Biomedical subjects

N Yanagihara

Publications and source records attributed to N Yanagihara.

At least 37 records · Page 2Linked to original sources

PubMed2000

Ossiculoplasty using hydroxyapatite prostheses: long-term results.

The surgical results of ossicular chain reconstruction using a hydroxyapatite prosthesis were evaluated in 106 ears of 101 patients who were followed up for > 5 years. Successful reconstruction was defined as: (1) postoperative air-bone gap of </= 20 db; or (2) postoperative air conduction better than 40 db; or (3) hearing gain better than 15 db. Success in hearing was obtained in 63/106 ears (59%) at 1 year; 44/65 ears (68%) in P-type (short columella) and 19/41 ears (46%) in T-type (long columella). By the fifth year, the overall success rate had deteriorated to 50%: i.e. 39/65 ears (60%) in P-type and 14/41 ears (34%) in T-type. Extrusion of the prosthesis occurred in 17 ears (16%) with a mean postoperative period of 27.7 months. The present results indicate that hydroxyapatite is a suitable material for an ossicular prosthesis, although the incidence of extrusion is high when it is placed in contact with the tympanic membrane.

Adolescent↗

PubMed2000

Edematous swelling of the facial nerve in Bell's palsy.

Surgical decompression of the intratemporal facial nerve from the geniculate ganglion to the stylomastoid foramen was carried out in 91 patients with Bell's palsy. All of the patients had denervation exceeding 95%, and a suprastapedial lesion. Edematous swelling of the nerve was assessed using the following three grades: + +, nerve swells beyond the bony facial canal; +, nerve swells beyond the nerve sheath, but within the bony canal, and -, no notable swelling observed. Varying degrees of swelling of the nerve were noted in all of the patients from onset to the end of the ninth week. The incidence of + + swelling was highest within 3 weeks of onset and then declined. + + swelling was most often noted in the vicinity of the geniculate ganglion, and was thought to be a manifestation of inflammation due to herpes simplex virus infection. There was a clear time dependency of the swelling in the horizontal and pyramidal segments, but not in the mastoid segment. After the ninth week, the incidence of swelling decreased sharply and no swelling of the nerve was observed in about one-third of the patients. Considering the etiology and the analysis of edematous swelling, we propose that the course of Bell's palsy be differentiated into an acute phase (the first 3 weeks after onset), a subacute phase (from the fourth to ninth weeks) and a chronic phase (after the tenth week).

Adolescent↗

PubMed2000

Histological rearrangement in the facial nerve and central nuclei following immediate and delayed hypoglossal-facial nerve anastomosis.

The timing of hypoglossal-facial nerve anastomosis is controversial. The present study was performed to clarify the influence of the timing of hypoglossal-facial nerve anastomosis on histological changes in the facial nerve and central nuclei using guinea pigs. The facial nerve was transected first at the labyrinthine portion, and then transected again at the stylomastoid foramen. Hypoglossal-facial nerve anastomosis was carried out immediately or 3 months later. Nerve regeneration and survival of the neurons in the facial and hypoglossal nuclei were evaluated by toluidine blue staining and horseradish peroxidase (HRP). Immediate anastomosis resulted in better nerve regeneration of the facial nerve, but the numbers of surviving neurons in the facial and hypoglossal nuclei were almost the same in both the immediate and delayed anastomosis groups.

Anastomosis, Surgical↗

PubMed2000

Inhibition by neuromuscular blocking drugs of norepinephrine transporter in cultured bovine adrenal medullary cells.

