Biomedical subjects

B H Hwang

Publications and source records attributed to B H Hwang.

At least 37 records · Page 2Linked to original sources

PubMed1991

Quantitative autoradiographic study on tyrosine hydroxylase mRNA with in situ hybridization and alpha 2 adrenergic receptor binding in the locus coeruleus of the spontaneously hypertensive rat.

alpha-2 Adrenergic (A2) receptors and tyrosine hydroxylase (TH) mRNA in the locus coeruleus (LC) were studied using [125I]iodoclonidine and [35S]TH oligonucleotide probe. Spontaneously hypertensive (SHR) rats contained less TH mRNA at their prehypertensive, but not at the well-established hypertensive stage, than age-matched Wistar-Kyoto rats. Furthermore, there is an up-regulation of A2 receptors in SHR rats which is parallel to their blood pressure elevation. The present data suggest that increased A2 receptors in conjunction with TH mRNA reduction in the LC are associated with initiation, but not maintenance of genetic hypertension.

Animals↗

PubMed1990

Increased density of glutamic acid decarboxylase-containing terminals in the medial preoptic nucleus and the area surrounding the paraventricular hypothalamic nucleus is associated with deoxycorticosterone acetate (DOCA)-salt hypertension.

gamma-Aminobutyric acid (GABA) is a major inhibitory neurotransmitter and has been shown to exert considerable influence on the neural control of the cardiovascular function. It is not clear, however, which GABAergic systems are involved in salt-induced hypertension. This study was designed to investigate the GABAergic neurons in specific regions of the brain possibly linked to salt-induced hypertension. After 4 weeks of deoxycorticosterone acetate (DOCA) and salt treatments, the rats developed cardiac hypertrophy. All of the animals were sacrificed for immunocytochemical localization of GABAergic terminals using specific antibodies to glutamic acid decarboxylase (GAD). GAD-positive GABAergic terminal densities in discrete regions of the brain were determined by using morphometric quantitation. Results showed that GABAergic terminal densities in the medial preoptic nucleus and the area lateral to the paraventricular hypothalamic nucleus were significantly increased in DOCA-salt-treated rats 4 weeks after the experiment as compared with 4 week controls. This study provides new evidence to support further the idea that central GABAergic neurons are closely associated with pathogenesis of salt-induced hypertension. Different hypertensive mechanisms between salt-induced hypertension and genetic hypertension are also discussed.

Animals↗

PubMed1990

Increased number of GABAergic terminals in the nucleus accumbens is associated with alcohol preference in rats.

Ethanol is known to be anxiolytic and this effect may be mediated through GABA transmission acting on the GABAA-benzodiazepine-Cl- ionophore complex. Recent studies from our laboratory have suggested that GABA transmission and the GABAA-benzodiazepine-Cl- ionophore complex might be involved in the rewarding action of ethanol in alcohol-preferring rats. We report here immunocytochemical and morphometric studies analyzing the GABAergic terminal density in the nucleus accumbens (NA), corpus striatum, nucleus tractus solitarius, and lateral septum of the selectively bred P (alcohol-preferring) and the NP (alcohol-nonpreferring) lines of rats, as well as of the high-alcohol-drinking (HAD) and low-alcohol-drinking (LAD) lines of rats. The NA was included for analysis because this structure has been implicated as an important component of the brain reward system. An increase of GABAergic terminal density was found in the NA of the P rats, when compared with the NP rats. Similarly, there were more GABAergic terminals in the NA of HAD rats than of the LAD rats. No differences between the lines were seen in the other brain regions examined. The results suggest that alcohol preference in P and HAD rats may be related to increased GABA terminals and enhanced GABAergic inhibition within the NA.

Alcohol Drinking↗

PubMed1986

Increased delta, but not mu, opiate receptor binding in the medulla oblongata of Long-Evans rats following 5-day water deprivation.

