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Biomedical subjects

K Seto

Publications and source records attributed to K Seto.

At least 163 records · Page 9Linked to original sources
PubMed1986

Efferent pathways from the region of the subfornical organ to hypothalamic paraventricular nucleus: an electrophysiological study in the rat.

Twenty-three neurons in the region of the subfornical organ (SFO) were antidromically activated by electrical stimulation of the hypothalamic paraventricular nucleus (PVN) in male rats under urethane anesthesia. Microiontophoretically (MIPh) applied angiotensin II (AII) excited the activity of all units in the region of the SFO and the effect of AII was blocked by MIPh applied saralasin (Sar), an AII antagonist, but not by atropine (Atr), a muscarinic antagonist. In these units, 12 were also excited by MIPh applied acetylcholine (ACh) while 11 were not affected and the effect of ACh was attenuated by not only MIPh applied Atr, but also Sar, suggesting that not only neurons specific for AII, but also neurons sensitive to both AII and ACh project to the PVN in the region of the SFO. Intravenously administered AII excited the activity of both types of units in the region of the SFO. Microinjected AII or ACh into the region of the SFO excited the activity of putative vasopressin (VP)-secreting units in the PVN. These results suggest that neurons projecting to the PVN in the region of the SFO may act to enhance the activity of putative VP-secreting neurons in the PVN in response to circulating AII.

Acetylcholine↗
PubMed1986

Ventrolateral medullary neurons projecting to the medial preoptic/anterior hypothalamic area through the medial forebrain bundle: an electrophysiological study in the rat.

A total of 152 ventrolateral medullary neurons was antidromically stimulated from both the medial preoptic/anterior hypothalamic area (MPOAH) and the medial forebrain bundle (MFB) in urethane anesthetized rats. These neurons were located primarily dorsal to the lateral reticular nucleus and could be readily classified in at least two groups, type I and type II cells on the basis of electrophysiological properties. The action potentials of type I cells had a shorter duration, and their conduction velocities ranged from 0.45 to 3.1 m/s. By contrast, type II cells, most predominantly observed, were characterized by a longer duration and an unusual shape of their action potential, and the antidromic propagation into the somatodendritic complex was often blocked. The conduction velocity (mean = 0.21 m/s) and absolute refractory period (mean = 2.63 ms) of type II cells are consistent with them having fine non-myelinated axons. Injection of 6-hydroxydopamine (6-OHDA), but not 5,7-dihydroxytryptamine, directly into the MFB blocked antidromic responses of 57% of type II cells tested. The residual type II cells whose antidromic responses were not affected by 6-OHDA were located significantly rostral to the 6-OHDA sensitive cells. Neither antidromic response of type I cells tested, on the other hand, was affected by 6-OHDA. The majority of type I cells were dramatically activated by noxious pinches of the tail, whereas the noxious stimuli produced no detectable change in the firing of type II cells. These data demonstrate that ventrolateral medullary neurons projecting to the MPOAH through the MFB are comprised of at least three distinct populations: 6-OHDA resistant fast conducting cells with somatic afferents, 6-OHDA sensitive and resistant slow conducting cells.

Action Potentials↗
PubMed1986

Role of the suprachiasmatic nuclei of the hypothalamus on diurnal rhythm in cardiac arrhythmias.

Ambulatory EGG and EEG recordings were recorded under a 14/10-h light-dark illumination schedule using rats. The rats consisted of two groups: a suprachiasmatic (Sch) lesioned group (n = 5) and a normal control group (n = 5). Bilateral Sch nuclei were lesioned electrically (DC, 2.5 mA, 30 s for each) using a pair of platinum electrodes 0.3 mm in diameter. After recovery from surgery, recordings of ECGs (leads I, II, and III) and EEGs from the cortex and the left dorsal hippocampus were continued for 6 days. Diurnal periodicity in bradyarrhythmia (sinoatrial block, atrioventricular block) and heart rate was analyzed by the least square fit of 24-h cosines. Significant diurnal rhythm was observed in control rats, whereas Sch-lesioned rats showed no significant diurnal rhythm. The integrity of the Sch nuclei, therefore, is necessary for the generation and/or the expression of diurnal periodicity in bradyarrhythmia in rats.

Animals↗
PubMed1986

Action of the lateral hypothalamic area on subfornical organ neurons projecting to the supraoptic nucleus in the rat.

