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Biomedical subjects

Y Tadokoro

Publications and source records attributed to Y Tadokoro.

At least 37 records · Page 2Linked to original sources

[Surgical treatment of torticollis in cases of congenital nystagmus with strabismus].

To correct compensatory head turn in twelve cases with congenital nystagmus, they were classified into two types according to the relative visual lines of both eyes to each other with respect to the sagittal axis of the head or the median plane of the body. One was termed the symmetrical pattern and the other was termed the asymmetrical pattern. In cases of the symmetrical pattern, a neutral zone exists in which the dominant eye in in the adducted position of gaze with esotropia and in the abducted position of gaze with exotropia. However, in the case of the asymmetrical pattern the neutral zone of the dominant eye is located in the abducted position of gaze with esotropia and in the abducted position of gaze with exotropia. Surgery was performed by shifting the dominant eye to the direction of the sagittal axis of the head in accordance with the degree of ocular deviation in the primary position. In asymmetrical pattern cares, both eyes were surgically shifted in parallel to the direction of the sagittal axis of the head without regard to the types of strabismus. The operation was based on the degree of compensatory head turn. We compared the surgical results the two types. In symmetrical cases, decreasing strabismus was disappointing compared to the head turn, while in asymmetrical cases decreasing head turn was disappointing as compared to strabismus. From these results surgery should be confined to the dominant eye in symmetrical cases, taking as the basis for operation the degree of head turn and not the ocular deviation.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Osmoreceptor mechanism for oxytocin release in the rat.

In order to determine whether oxytocin release is controlled by an osmoreceptor mechanism identical with that for vasopressin release, the plasma oxytocin concentration and plasma osmolality were measured during intraatrial infusion and after intraventricular injection of various osmotic solutions in unanesthetized rats. Intraatrial infusion of 0.6 M NaCl Locke solution (L.S.) or 1.2 M mannitol L.S. elevated plasma oxytocin significantly, while 1.2 M urea L.S. caused only a small increase and isotonic L.S. did not change in plasma oxytocin. All hypertonic solutions produced significant and similar increases in the plasma osmolality. Plasma oxytocin was positively correlated with plasma osmolality in the animals infused with hypertonic NaCl or mannitol but not in the animals infused with hypertonic urea. The injection of 2 microliters of 0.6 M NaCl artificial cerebrospinal fluid (CSF) or 1.2 M mannitol CSF into the third ventricle caused a significant increase in plasma oxytocin immediately (5 min after injection) without changing plasma osmolality, while the intraventricular injection of 1.2 M urea CSF or isotonic CSF produced no significant change in plasma oxytocin. These results indicate that oxytocin release is controlled by osmoreceptors rather than Na receptors, that the adequate stimulus for the osmoreceptors is one which produces cellular dehydration and that the osmoreceptors are located in the brain region which is accessible to osmotic agents from both the outside and inside of the blood-brain barrier. Since the organum vasculosum of the lamina terminalis (OVLT) lacks a blood-brain barrier and is known to be involved in osmotic control of vasopressin release, a lesion was made in the anteroventral region of the third ventricle which encompasses the OVLT and the effect of hypertonic NaCl infusion on oxytocin release was examined. No significant increase in plasma oxytocin was observed after intraatrial infusion of 0.6 M NaCl L.S. in the lesioned rats. All of these findings lead to the conclusion that oxytocin release is under the control of osmoreceptors identical to those for vasopressin release.

Animals↗

Vaginal distension induces milk ejection-related burst of oxytocin neurones interacting with suckling stimuli in lactating rats.

Milk ejection-related bursts of action potentials recurred at fairly regular intervals during suckling in oxytocin cells of anesthetized lactating rats. Additional milk ejection-related bursts were frequently induced in response to vaginal distension. The latency for the induced response was 2.9 +/- 0.2 s and the size of the induced bursts was similar to that of spontaneous ones. When animals were not suckled, the burst was in no case induced by the stimulus. The findings indicate that the two afferent stimuli arising from the mammary gland and vagina can interact with each other in generating milk ejection-related bursts of oxytocin cells.

Action Potentials↗

Activation of neurosecretory cells by osmotic stimulation of anteroventral third ventricle.

Extracellular action potentials of paraventricular neurosecretory cells were obtained from urethan-anesthetized rats during microinjection of a hyper- or hypotonic solution into the anteroventral third ventricle (AV3V), third ventricle, or the vicinity of the recording site. The injection of a 0.2-microliter NaCl solution with a concentration range from 0.16 to 0.8 M into the AV3V excited most of the neurons tested. However, the magnitude of the response was dose related. In most cases, arterial blood pressure recorded simultaneously with the excitatory response of the neuron did not change after the injection. Distilled water (0.2 microliter) was injected into the AV3V after the intraperitoneal injection of a 1.5 M NaCl solution (1 ml), which decreased the firing rate in 67% of the neurons tested. The small volume (0.2 microliter) of hypertonic saline, which was effective when injected into the AV3V, excited none of the neurons tested when injected into the third ventricle or the vicinity of the recording site. These results strongly suggest that the AV3V is sensitive to the osmotic stimulus within a physiological range and that the region plays an important role as an osmoreceptor site for the osmoregulation of paraventricular neurosecretory cells.