Opiate receptors of the mu type were labeled with [125I]D-Ala2,N-Me-Phe4,Met-(O)5-ol-enkephalin (FK-33824). delta receptors were labeled with [125I]D-Ala2-D-Leu5-enkephalin (DADLE) in the presence of excess (N-Me-Phe3,D-Pro4)-morphiceptin (PL017). Since DADLE binds mu and delta receptor sites, and PL017 blocks mu receptors, this protocol improves specific labeling of delta receptors. Quantitative autoradiography showed that chronic dehydration causes no changes in mu receptor binding in the medulla oblongata of Long-Evans rats. However, there is increased delta receptor binding in the solitary, hypoglossal and gracilis nuclei, and the spinal nucleus of trigeminal system of dehydrated animals, suggesting that delta opiate receptors participate in the physiological response to dehydration.

Animals↗

PubMed1986

Effects of chronic dehydration on angiotensin II receptor binding in the subfornical organ, paraventricular hypothalamic nucleus and adrenal medulla of Long-Evans rats.

Angiotensin II (AII) is an important peptide known to regulate blood pressure and body fluid. In the present study we used a potent AII antagonist, 125I-(Sar1,Ile8)-AII (125I-SI-AII), to study AII receptor binding in Long-Evans rats 5 days after water deprivation. Specific structures evaluated include the subfornical organ (SFO) and adrenal gland. With quantitative autoradiography, we have found that there is an increase of 125I-SI-AII binding in the SFO, whereas there is a decrease in AII binding in the adrenal medulla. These observations suggest that central and peripheral AII target tissues are affected differently by dehydration. The increase in SI-AII binding in the SFO may indicate participation of this structure during dehydration, as angiotensin stimulation of SFO causes thirst and vasopressin release.

1-Sarcosine-8-Isoleucine Angiotensin II↗

PubMed1986

Plasticity of catecholaminergic terminals in rat paraventricular hypothalamic nucleus after 6-hydroxydopamine lesion: an emphasis on bouton sizes and synaptic frequency.

Catecholaminergic (CA) nerve terminals in the paraventricular hypothalamic nucleus (PVN) of adult rats were studied at 4, 21, 56 and 180 days after a single injection of 6-hydroxydopamine (6-OHDA) neurotoxin into the right lateral ventricle of the brain. We previously described and quantified the extent of CA terminal sprouting in the PVN after 6-OHDA lesions. For this communication we studied parameters, specifically the bouton sizes and the synaptic frequencies of CA terminals during the renewal process, and evaluated how changes of these parameters are related to axonal sprouting. The CA boutons were identifiable in the electron microscope by exhibiting small granular vesicles (SGVs) after central administration of 5-hydroxydopamine (5-OHDA) marker. The marked CA boutons were measured and further categorized according to whether or not they were associated with distinct synaptic specializations at various post-lesion stages. The average sizes of CA boutons were strikingly similar in their diameters (1.0 micron) for both control and experimental tissues. However, CA boutons larger than 2.1 micron were rare and seen more often in the experimental tissues with 6-OHDA lesion and were sustained up to 180 days after lesions. Catecholaminergic profiles with ultrastructural features of growth cones were also seen in the PVN following the 6-OHDA lesions, indicating that there is growth activity in the PVN after 6-OHDA lesion. There were 33% of CA boutons in the PVN from the control tissues that appeared to have synaptic contacts.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic Fibers↗

PubMed1986

Different pharmacological anatomy in the paraventricular hypothalamic nucleus, supraoptic nucleus, and suprachiasmatic nucleus of rats: quantitative autoradiography on angiotensin II receptor binding sites.