The activity of all subfornical organ neurons (N = 20) that were antidromically identified by electrical stimulation of the rat hypothalamic supraoptic nucleus region was excited by microiontophoretically applied angiotensin II. Electrical stimulation of the lateral hypothalamic area produced either an excitatory response (N = 12) or no effect (N = 8) in the activity of identified subfornical organ neurons. The excitatory responses to iontophoretically applied angiotensin II or stimulation of the lateral hypothalamic area were blocked by iontophoretically applied saralasin, an antagonist of angiotensin II.

Angiotensin II↗
PubMed1986

Subfornical organ efferents influence the activity of median preoptic neurons projecting to the hypothalamic paraventricular nucleus in the rat.

Twelve neurons in the median preoptic nucleus were antidromically activated by electrical stimulation of the hypothalamic paraventricular nucleus in the rat. Electrical stimulation of the subfornical organ produced excitation (N = 7) or inhibition (N = 4) of the activity of these identified units. The activity of all identified units that were excited by stimulation of the subfornical organ was also excited by microiontophoretically applied angiotensin II whereas the remaining units were not affected. The excitatory responses of the identified units to subfornical organ stimulation or applied angiotension II were blocked by saralasin, an angiotensin II antagonist.

Angiotensin II↗
PubMed1986

Angiotensin II-sensitive neurons in the rat lateral hypothalamic area with efferent projections to the subfornical organ.

Thirteen neurons in the lateral hypothalamic area were antidromically activated by electrical stimulation of the subfornical organ in the rat. The activity of almost all identified neurons (N = 11) was excited by microiontophoretically applied angiotensin II. On the other hand, of the antidromically unidentified lateral hypothalamic area neurons (N = 10) tested, 4 were excited by microiontophoretically applied angiotension II and 6 were not affected. The excitatory responses of identified and unidentified lateral hypothalamic area neurons to angiotensin II were blocked by microiontophoretically applied saralasin, an angiotensin II antagonist.

Action Potentials↗
PubMed1986

Influence of microinjection of insulin into hippocampus on hepatic acetate metabolism in rabbits.

Insulin was injected directly into the dorsal hippocampus (DHPC) of rabbits, and changes in hepatic acetate metabolism were studied. The injection of 50 microU insulin into the DHPC decreased the rates of 14C transfer from 14C-1-acetate into glucose and ketone bodies, and increased 14C transfer into cholesterol ester, triglyceride, free cholesterol and free fatty acids. But after insulin injection into the DHPC of rabbits with lesions of dorsal fornix (DFX), hepatic acetate metabolism did not differ from that of control rabbits, which received saline injection into the same brain region. From these results it might be suggested that the DHPC are parts of insulin-sensitive brain regulator system in the hepatic acetate metabolism.

Acetates↗
PubMed1986

Influence of lesions of the limbic-hypothalamic system on metabolic response of pyruvate to daily repeated immobilization stress in rabbits.

The pyruvate metabolic response to the 1st exposure (exposure on the 1st day) to immobilization stress (IMO) were considerably altered by lesions of the periventricular arcuate nucleus (ARC), ventromedial hypothalamus (VMH), stria terminalis (ST) and dorsal fornix (FX). The pyruvate metabolic responses to IMO were completely abolished by seven times repetition of exposure to IMO in the rabbits with lesions of ARC and VMH; they were similar to sham-operated groups. In rabbits with lesions of ST and FX, the pyruvate metabolic responses to the 7th exposure (exposure on the 7th day) to IMO were almost the same as those after the 1st exposure to IMO, but these metabolic responses were completely abolished by the seven times repetition of exposure to IMO in the sham-operated animals. These results suggest that firstly the ARC, VMH, amygdala (AMYG)-ST system and dorsal hippocampus (HPC)-FX system are involved in the pyruvate metabolic responses to the 1st exposure to IMO, and secondly, that the AMYG-ST system and the HPC-FX system are involved in the disappearance process of pyruvate metabolic responses to IMO by the daily repetition of exposure to IMO.

Animals↗
PubMed1986

Enumeration, isolation, and species identification of mycoplasmas in saliva sampled from the normal and pathological human oral cavity and antibody response to an oral mycoplasma (Mycoplasma salivarium).

