period. This treatment had no effect on the amount of each sleep stage in the total 24-h period or in the light period, but caused significant increases in slow-wave sleep and REM sleep in the dark period. Equivalent decrease in the awake stage during the dark period was also observed. As a result, histamine depletion decreased the light:dark ratio of slow-wave sleep. These findings suggest that decrease of the histamine content of the brain attenuated the circadian amplitude of sleep-wakefulness by suppressing the surge of wakefulness during the dark period. From these results, histamine is suggested to modulate the circadian amplitude of the sleep-wakefulness cycle.

Animals

Effects of histamine and alpha-fluoromethylhistidine injections on circadian phase of free-running rhythms.

Sequential IP injections of alpha-fluoromethylhistidine at CT-6 and CT-18 elicited transient delay during the injection period in the onset of activity in the free-running circadian rhythms of locomotor and drinking activities. Histamine injection ICV resulted in various changes, permanent or transient, in the circadian phase of the free-running rhythms depending on the subjective time of the injection: it caused transient advance in onset of activity when injected at CT-0, 3, 6, 9, 18 or 21, whereas it caused permanent phase-delay when injected at CT-12 or 15. These permanent effects were plotted in a phase-response curve. Histamine administration at CT-6 and CT-18 resulted in transient, reciprocal changes of almost equivalent amplitude changes to those of histamine depletion at the corresponding subjective times. Although this transient shift may represent a masking effect of the drug, HA may modulate the circadian synchronization mechanism(s) during the advance sensitive phase. Moreover, HA seems to elicit phase-delay by affecting the light-relaying tract.

Animals

Development of a computer program classifying rat sleep stages.

We developed a simple and precise program for the on-line judgement of the sleep stages of four rats simultaneously for an unlimited period, using a commercially available general purpose signal processor (NEC-Sanei 7T17; 32-bit, 5 MHz, 4 Mbyte, 1 Mbyte 1 floppy disc drive). EEG and EMG were recorded with an 8-channel polygraph (NEC-Sanei, System 380) through electrodes chronically implanted into the brain. The signals were A/D converted every ms and integrated for 2760 ms after full-wave rectification, and the subsequent 2240 ms was used for calculation and further analysis. All data were handled with this 5000 ms as the minimum unit. Then 3 sleep stages, i.e., waking, slow-wave sleep, and REM sleep, were determined by a template matching method from the relative amplitudes and durations of the integrated EEG, EMG and EMG surge data based on algorithms of standard visual amplitude analysis criteria for the sleep-stage classification. An agreement matrix was constructed between the data scored by the visual and by the automatic analysis, and the agreement value was satisfactory, although slight variability was seen in the REM sleep-stage determination. This result indicated that EEG and EMG data analysis is appropriate for researching the circadian rhythmic mechanism of the sleep-wake cycle.

Animals

Effects of histamine on thermosensitive neurons in rat preoptic slice preparations.

Single neuronal activities were recorded extracellularly from slice preparations of the rat preoptic area and effects of histamine (0.01 10 microM) on the activities were examined with regard to thermosensitivies of the neurons. Superfusion of histamine increased the firing rate in 52 of 75 warm-sensitive neurons and in 22 of 41 thermally insensitive neurons in a dose-dependent manner. Ten (3%) warm-sensitive neurons and 6 (15%) thermally insensitive neurons were inhibited by histamine. Mepyramine (10 microM) (H1-antagonist), but not famotidine (H2-antagonist), blocked the histamine (10 microM) induced excitation in 19 (76%) of 25 warm-sensitive neurons and in 6 (75%) of 8 thermally insensitive neurons. These results suggest that histamine excites both warm-sensitive and thermally insensitive neurons in the preoptic area mainly via the H1-receptor.

Animals

Effect of histamine depletion on circadian variations of corticotropin and corticosterone in rats.

The effects of cerebral histamine depletion induced by alpha-fluoromethylhistidine (FMH) on corticotropin (ACTH) and corticosterone secretions were examined. Neither acute nor chronic FMH treatment altered the corticoadrenal responses to three types of stress: transposition, immobilization and water immersion. And exposure to stress did not affect the hypothalamic content of histamine. However, chronic intracerebral treatment with FMH had a significant effect on the circadian rhythm of the plasma corticosterone (CS) level in rats. Namely, it caused a marked attenuation of the amplitude of the peaks of the CS level resulting in an almost arrhythmic state. The maximum differences between FMH treated and untreated groups were seen at 8.00 and 20.00 h, the times when the illumination condition changed (light onset 8.00 h). This treatment with FMH also had a similar effect on the plasma ACTH concentration; namely the plasma ACTH level in the saline treated group was lower than that of the FMH-treated group at light onset and higher than the latter at dark onset, but was similar to the latter at other sampling points. These results indicate the histaminergic modulation of the circadian rhythm of hormonal secretion of the adrenal cortex and show that this phenomenon is mediated through the central nervous system by an influence on the rhythm of hypophyseal ACTH secretion possibly through alteration in the concentration of corticotropin-releasing factor.

Adrenocorticotropic Hormone

Changes in the feeding behavior of rats elicited by histamine infusion.

In this study, we examined the effect of a putative neurotransmitter or a neuromodulator histamine (HA) on the feeding behavior to elucidate its physiological function in the central nervous system. Rats were implanted with a cannula into the suprachiasmatic nucleus through which HA was continuously infused for 200 hours with an Alzet osmotic minipump. The food intake was recorded automatically. This infusion resulted in decrease in food intake during the dark period and increase in it during the light period which contributed to the decrease in total food intake and increase in the percentage of food intake during the light period. Percentage of food intake during the light period is a good index of the amplitude of the circadian rhythm. Presumably, HA is concerned not only in the meal size, but also in the chronological aspect of the feeding behavior. The administration of H1-antagonist, pyrilamine, antagonized the HA induced increase in food intake during the light period. These findings suggest that continuous infusion of HA affected the feeding behavior which is possibly mediated through the H1-receptors in rat brain.

Animals

Histaminergic neuron system in the brain: distribution and possible functions.

Recent immunocytochemical studies have identified the histaminergic neuron system in the brain. In the rat brain, histaminergic neuronal cell bodies are located in the tuberomammillary nucleus in the posterior hypothalamus, while histaminergic fibers are distributed in almost all regions of the brain. Similar distributions of histaminergic neuronal cell bodies and fibers have been reported in the brains of other mammals and nonmammalian vertebrates. As expected from the widespread distributions of the efferent fibers, the central histaminergic neuron system seems to be involved in multiple functions in the brain. The results of intracerebral injection of histamine and administration of alpha-fluoromethylhistidine (FMH), which depletes brain histamine level, suggest that the central histaminergic system may modulate feeding, drinking and sexual behaviors, sleep-wakefulness and circadian rhythm, neuroendocrine and cardiovascular controls and thermoregulation.

Animals