Angiotensin II (AII) and vasopressin (VP) play important roles in cardiovascular function. Using 125I-[Sar1,Ile8]-angiotensin II (125I-SI-AII), a potent AII antagonist, AII receptor binding sites were autoradiographically localized in three VP-producing areas of the hypothalamus and compared in hypertensive and normotensive rats. Within three major VP-producing areas, AII receptor binding was highest in the paraventricular hypothalamic nucleus and lowest in the supraoptic nucleus, suggesting that a differential AII regulation of separate VP systems exists in the brainstem. No statistical difference in 125I-SI-AII receptor binding was found between WKY and SHR rats in each of the three major VP-producing nuclei studied. These results are consistent with a role of AII receptors in a subtle and complicated regulation of VP in cardiovascular function.

Angiotensin II↗

PubMed1986

Increased synaptic contacts of catecholaminergic boutons in the cerebral cortex and paraventricular hypothalamic nucleus of rats after prenatal and perinatal ethanol exposure.

Prenatal/perinatal exposure to ethanol caused no obvious changes of catecholaminergic terminal density in the cerebral cortex and hypothalamus. However, ethanol induced significant increases of catecholaminergic synaptogenesis in these two regions. Such increased catecholaminergic synaptogenesis may thus be a basis for the etiology of alcohol-induced hyperactive behavior.

Animals↗

PubMed1986

Quantitative autoradiography of 125I-[Sar1, Ile8]-angiotensin II binding in the brain of spontaneously hypertensive rats.

The brain contains its own angiotensin II (AII) system. To better understand the role of central AII in cardiovascular regulation, we used 125I-[Sar1, Ile8]-AII (125I-SI-AII), radioactive AII antagonist, to autoradiographically localize putative AII receptor binding in many parts of the central nervous system of the spontaneously hypertensive (SHR) and normotensive Wistar-Kyoto (WKY) rats. With 125I-SI-AII binding on brain membrane preparations. Scatchard analysis indicated that Kd values were from 0.10 +/- 0.04 nM to 0.13 +/- 0.05 nM, whereas Bmax values (femtomol/mg protein) were found to be from 6.95 +/- 1.60 to 15.52 +/- 4.99 among brain regions studied. Various SI-AII receptor binding activities among brain regions revealed in this study were therefore most likely due to differences in AII receptor density with high affinity binding of 125I-AII. Using 125I-SI-AII, specific binding for SI-AII was found in the nucleus tractus solitarius (NTS), paraventricular hypothalamic nucleus (PVN), subfornical organ (SFO), suprachiasmatic nucleus (SCN), area postrema, the dorsal motor nucleus of the vagus (DMX), and the nucleus of spinal tract of the trigeminal system (NSV). With quantitative receptor autoradiography in conjunction with radioactive standards, we have observed that the NTS possesses the highest SI-AII binding, followed by the PVN, SFO, NTS, DMX, and NSV. No significant differences were observed between the SHR and WKY rats in the SI-AII binding within the SFO, PVN and NTS. However, SHR at early hypertensive (7 weeks) and established hypertensive (16 weeks) stages contained significantly higher SI-AII bindings in the NSV, as compared to age-matched WKY rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗

PubMed1985

Heterogeneous localization of adenylate and guanylate cyclases in R3230AC rat mammary adenocarcinoma cells.

Adenylate and guanylate cyclase activities were demonstrated in R3230AC rat mammary adenocarcinomas by electron microscopic cytochemistry. Adenylate (AC) and guanylate (GC) cyclases were detected on plasma membrane of tumor epithelial cells, but not on fibroblasts and endothelial cells in the perivascular space. Both AC and GC activities were enriched in tumor epithelial cells at the periphery of the tumor lobular parenchyma rather than in cells in central core of the lobular parenchyma. Furthermore, the tumor cell plasma membranes facing the connective tissue stroma were in paucity or devoid of either enzyme activity. These heterogeneous distributions of both AC and GC among tumor epithelia suggest that R3230AC epithelial cells in different parts of the tumor mass may vary significantly in their regulation of cellular physiology.

Adenocarcinoma↗

PubMed1985

Effects of intracerebroventricular 6-hydroxydopamine on catecholaminergic fibers in the rat hypothalamus.