UNLABELLED: Pancuronium stimulates the cardiovascular system, whereas vecuronium, a derivative of pancuronium, has far fewer effects. The inhibition of norepinephrine transporter (NET) in the sympathetic nervous system may partly account for the stimulatory actions of pancuronium. To investigate the mechanism of action of pancuronium on NET, we examined the effects of pancuronium on NET activity by using cultured bovine adrenal medullary cells and compared pancuronium with other neuromuscular blocking drugs. Pancuronium (1-300 microM) inhibited desipramine-sensitive [(3)H]norepinephrine (NE) uptake in a concentration-dependent manner. Vecuronium (100-300 microM) and d-tubocurarine (300 microM) also decreased [(3)H]NE uptake but were less potent than pancuronium at clinical concentrations. Succinylcholine had little effect on [(3)H]NE uptake. Saturation analysis showed that pancuronium and vecuronium reduced an apparent maximum velocity (V(max)) of [(3)H]NE uptake without altering Michaelis-Menten constant, indicating noncompetitive inhibition. Pancuronium did not inhibit the specific binding of [(3)H]desipramine to plasma membranes isolated from bovine adrenal medulla. A protein kinase C inhibitor, GF109203X, did not affect the inhibition of [(3)H]NE uptake by pancuronium. Pancuronium enhanced the inhibition of NET induced by ketamine. These results suggest that pancuronium, with clinically relevant concentrations, inhibits NET activity by interacting with a site distinct from the recognition site for NE and the desipramine binding site on the transporter. IMPLICATIONS: In this study, pancuronium inhibited norepinephrine uptake and was the most potent of the neuromuscular blocking drugs we tested, including pancuronium, vecuronium, d-tubocurarine, and succinylcholine. Pancuronium may affect the sympathetic nervous system by inhibiting the activity of the presynaptic norepinephrine transporter at clinically relevant concentrations.

Adrenal Medulla↗

PubMed2000

Dual effects of intravenous anesthetics on the function of norepinephrine transporters.

BACKGROUND: Norepinephrine transporters (NETs) terminate the neuronal transmission of norepinephrine, which is released from noradrenergic neurons. To investigate the interaction with NET, the authors examined the effects of short- and long-term treatment with anesthetics on the activity and mRNA level of NET. METHODS: To assay [3H]norepinephrine uptake, bovine adrenal medullary cells in culture were incubated with [3H]norepinephrine in the presence of intravenous anesthetics, including propofol, thiamylal, and diazepam. To study the direct interaction between the anesthetics and NET, the effect of propofol on the binding of [3H]desipramine to the plasma membrane was examined. To study the long-term effect of anesthetics, [3H]norepinephrine uptake by cells pretreated with propofol for 6-24 h and [3H]desipramine binding after pretreatment for 12 h were measured. Simultaneously, we examined the effect of anesthetics on the expression of NET mRNA using the reverse transcriptase-polymerase chain reaction. RESULTS: All of the intravenous anesthetics inhibited [3H]norepinephrine uptake in a concentration-dependent manner. The active concentrations of propofol (1-3 microm) and thiamylal (< or = 30 microm) were similar to those encountered clinically. The kinetic analysis revealed that all the anesthetics noncompetitively inhibited [3H]norepinephrine uptake. Propofol inhibited [3H]desipramine binding with a potency similar to that observed in [3H]norepinephrine uptake. Scatchard analysis showed that propofol competitively inhibited [3H]desipramine binding. On the other hand, long-term treatment of cells with propofol (10 microm) enhanced the NET functional activity and [3H]desipramine binding, and also increased the level of NET mRNA. CONCLUSIONS: These results suggest that intravenous anesthetics have a dual effect on NET; short-term treatment causes inhibition, whereas long-term treatment leads to up-regulation. The interaction of intravenous anesthetics with NET may modulate the neuronal transmission of norepinephrine during anesthesia.

Adrenal Medulla↗

PubMed2000

ATP activates DNA synthesis by acting on P2X receptors in human osteoblast-like MG-63 cells.

In human osteoblast-like MG-63 cells, extracellular ATP increased [(3)H]thymidine incorporation and cell proliferation and synergistically enhanced platelet-derived growth factor- or insulin-like growth factor I-induced [(3)H]thymidine incorporation. ATP-induced [(3)H]thymidine incorporation was mimicked by the nonhydrolyzable ATP analogs adenosine 5'-O-(3-thiotriphosphate) and adenosine 5'-adenylylimidodiphosphate and was inhibited by the P2 purinoceptor antagonist suramin, suggesting involvement of P2 purinoceptors. The P2Y receptor agonist UTP and UDP and a P2Y receptor antagonist reactive blue 2 did not affect [(3)H]thymidine incorporation, whereas the P2X receptor antagonist pyridoxal phosphate-6-azophenyl-2',4-disulfonic acid inhibited ATP-induced [(3)H]thymidine incorporation, suggesting that ATP-induced DNA synthesis was mediated by P2X receptors. RT-PCR analysis revealed that MG-63 cells expressed P2X(4), P2X(5), P2X(6), and P2X(7), but not P2X(1), P2X(2), and P2X(3), receptors. In fura 2-loaded cells, not only ATP, but also UTP, increased intracellular Ca(2+) concentration, and inhibitors for several Ca(2+)-activated protein kinases had no effect on ATP-induced DNA synthesis, suggesting that an increase in intracellular Ca(2+) concentration is not indispensable for ATP-induced DNA synthesis. ATP increased mitogen-activated protein kinase activity in a Ca(2+)-independent manner and synergistically enhanced platelet-derived growth factor- or insulin-like growth factor I-induced kinase activity. Furthermore, the mitogen-activated protein kinase kinase inhibitor PD-98059 totally abolished ATP-induced DNA synthesis. We conclude that ATP increases DNA synthesis and enhances the proliferative effects of growth factors through P2X receptors by activating a mitogen-activated protein kinase pathway.