Saliva samples collected from 393 subjects with and without oral diseases were examined for concentrations of mycoplasmas and Mycoplasma species. Mycoplasmas were isolated from 383 (97%) of the 393 subjects. Viable counts ranged from zero to 7.6 X 10(7) CFU/ml (median, 6.9 X 10(4)) and were significantly (P less than 0.01) higher in diseased subjects, except for those with arthrosis temporomandibularis, than in controls. Of 1,400 isolates, 897 (64%), 442 (30%), and 8 (1%) were identified as Mycoplasma salivarium, M. orale, and M. hominis, respectively, and the remaining 73 isolates (5%) were unidentifiable. More than two-thirds of the isolates from diseased subjects versus only half from controls were identified as M. salivarium. In diseased subjects other than those with ostitis (especially those with arthrosis temporomandibularis), the incidence of M. salivarium was higher than that of M. orale, whereas the former occurred about as frequently as the latter in the controls. Antibodies to M. salivarium were also measured in sera from some subjects by the metabolism inhibition test. Sera with metabolism inhibition titers of 16 or greater were rated positive. There was no significant difference in the prevalence of antibodies between diseased subjects (60%) and controls (40%), but the mean titers (97 to 220) of all positive sera from diseased subjects were two to four times those for sera from controls. In addition, a fourfold or greater rise or fall of antibody titers to the organism was shown in paired sera from some subjects. On the basis of these results, M. salivarium was strongly suggested to participate etiologically in some cases of oral infection.

Adolescent↗
PubMed1986

Effects of adrenoceptor agonists and antagonists on the firing of neurons in the rat A1 noradrenergic region.

Noradrenaline (NA), but not clonidine applied microiontophoretically, inhibited the firing of neurons in the rat A1 noradrenergic region, whereas intravenous clonidine dose-dependently inhibited their firing (ED50 = 18.3 micrograms/kg). The NA-induced inhibition was blocked by the beta-antagonist timolol, but not by the alpha-antagonists phentolamine or piperoxane. These results suggest that neurons in the A1 region possess beta-adrenoceptors rather than alpha-adrenoceptors near their cell bodies, and that systemically administered clonidine acts indirectly on these cells.

Adrenergic Agonists↗
PubMed1985

Subfornical organ neurons with efferent projections to the hypothalamic paraventricular nucleus: an electrophysiological study in the rat.

Seventeen neurons in the subfornical organ (SFO) were antidromically activated by electrical stimulation of the paraventricular nucleus (PVN) in the rat. The activity of all identified SFO neurons was excited by microiontophoretically (MIPh) applied angiotensin II (AII) and the effect of AII was blocked by MIPh-applied saralasin (Sar), an AII antagonist, but not by atropine (Atr), a muscarinic antagonist. In these identified SFO neurons, 9 were also excited and 8 were not affected by MIPh-applied acetylcholine (ACh) and the effect of ACh was attenuated by not only MIPh-applied Atr but also by Sar. These results suggest that there are specific AII- and both AII- and ACh-sensitive types of SFO neurons with efferent projections to the PVN.

Acetylcholine↗
PubMed1985

Electrophysiological evidence that circulating angiotensin II sensitive neurons in the subfornical organ alter the activity of hypothalamic paraventricular neurohypophyseal neurons in the rat.

Thirteen neurons in the subfornical organ (SFO) were antidromically activated by electrical stimulation of the paraventricular nucleus (PVN) in the rat. The activity of these identified SFO neurons was excited by intravenous injection of angiotensin II (AII). Electrical stimulation of the SFO produced orthodromic excitation (40%) and inhibition (40%) of the activity of putative vasopressin (VP)-secreting PVN neurons. These results suggest that circulating AII sensitive SFO neurons with efferent projections to the PVN have both excitatory and inhibitory influences on the activity of putative VP-secreting neurons in the PVN.

Angiotensin II↗
PubMed1985

Inputs from the A1 noradrenergic region to hypothalamic paraventricular neurons in the rat.

Electrical stimulation of the rat A1 noradrenergic region produced excitation (77%) of the activity of putative vasopressin (VP)-secreting neurons in the paraventricular nucleus (PVN) and produced excitation (4%), inhibition (26%) and excitation-inhibition (11%) of the activity of PVN neurons that were not antidromically identified by neurohypophysial stimulation. The excitatory response of putative VP-secreting neurons was blocked by microiontophoretically applied phentolamine, an alpha-adrenoceptor antagonist, but not by timolol, a beta-adrenoceptor antagonist. The inhibitory response of unidentified PVN neurons, on the other hand, was blocked by timolol, but not by phentolamine.

Adrenergic Fibers↗