Regeneration in the central nervous system has been claimed to be very limited and abortive, although functional regeneration of some of its pathways after destruction has been observed. The exact mechanisms by which axons regenerate fully or fail to have functional regeneration remain to be studied further. We explored whether or not there is a regional difference in regeneration of central catecholaminergic (CA) neurons in the hypothalamus of young adult rats after 6-hydroxydopamine (6-OH-DA) treatment. Four days after treatment, the numbers of CA terminals and axons were significantly reduced in the paraventricular hypothalamic nucleus, periventricular hypothalamic nucleus, supraoptic commissure (SOC), and dorsomedial hypothalamic nucleus as assessed by a morphometric quantitation on fluorescence microscopy micrographs; CA axons were gradually increased in numbers after the treatment. The number of CA varicosities in the supraoptic commissure was restored to 96% of control 180 days after the 6-OH-DA lesion, whereas the actual numbers of CA varicosities in the paraventricular, periventricular, and dorsomedial hypothalamic nuclei were attained at 79, 79, and 68% of control values, respectively. Our results indicate that CA fibers in the supraoptic commissure possess more regenerative potential than the three other hypothalamic regions studied, suggesting a regional difference in CA nerve sprouting during neuroplasticity within the hypothalamus. The favorable regeneration of CA axons in the supraoptic commissure implies to us that some trophic features along that pathway, particularly near the third ventricle, may have been stimulated after chemical lesion using 6-OH-DA, and gradually released in the distal field of the supraoptic commissure to attract CA stumps to sprout. These factors may thus induce both regenerative sprouting and collateral sprouting resulting in vigorous regrowth of CA fibers in the supraoptic commissure.

Animals↗

PubMed1985

Effects of triiodothyronine and propylthiouracil on regeneration of catecholaminergic nerve terminals in the paraventricular hypothalamic nucleus of the adult rat.

Effects of triiodothyronine and the antithyroid drug, propylthiouracil, on regeneration of catecholaminergic nerve terminals in the paraventricular hypothalamic nucleus of adult rats were studied. Lesions were produced by 6-hydroxydopamine neurotoxin and then the animals were treated with triiodothyronine or propylthiouracil inducing hyperthyroidism or hypothyroidism, respectively, as determined by radioimmunoassay. Although catecholaminergic varicosities increased with time in the paraventricular hypothalamic nucleus of rats after lesion, fluorescent microscopic quantitation showed no statistical difference in their number between rats treated with triiodothyronine and the vehicle for as long as 56 days. Furthermore, electron microscopic quantitation at 56 days postlesion showed no significant difference between the triiodothyronine-treated and control rats in terms of the density, proportion, size, types of synapses, and synaptic frequency of catecholaminergic nerve terminals. There were growth cones in the paraventricular hypothalamic nucleus, suggesting growth activity after lesion. However, we found that exogenous administration of large doses of triiodothyronine at 25 micrograms/kg had little effect on the enhancement of regeneration of central catecholaminergic terminals after their destruction by 6-hydroxydopamine.

Animals↗

PubMed1984

Ultrastructural studies on catecholaminergic terminals and GABAergic neurons in nucleus tractus solitarius of the rat medulla oblongata.