Adenosine Triphosphate↗

PubMed2000

Assessment of stapes mobility by use of a newly developed piezoelectric ceramic device. A preliminary experiment in dogs.

A piezoelectric device was developed for assessment of stapes mobility during middle ear surgery. The device comprises a pair of ceramic bimorph elements: one for activation of the stapes and the other to pick up the vibration as an electric output, which varies in accordance with the stapes mobility, ie, the inverse of the cochlear input impedance (Zsc). The device is compact and easily manipulated even in the narrow surgical field of the ear. However, the measuring range is restricted to between 1 and 10 kHz. Measurement of Zsc was conducted with this device in 5 ears of 5 dogs. The mean magnitude of Zsc increased with frequency in the range from 1 to 10 kHz: 0.95 megohm at 1 kHz and 8.8 megohms at 10 kHz. After fixation of the stapes with dental cement, the magnitude increased to more than 10 megohms, except at 1 kHz. The results suggest that the device is useful in detecting decreases in stapes mobility in patients with chronic otitis media.

Animals↗

PubMed2000

Interleukin (IL)-4 and IL-13 inhibit the differentiation of murine osteoblastic MC3T3-E1 cells.

Interleukin-4 (IL-4) inhibits the spontaneous and stimulated bone resorption resulting from the inhibition of osteoclast formation, as well as osteoclastic activity. Since IL-13 shares some biological properties with IL-4, it was recently reported that IL-13 inhibits bone resorption. The present study was designed to determine the effects of murine IL-4 (IL-4) and murine IL-13 (IL-13) on the murine osteoblastic cell line MC3T3-E1. IL-4 and IL-13 stimulated 3H-thymidine incorporation in the MC3T3-E1 cells and its proliferation in dose dependent manners. A spontaneous increase in alkaline phosphatase (ALP) activity in the cells after plating was inhibited by IL-4 or IL-13, and both cytokines blunted an increase in ALP activity by human parathyroid hormone (PTH) (1-34). PTH-stimulated cyclic AMP (cAMP) production was inhibited by pretreatment with IL-4 and IL-13 for 48 hr in dose dependent manners. Pretreatment with IL-4 and IL-13 for 48 hr caused a decrease in PTH-induced cAMP production at any stimulatory concentration. However, the effective dose (ED50) was unchanged by the pretreatment with these cytokines. Pretreatment with IL-4 and IL-13 did not modulate cAMP generation by forskolin. In contrast, cAMP generation by PGE2 is greater in the cells treated with the cytokines compared to those without the cytokines. These results indicate that IL-4 and IL-13 act on MC3T3-E1 cells in the same manner, stimulating cell proliferation, but inhibiting cell differentiation. The inhibition of osteoblast differentiation by IL-4 and IL-13 may be associated with a decrease in PTH actions on osteoblasts.

Alkaline Phosphatase↗

PubMed2000

[Treatment of Bell's palsy with acyclovir and prednisolone].

Many current studies have suggested that herpes simplex virus is a probable cause of Bell's palsy, and that treatment with antiviral agents such as acyclovir might benefit the patients. In the present study, 69 patients with Bell's palsy were treated with oral administration of acyclovir (2000 mg/day) and prednisolone (60-40 mg/day) at Ehime University Hospital between Oct. 1995 and Dec. 1998. Patients enrolled in this study met the following criteria: 1) severe or complete paralysis with a score lower than 20 by the 40-point Japanese grading system, and 2) treatment started within 7 days of onset. The overall recovery rate was 95.7% (66/69). The rate in patients who started this treatment within 3 days after disease onset was 100%, and this early treatment was highly efficacious in the prevention of nerve degeneration and resulted in a significantly better recovery. By comparison, the recovery rate in patients whose treatment was started 4 days or more after onset was only 84.2%. All patients who were given a diagnosis of zoster sine herpete and treated with acyclovir-prednisolone had a good outcome. These results suggest that early treatment, within 3 days after palsy onset, is necessary for effective acyclovir-prednisolone therapy of Bell's palsy.