Animals↗

Dopaminergic involvement in the estrogen-induced suppression of frequency of pulsatile luteinizing hormone secretion in the ovariectomized rat.

This experiment examined whether various catecholaminergic synthesis inhibitors and receptor blockers affect the inhibitory effect on the frequency of pulsatile luteinizing hormone (LH) secretion induced by local application of estradiol benzoate (EB) into the preoptic suprachiasmatic area (POSC) of ovariectomized rats. Ovariectomized rats were pretreated with either alpha-methyl-p-tyrosine (AMPT; tyrosine hydroxylase inhibitor), AMPT plus threo-dihydroxyphenylserine (DOPS; norepinephrine precursor), diethyldithiocarbamate (DDC; dopamine-beta-hydroxylase inhibitor), pimozide (dopaminergic receptor blocker), phenoxybenzamine (alpha-adrenergic receptor blocker), propranolol (beta-adrenergic receptor blocker), or their vehicles. EB implantation into the POSC reduced the frequency of existing pulsatile LH secretion in vehicle-treated rats. Pretreatment of the rat with AMPT, AMPT plus DOPS, or pimozide did not affect the basal pulsatile LH secretion but eliminated the suppressive effect of EB implantation on the LH pulse frequency. In rats pretreated with DDC or phenoxybenzamine, basal pulsatile LH secretion was significantly inhibited, and EB implantation did not lower serum LH further in these rats. Propranolol had no obvious effect on either basal pulsatile LH secretion or EB-induced suppression of LH pulse frequency. These findings suggest that, in addition to the alpha-adrenergic involvement in maintaining the basal pulsatile LH secretion, the intact dopaminergic system is required for the suppression of the frequency of LH pulses induced by estrogen.

Animals↗

Detailed analysis of blood oxytocin levels during suckling and parturition in the rat.

A detailed secretory profile of oxytocin during suckling and parturition was determined in unanaesthetized freely moving rats. Ten pups were reunited with their mothers after 12-15 h of separation. Unless the milk-ejection reflex occurred, there was no difference in serum oxytocin levels before separation and during the suckling of either four or five, or nine or ten pups. Serum oxytocin levels increased abruptly by 50.1 +/- 4.2 (S.E.M.) pmol/l (n = 9) at milk ejection, and declined rapidly with a half-life of about 1.5 min. The peak concentration of blood oxytocin at each milk ejection was independent of the previous suckling period; values from the first three milk-ejection reflexes following the introduction of the pups and those observed 3-5 h after introduction were similar. The process of parturition was monitored by recording intra-uterine pressure with a balloon implanted in the uterus. On day 22 or 23 of pregnancy, continuous and rhythmical contractions of the uterus occurred (onset of parturition), but serum levels of oxytocin (21.1 +/- 1.9 pmol/l; n = 13) did not alter until the expulsive phase. During the expulsive phase, fetuses were delivered after fetus-expulsion reflexes which were recorded as sudden large increases in intra-uterine pressure. Basal levels of oxytocin in the blood increased during this phase (32.5 +/- 4.4 pmol/l; n = 13) and, in addition, rose by about 15 pmol/l and declined slowly after fetus-expulsion reflexes. The increase, however, was quite different from that seen at milk-ejection reflexes.

Animals↗

[Studies on the feedback regulation of pulsatile luteinizing hormone secretion. II. Role of the catecholaminergic system in estrogen-induced suppression of the frequency of pulsatile LH secretion in ovariectomized rats].