Synaptogenesis of catecholamine (CA) boutons in the nucleus tractus solitarius (NTS) was compared between spontaneously hypertensive (SHR) rats and Wistar-Kyoto (WKY) rats at different ages. On the average, there were about 32 CA varicosities per 2200 microns2 area of the NTS in both SHR and WKY rats as revealed by glyoxylic acid fluorescence microscopic (FM) morphometric study. The FM analysis indicated that there were no significant changes in the CA varicosity density between SHR and WKY rats. The CA boutons were labeled with 5-hydroxydopamine and appeared to contain small granular vesicles at the electron microscopic (EM) level. A total of 1402 CA boutons were studied in a 540,000 micron2 area of the NTS. The number of CA boutons involved in synaptic contacts vs the number of total CA boutons was used to obtain synaptic frequency which was taken as an index for synaptogenesis. A reduction of approximately 18% and 14% of synaptogenesis of CA boutons was observed in the NTS of SHR rats at 4 weeks (prehypertensive stage) and 12 weeks (early hypertensive stage) of age respectively, as compared to age-matched WKY rats. No significant difference of synaptogenesis of CA neurons was found between SHR and WKY rats at 16 weeks of age, a stage in which hypertension is well established and maintained in SHR rats. These results suggest that CA neurons with fewer synaptic contacts in the NTS may play a more important role in the initiation than in the maintenance of hypertension in the SHR rats. In addition to CA terminals, there were numerous GABAergic cell bodies in the NTS which were identified by immunocytochemistry using antibodies to the GABA synthesizing enzyme, L-glutamate decarboxylase (GAD). GABAergic dendrites with GAD-positive reaction were often seen to receive several GAD-negative synapses at EM random profiles. In the text, a viewpoint is thus discussed that emphasizes that a synaptic abnormality of CA terminals with fewer synaptic contacts affecting GABAergic neurons may participate in the pathogenesis of hypertension. However, it remains to be determined as to whether or not there is a direct contact between CA boutons and GABAergic dendrites.

Animals↗

PubMed1984

Catecholamine synapses and contents in the paraventricular hypothalamic nucleus and nucleus tractus solitarius of DOCA-salt hypertensive rats.

Central catecholamine (CA) neurons in the nucleus tractus solitarius (NTS) and paraventricular hypothalamic nucleus (PVN) were studied in Wistar rats that had been unilaterally nephrectomized. The experimental animals were then treated with deoxycorticosterone acetate (DOCA) and salt water. The control animals were treated with the vehicle and tap water. Blood pressure of animals 4 weeks after DOCA/salt treatment was significantly elevated when compared to control rats. Morphologically, CA terminals showed no noticeable changes in the DOCA/salt hypertensive rats. Furthermore, the density of CA terminals either in the NTS or in the PVN of the DOCA/salt hypertensive rats was not statistically different from that of normotensive controls, suggesting that salt does not cause lesions or destruction of CA terminals. However, an extensive electron-microscopic morphometric analysis indicated that there was an enhancement of CA synaptogenesis (expressed by increased synaptic frequency among all CA boutons labeled with 5-hydroxydopamine) in the PVN, but not in the NTS of DOCA/salt hypertensive rats. In addition, the high-performance liquid chromatography revealed decreased CA contents in the PVN, but not in the NTS, of DOCA/salt hypertensive animals. Since synapses are primary sites for neurotransmitter release, the above results collectively suggest that more CA synapses formed in the PVN may reflect a net CA release from CA terminals resulting in the decreased CA content in the axonal terminals. Such an increased CA release and enhanced CA synaptogenesis may consequently enhance CA function in the PVN of hypertensive rats 4 weeks after DOCA/salt treatment, and relate to the development and/or maintenance of hypertension in the DOCA/salt rats.

Animals↗

PubMed1982

Fluorescence and electron microscopic study of the tree shrew pineal organ.

The fine structure of the pineal gland and the pineal innervation in the tree shrew were studied by electron microscopy and glyoxylic acid-induced fluorescence microscopy respectively. The parenchymal cells consist of pinealocytes, glial cells and pigment-containing cells. The pinealocytes are characterized by the presence of granular vesicles, synaptic ribbons, electron-dense bodies and small profiles of rER with dilated cisternae. Glial cells contain light cytoplasmic bodies, lipofuscin granules, bundles of microfilaments, and elongate profiles of rER with flattened cisternae which are often stacked together with light cytoplasmic bodies; the pigment-containing cells are unique in possessing giant pigment granules in the cytoplasm. The pinealocyte/glial cell/pigment cell in tree shrew pineals may be the same cell line of parenchymal cells at different ontogenetic stages. Pigment-containing cells contain pigment granules as a prominent cytoplasmic inclusion, suggesting they are senscent in secretory function. Both pinealocytes and glial cells contain structures suggesting secretory function such as well-developed Golgi complex and granular vesicles. The antigonadotrophic substances may be stored in granular vesicles. The present ultrastructural study supports the conclusion that tree shrew pineal organ is an endocrine gland which is heavily innervated by adrenergic nerves and possibly by cholinergic nerves.