Acyclovir↗

PubMed2000

Ramsay Hunt syndrome in children.

In a retrospective study, 52 children were diagnosed with Ramsay Hunt syndrome. The facial palsy was milder and complete recovery of the function was achieved in 78.6% of patients. Associated cranial neuropathies were less common in children than in adults. The timing of vesicle appearance tended to be delayed in children. In preschool children, Ramsay Hunt syndrome was rare, although the frequency has recently increased. The syndrome is relatively common in older children. This study suggested that vaccination can prevent or reduce the occurrence of Ramsay Hunt syndrome.

Adolescent↗

PubMed1999

Progressive association of a "soluble" glycolytic enzyme with the detergent-insoluble cytoskeleton during in vitro morphogenesis of MDCK epithelial cells.

In MDCK epithelial cells, cell contact at confluency initiates a protracted process of morphogenesis during which several proteins known to bind the cytoskeleton become progressively associated with the detergent-resistant cell fraction and distributed to their characteristic polarized domains. Using extraction protocols that identify this tight cytoskeletal linkage, here we show a similar but slower, time-dependent enrichment in the detergent resistant fraction of glyceraldehyde-3-phosphate dehydrogenase (GAPDH), a highly abundant glycolytic enzyme that is traditionally considered soluble. Similar enrichment did not occur for two other glycolytic enzymes, phosphoglycerate mutase or lactate dehydrogenase. Insoluble GAPDH was not homogeneously distributed in the cytoplasm but rather displayed several discrete patterns that varied within and among MDCK cells. It also localized prominently to a few nuclei in the phenotypically heterogeneous cells of late confluency cultures. Disruptors of cytoskeletal filaments were relatively ineffective in the postconfluent epithelial monolayers, although use of disrupting agents implicated actin as the cytoplasmic filament that tethers insoluble GAPDH. Catalytic activity could be demonstrated in the insoluble fraction of GAPDH from postconfluent cultures, but only after release by mechanical disruption of insoluble extracts. Treatment of postconfluent cells with agents that deplete ATP diminished the fraction of cytoskeletally associated GAPDH, and levels of insoluble GAPDH were restored with ATP repletion, suggesting that ATP levels may regulate cytoskeletal linkage and thereby local enzyme activity. We conclude that the highly abundant and ubiquitous enzyme GAPDH becomes progressively enriched in detergent stable subcellular compartments during the process of epithelial morphogenesis. The process that produces GAPDH compartments is slow, suggesting that epithelial cells just at confluency, when they are typically analyzed, have not yet maximized the organizational state that can be attained in monolayer culture.

Acrylamide↗

PubMed1999

Modification of low density lipoprotein potentiates its inhibitory effect on catecholamine secretion in cultured bovine adrenal medullary cells.

Low density lipoprotein (LDL) and lipoprotein(a) suppress catecholamine secretion in cultured adrenal medullary cells. Modification of LDL by oxidation or acetylation potentiates various atherogenic actions of LDL. In the present study, we investigated whether the modification of LDL influences catecholamine secretion in cultured bovine adrenal medullary cells. The exposure of LDL to CuSO4 caused a time-dependent oxidation of LDL. Maximal oxidation of LDL was observed after exposure to CuSO4 for 24 h. Native LDL inhibited catecholamine secretion induced by carbachol to 68.5% of control. Oxidized LDL caused further inhibition of carbachol-evoked secretion to 37.6% of control. Acetylated LDL inhibited it to 41.0% of control. There was a good correlation between the extent of LDL oxidation and the inhibition of catecholamine secretion. These results suggest that oxidation or acetylation of LDL augments its inhibitory effect on the secretion of catecholamines. Since catecholamines are a risk factor of atherosclerosis, the inhibitory effect by such modified LDL may be a mechanism inhibiting atherosclerotic progression.

Adrenal Medulla↗

PubMed1999

Age-related scattered hypofluorescent spots on late-phase indocyanine green angiograms.