The pattern of pulsatile secretion of luteinizing hormone (LH) is affected by the circulating gonadal hormone levels. In the rat the frequency and amplitude of the LH pulse increase after ovariectomy and decrease after estrogen replacement. Since estrogen is known to affect the catecholaminergic activities in the rat hypothalamus, the present study examined whether the catecholaminergic mechanisms are involved in the estrogen-induced suppression of pulsatile LH secretion. Recently, we have elucidated that the preoptic suprachiasmatic area (POSC) is a specific site of action of estradiol in reducing the LH pulse frequency. Subsequently, in this paper, we report the effects of various catecholamine synthesis inhibitors and synaptic blockers on the basal pulsatile LH secretion and on the frequency suppression induced by local implantation of EB in the POSC. Female rats of the Wistar strain were ovariectomized about 4 weeks before the experiment. Blood samples were obtained at 6-min intervals for 4 h without anesthesia through the indwelling atrial catheter. The rats were given i.p. injection with the drug or the vehicle 1 or 3h before bleeding. The steroid was implanted into the POSC via the chronically-implanted cannula 1 h after the initiation of the bleeding. Serum LH concentrations were determined by radioimmunoassay. The following results were obtained. EB implantation into the POSC suppressed the frequency of existing pulsatile LH secretion in vehicle-treated rats. Pretreatment of the rat with alpha-methyl-p-tyrosine (AMPT), AMPT + threo-dihydroxyphenylserine (DOPS) or pimozide did not affect the basal pulsatile LH secretion but prevented suppressive effect of EB implantation on the LH pulse frequency. In rats pretreated with diethyldithiocarbamate (DDC) or phenoxybenzamine the basal pulsatile LH secretion was abolished. Further suppression by EB implantation was not clear. Pretreatment of the rats with propranolol did not affect the basal pulsatile LH secretion nor the EB-induced suppression of the LH pulse frequency. These results support the hypothesis that the alpha-adrenergic mechanism is required for maintaining the basal pulsatile LH secretion in ovariectomized rats. Furthermore, the dopaminergic system is obligatorily necessary for the manifestation of the inhibitory action of EB implanted in the POSC on the LH pulse frequency.

Animals↗

[Studies on the feedback regulation of pulsatile luteinizing hormone secretion: effect of ovarian steroid implantation into the forebrain and basal hypothalamus on pulsatile LH secretion in ovariectomized rats].

Recent studies have demonstrated that ovarian steroids are involved in the regulation of pulsatile LH secretion. In order to identify the site of action of ovarian steroids in modulating pulsatile LH secretion, the effect of local administration of estradiol benzoate (EB) or progesterone (P) into various brain regions on the characteristic of LH pulses was investigated in ovariectomized rats. Female rats of the Wistar strain were ovariectomized about 3-4 weeks before the experiment. Blood samples were obtained at 6-min intervals for 4h without anesthesia through the indwelling atrial catheter. The steroid was implanted into the brain via the chronically-implanted cannula 1h after the initiation of the bleeding. Serum LH concentrations were determined by radioimmunoassay. The following results were obtained. Pulsatile LH secretion occurred at intervals of approximately 20-30 min and mean LH pulse amplitude was 4.85-5.27 ng/ml h in intact ovariectomized rats. Implantation of cholesterol, as a control, in various brain areas did not induce any changes in the pattern of pulsatile LH secretion. Implantation of EB into the preoptic suprachiasmatic area (POSC) rapidly decreased the mean serum concentration of LH within 1h as compared to the pre-implantation value. The LH pulse frequency, but not the amplitude, was also decreased rapidly and significantly within 1h after EB was implanted into the POSC. In rats with EB implanted into the diagonal band of Broca (DBB), LH pulse frequency began to decrease with 2h, followed by a decline in the mean LH concentration within 3h after the implantation. Implantation of EB into the medial part of the amygdala (m-AMYG) decreased the pulse frequency within 2h, and lowered the average LH level within 3h. The mean amplitude of LH pulses did not change after the implantation. Mean LH concentrations and LH pulse amplitudes began to decrease 1-2h after EB was implanted into the medial basal hypothalamus (MBH), whereas there was no change in the pulse frequency. Rats with the EB implant in the bed nucleus of the stria terminaris, the medial preoptic area, the medial septal nucleus or the anterior hypothalamic area did not show any changes in either the amplitude or the frequency of pulsatile LH secretion. Implantation of P into the DBB, POSC or MBH of ovariectomized rats did not induce any significant change in the pattern of pulsatile LH secretion. These results suggest that the sites of estradiol action in modulating characteristics of pulsatile Lh secretion are not widespread but rather concentrated within the specific brain regions.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

Differential changes in the mechanisms controlling luteinizing hormone and prolactin secretion in middle-aged female rats.

Serum luteinizing hormone (LH) and prolactin (PRL) concentrations were measured in young (3-4 month old) and middle-aged (10-12 month old) intact female rats on proestrus, in ovariectomized rats after two estrogen injections (estradiol benzoate; EB, 10 micrograms/100 g body weight, s.c.) or after preoptic stimulation in EB-primed ovariectomized rats. Only animals showing regular 4-day estrous cycles were selected for the experiment. The magnitude of proestrous LH surge was significantly smaller in middle-aged than in young rats. Two BE injections, at noon on Days 0 and 3, in ovariectomized middle-aged rats failed to induce surges in LH secretion on Day 4 whereas the same treatment produced LH surges in ovariectomized young rats. The preoptic electrochemical stimulation (50 microA for 60 sec) produced a prompt rise in serum LH levels in ovariectomized EB-primed young but not in middle aged rats. The preoptic stimulation with a larger current (200 microA) induced LH secretin in middle-aged rats. In none of these situations serum PRL concentrations were different between young and middle-age rats. These results suggest differential aging rates in the preoptic mechanisms governing LH and PRL secretion in the rat. The function of the preoptic ovulatory center in responding to the estrogen positive feedback action and inducing LH secretion may become impaired and independent of the PRL control mechanism, even before the regular estrous cycle terminates.