Animals↗

PubMed1982

Characterization of monoaminergic terminals in the neostriatum of neonatal rats: an electron microscopic morphometric analysis.

Monoaminergic (MA) boutons in the neostriatum of neonatal rats were studied by using 5-hydroxydopamine. We found: (a) bouton size averaged 0.6 micron in diameter; (b) terminal density was 68 boutons per 7200 micron2 area; (c) synaptic frequency was 33.2%; and (d) MA neurons constituted 9.2% of all boutons. This population was much lower than that reported in immature neocortex where MA neurons are a major innervation.

Animals↗

PubMed1980

Changes induced by 6-hydroxydopamine in the paraventricular nucleus. A correlated fluorescence microscopic/electron microscopic evaluation.

Remodelling of catecholaminergic (CA) fibers after cerebral intraventricular 6-hydroxydopamine (6-OH-DA) administration was evaluated quantitatively in the paraventricular nucleus ( PAR) of young adult rats, using fluorescence microscopy (FM) and electron microscopy (EM). Fluorescent CA varicosities and CA boutons (marked with 5-OH-DA) were counted after survival periods of 4, 21, 56 or 180 days. Four days after 6-OH-DA treatment, the number of fluorescent varicosities dropped to 45% of control numbers but was restored to 79% of control values by 180 days. In the EM study, marked boutons had dropped more dramatically: to 12% of control numbers, after 4 days and 54% by 180 days post-neurotoxin. These data provide strong evidence that substantial but incomplete restoration of CA terminals occurred in PAR. It is of interest that, in all survival intervals, percentage reductions in numbers of CA terminals were more extreme when EM was used for quantification. Nevertheless, the trends indicating partial restoration of terminal numbers with time were parallel in the FM and EM studies. Structures identified as CA growth cones in PAR contained a feltwork of fine filaments together with mitochondria, granular vesicles (often with electron-dense cores marked by the 5-OH-DA label), vacuoles and smooth-surfaced reticulum. The presence of growth cones, some of which persisted 11 months after neurotoxin administration, further supports the inference that a regenerative response of CA elements was evoked in PAR by the 6-OH-DA treatment.

Adrenergic Fibers↗

PubMed1979

Age as a factor in 6-hydroxydopamine-induced plasticity in the hypothalamus.

The question of age as a possible factor influencing the regenerative response of catecholaminergic varicosities in the hypothalamus was investigated in the supraoptic commissure and the paraventricular, periventricular, and dorsomedial hypothalamic nuclei of rats that had received intraventricular injections of the neurotoxin 6-hydroxydopamine when they were (1) neonates, (2) young adults, or (3) senescent adults. After post-neurotoxin survival for 4, 21, 56, or 180 days, the animals were perfused, and the hypothalamic tissue sections were cut and processed using a glyoxylic acid method for localizing catecholamines. Four days following neurotoxin administration, counts of fluorescent varicosities showed a significant loss of catecholamine varicosities in each of the four areas. Subsequently, at least partial restoration of numbers of catecholamine varicosities occurred in all hypothalamic areas in all three age groups. It is concluded that, following selective lesions induced by the neurotoxin 6-OH-DA, catecholamine varicosities were restored both in immature and mature groups. According to the evidence obtained experimentally, the rate of restoration was greater in the neonate group, whereas the percentage restoration attained varies according to the hypothalamic area studied and the age of the animal.

Age Factors↗