PURPOSE: Scattered hypofluorescent spots may be seen on indocyanine green (ICG) angiograms of regions that do not show abnormalities when viewed with an ophthalmoscope. Hypofluorescent spots are found in several pathologic conditions, typically in inflammatory diseases. In this report, we describe hypofluorescent spots in normal fundi and show that such spots can be age-related. METHODS: Video-fundus camera ICG angiograms of 115 eyes of 109 patients aged 12 to 85 years with normal fundi or with only age-related maculopathy were reviewed. The relation between age and scattered hypofluorescent spots, and between age-related maculopathy and spots was examined utilising regression analysis. RESULTS: Scattered hypofluorescent spots were seen throughout the posterior pole in 24 eyes of 23 patients and in a portion of the posterior pole in 30 eyes of 29 patients. The hypofluorescent spots were noted between 26 and 37 minutes after dye injection. Patient age ranged from 51 to 80 years, and regression analysis showed that the frequency of hypofluorescent spots increased significantly with aging (p < 0.05). However, age-related maculopathy did not show a significant relation to the spots. CONCLUSION: Scattered hypofluorescent spots seen in the posterior pole during the late-phase of ICG angiograms can apparently be due to aging of the fundus.

Adolescent↗

PubMed1999

Effect of retinoic acid on proliferation and polyamine metabolism in cultured bovine retinal pigment epithelial cells.

Reports regarding the effect of all-trans-retinoic acid (RA) on the cell growth of retinal pigment epithelial cells (RPE) have been contradictory. The aims of this study are to clarify the in vitro effect of RA on RPE cells and to examine polyamine metabolism after RA stimulation. A 4-day incubation of fetal-calf-serum (FCS)-stimulated RPE cells with 10 or 25 microM RA significantly increased both cell number and [3H]thymidine incorporation. RPE cells grown over an extended period for 8 days also increased in number and reached full confluency. However, if the incubation was further extended to 12 days, no further increase in cell number was detected. RA treatment of FCS-stimulated RPE cells shifted the peak of ornithine decarboxylase (ODC) activity from 16 to 4 h. S-adenosylmethionine decarboxylase (SAMDC) activity and spermidine/spermine N1-acetyltransferase (SAT) activity of RA-treated RPE cells were significantly greater until 8 and 16 h after incubation, respectively. The putrescine content was significantly increased in RA-treated RPE cells up until 24 h, while spermidine, spermine and N1-acetylspermidine contents were significantly increased until 16 h. Our findings suggest that RA treatment increases the intracellular polyamine concentration of RPE cells via activation of ODC, SAMDC and SAT and that this results in the promotion of RPE cell growth until the cells reach full confluency.

Adenosylmethionine Decarboxylase↗

PubMed1999

Combined rupture of Reissner's membrane and round window: an experimental study in guinea pigs: experimental double-membrane rupture.

OBJECTIVE: Hearing loss caused by combined rupture of Reissner's membrane and the round window (RW) membrane (the double-membrane rupture) may differ depending on the site of the lesion on Reissner's membrane. The purpose of this experimental study was to reveal the relationship between the hearing impairment and the site of the lesion on Reissner's membrane. BACKGROUND: According to experimental studies on perilymphatic fistula (PLF), profound hearing loss is not induced by rupture of RW alone, but by the double-membrane rupture. However, the mechanism responsible for hearing loss in the double-membrane rupture remains unclear. METHODS: Compound action potentials (CAPs) of the cochlear nerve in response to tone pip stimuli (1, 2, 4, and 8 kHz) were recorded before the lesion, 90 minutes after the Reissner's membrane rupture, and 90 minutes after subsequent laceration of the RW. Reissner's membrane was ruptured at one of the four turns for comparison. RESULTS: The double-membrane rupture caused a more severe increase in CAP thresholds than seen with separate ruptures, when the Reissner's membrane was ruptured at the second turn. Such pronounced increase in threshold was not seen in ears with the rupture at other turns. CONCLUSIONS: The double-membrane rupture causes varying degrees of hearing loss depending on the site of the lesion of Reissner's membrane. When the Reissner's membrane was ruptured at the second turn, the most severe hearing loss was detected.

Animals↗

PubMed1999

Prostaglandin E2 induces Ca2+ release from ryanodine/caffeine-sensitive stores in bovine adrenal medullary cells via EP1-like receptors.