Aging↗

Regional specificity in the effect of estrogen implantation within the forebrain on the frequency of pulsatile luteinizing hormone secretion in the ovariectomized rat.

Pulsatile secretion of luteinizing hormone (LH) in ovariectomized rats was evaluated before and after local implantation of crystalline estradiol benzoate (EB) into various regions within the forebrain. Serum concentrations of LH were measured by radioimmunoassay in samples collected at 6-min intervals through indwelling cardiac catheters. In rats with EB implanted in the preoptic suprachiasmatic area (POSC), and in the nucleus of the tractus diagonalis and the diagonal band of Broca (DBB) to a lesser extent, the mean LH concentration and LH pulse frequency decreased rapidly while the pulse amplitude did not change for 3 h after implantation. Rats with the EB implant in the bed nucleus of stria terminalis, the medial preoptic area, the medial septal nucleus, the anterior hypothalamic area or the third ventricle showed unchanged frequencies of LH secretory pulses. Implantation of progesterone into the POSC of ovariectomized rats produced no significant change in LH secretory profiles. It was suggested that the sites of action of estrogen in decreasing the LH pulse frequency are not widespread but rather restricted within a small part of the brain, including the POSC and DBB, in the ovariectomized rat.

Animals↗

Changes in the characteristics of pulsatile LH secretion after estradiol implantation into the preoptic area and the basal hypothalamus in ovariectomized rats.

Intracranial actions of estradiol benzoate (EB) in modulating the characteristics of pulsatile LH secretion were examined in ovariectomized rats. A minute amount of crystalline EB was implanted into the medial basal hypothalamus (MBH) or the preoptic suprachiasmatic area (POSC) and blood samples were collected at 6-min intervals for radioimmunoassay of serum LH concentrations. In rats with EB implanted in the MBH, the LH pulse amplitude decreased while the frequency did not change for 3 h after implantation. In rats bearing EB implants in the POSC, in contrast, the LH pulse frequency decreased without a significant variation in the pulse amplitude. Control animals with empty cannulae inserted into the MBH or POSC exhibited unchanged amplitude and frequency of LH secretory pulses. These results indicate that estrogen can regulate the amplitude and frequency of pulsatile LH secretion via mechanisms independent of each other. It appears that MBH and/or the pituitary is a site of the action of estrogen in decreasing LH pulse amplitude, while the POSC is a site of the steroid action in decreasing the pulse frequency.

Animals↗

A laboratory report on vibration etching for fissure sealants.

We have developed a vibration etching technique in which occlusal pits and fissures are simultaneously cleansed and acid-etched using a fissure needle mounted on an electromagnetic vibrator. When tested on extracted teeth, the needle completely cleansed the fissures by removing the contents and the prismless enamel layer, and widened them to from 100 to 150 micrometers to the depth reached by the needle. The sealant penetrated readily and adhered to the reduced and etched fissure walls interlocking with resin tags.

Acid Etching, Dental↗

Participation of the lower brain stem in induction of preovulatory gonadotropin surges in female rats.

The role of the lower brain stem in controlling preovulatory gonadotropin surges was investigated in female rats under acute experimental conditions. Electrolytic lesions or diethyldithiocarbamate implantations in the ventrolateral part of the medulla oblongata (VLMO), which were carried out at 1100-1330 h on the day of proestrus, resulted in a blockade of the preovulatory surges of LH, FSH and PRL as well as subsequent ovulation. Such treatments in the dorsomedial part of the medulla oblongata did not affect gonadotropin surges or ovulation. By means of electrolytic lesions in the VLMO, norepinephrine concentrations were significantly reduced in the preoptic-anterior hypothalamic area at 1700-1800 h on proestrus, though they did not change in the mid-posterior hypothalamus. Electrochemical stimulations of the suprachiasmatic part of the preoptic area or norepinephrine injections into the third ventricle at 1400-1500 h on proestrus in animals with VLMO lesions succeeded in induce gonadotropin surges and ovulation. These results suggest that the lower brain stem is involved in the induction of preovulatory gonadotropin surges and that the process may be mediated by the ascending noradrenergic system which originates in the VLMO.

Animals↗