Prostaglandin E2 (PGE2) causes Ca2+ release from intracellular Ca2+ stores and stimulates phosphoinositide metabolism in bovine adrenal medullary cells. These results have been interpreted as PGE2 induces Ca2+ release from inositol trisphosphate (IP3)-sensitive stores. However, we have recently shown that pituitary adenylate cyclase-activating polypeptide (PACAP), bradykinin, and angiotensin II release Ca2+ from caffeine/ryanodine-sensitive stores, although they cause a concomitant increase of intracellular IP3. In light of these results, the mechanism of PGE2-induced Ca2+ release was investigated in the present study. PGE2 dose-dependently caused a transient but consistent Ca2+ release from internal Ca2+ stores. The PGE2-induced Ca2+ release was unaffected by cinnarizine, a blocker of IP3-induced Ca2+ release. By contrast, it was potently inhibited by prior application of caffeine and ryanodine. Although IP3 production in response to PGE2 was abolished by the phospholipase C inhibitor U-73122, Ca2+ release in response to PGE2 was unaffected by U-73122. The PGE2-induced Ca2+ release was unaffected by Rp-adenosine 3',5'-cyclic monophosphothioate, an inhibitor of protein kinase A, and forskolin, a cyclic AMP (cAMP)-elevating agent, did not cause Ca2+ release. The EP1 agonist 17-phenyl-trinorPGE2 and the EP1/EP3 agonist sulprostone mimicked the Ca(2+)-releasing effects of PGE2, whereas the EP2 agonist butaprost or the EP2/EP3 agonist misoprostol caused little or no Ca2+ release. The EP1 antagonist SC-51322 significantly suppressed the Ca2+ release response induced by PGE2, whereas the EP4 antagonist AH-23828B had little effect. These results suggest that PGE2, acting on EP1-like receptors, induces Ca2+ release from ryanodine/caffeine-sensitive stores through a mechanism independent of IP3 and cAMP and that PGE2 may share the same mechanism with PACAP and the other peptide ligands in causing Ca2+ release in bovine adrenal medullary cells.

Adrenal Medulla↗

PubMed1998

Adrenomedullin increases intracellular Ca2+ and inositol 1,4,5-trisphosphate in human oligodendroglial cell line KG-1C.

The effects of adrenomedullin (AM), a hypotensive peptide, were investigated in cultured human oligodendroglial cell line KG-1C. Human AM increased the intracellular Ca2+ concentration ([Ca2+]i) at concentrations greater than 10(-7) M. Human calcitonin gene-related peptide (CGRP), a peptide structurally related to AM, also increased [Ca2+]i with a potency similar to that of AM. AM increased [Ca2+]i in the absence of extracellular Ca2+. Further, AM increased inositol 1,4,5-trisphosphate (Ins(1,4,5)P3) level in a concentration-dependent manner similar to that of AM-induced [Ca2+]i, suggesting that AM-induced elevation of [Ca2+]i is due to Ca2+ release from Ins(1,4,5)P3-sensitive stores. AM (10(-9) to 10(-6) M) increased cAMP in a concentration-dependent manner. Forskolin also increased cAMP, but did not mimic the [Ca2+]i-raising effect of AM. These findings suggest that functional AM receptors are present in oligodendroglial KG-1C cells and that AM increases [Ca2+]i through a mechanism independent of cAMP.

Adrenomedullin↗

PubMed1998

Activation of inwardly rectifying K+ channels by GABA-B receptors expressed in Xenopus oocytes.

In Xenopus oocytes coinjected with poly(A)+ RNA derived from the rat cerebellum and cRNAs for the cloned G protein-gated inwardly rectifying K+ channel (GIRK), GIRK1 and GIRK2, the GABA-B agonist baclofen elicited inwardly rectifying K+ currents. The inward K+ currents elicited by baclofen were inhibited by the selective GABA-B antagonists 2-OH saclofen and CGP 35348, and by the GIRK inhibitor Ba2+. In contrast, baclofen caused no currents in oocytes injected with the cerebellar poly(A)+ RNA alone, the poly(A)+ RNA and cRNA for GIRK1 or GIRK2, or only cRNAs for GIRK1 and GIRK2. These findings indicate that GABA-B receptors in the rat cerebellum were functionally expressed in Xenopus oocytes and activated the cloned GIRKs composed of GIRK1 and GIRK2 as heteromultimers.

Animals↗