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Biomedical subjects

K C Choi

Publications and source records attributed to K C Choi.

At least 55 records · Page 3Linked to original sources
PubMed1999

Effectiveness of preoperative transarterial chemoembolization in presumed inoperable hepatoblastoma.

PURPOSE: To evaluate the effectiveness and therapeutic role of preoperative transarterial chemoembolization (TACE) of hepatoblastoma. MATERIALS AND METHODS: Four patients (one boy, three girls) with unresectable hepatoblastoma were treated twice with preoperative TACE in an effort to improve the surgical and clinical outcome. The patients ranged in age from 8 to 27 months (mean, 15 months). The first TACE was performed superselectively in tumor feeding arteries. The second TACE was performed 3 weeks later. Surgical hepatic resection was performed 1 month after the second TACE. Contrast-enhanced computed tomography (CT) was used to evaluate changes in size, volume, internal texture, and margin of the masses. The toxicity of the chemotherapeutic drugs was evaluated by blood chemistry analysis (AST/ALT, alpha-FP) performed before and after TACE, and after surgery. RESULTS: TACE allowed subsequent surgical resection in all four patients, who remained disease free 16-52 months after operation. There were no major problems related to TACE. There was no chemotherapeutic agent toxicity from TACE. The average largest diameters and volumes of the tumors decreased by 31% (8.3 to 5.6 cm) and 69% (317 to 93 cm2), respectively. CONCLUSION: TACE provided subsequent successful surgical resection and good long-term results in all four patients. The hepatoblastomas were initially considered inoperable because of extensive hepatic involvement and indistinct margins.

Antineoplastic Agents↗
PubMed1999

Effects of L-arginine on cyclosporin-induced alterations of vascular NO/cGMP generation.

BACKGROUND: Cyclosporin (CsA)-induced vascular dysfunction has been attributed to a diminished role of the nitric oxide (NO)/cGMP-mediated vasodilator mechanism. The present study was aimed at investigating whether L-arginine, the substrate of NO synthesis, ameliorates CsA-induced vascular dysfunction. METHODS: Male Sprague-Dawley rats were used throughout the study. The thoracic aorta was isolated from normal rats and acutely treated with CsA (10(-4) mol/l, 60 min) in vitro, or the aorta was taken from rats treated with CsA (25 mg/kg/day, i.m., 1 week). The vascular relaxation response to acetylcholine, and tissue levels of NO metabolites and cGMP were determined. The vascular expression of NO synthase (NOS) isoforms was also determined by western blot analysis. RESULTS: Acute treatment with CsA in vitro markedly attenuated the vasorelaxation response to acetylcholine, which was completely restored by L-arginine. The vascular accumulation of NO metabolites in response to acetylcholine was decreased significantly by CsA, which was prevented by cotreatment with L-arginine. CsA decreased the cGMP accumulation in response to both acetylcholine and sodium nitroprusside. L-Arginine restored, although not completely, acetylcholine-stimulated cGMP generation, whereas it did not affect sodium nitroprusside-stimulated cGMP generation. Following chronic CsA treatment in the whole animal, the vasorelaxation response to acetylcholine was decreased significantly along with tissue levels of NO metabolites; this was preserved by L-arginine-supplementation. Vascular expression of iNOS protein was decreased by CsA treatment along with decreased tissue accumulation of NO metabolites. L-Arginine supplementation did not modify the altered expression of NOS proteins. CONCLUSION: These results suggest that CsA causes an L-arginine-sensitive vascular dysfunction which is associated with impaired generation of NO and cGMP.

Acetylcholine↗
PubMed1999

Analgesia, pruritus, and ventilation exhibit a dose-response relationship in parturients receiving intrathecal fentanyl during labor.

UNLABELLED: Several studies have characterized the 50% and 95% effective doses (ED50 and ED95, respectively) of intrathecal sufentanil for labor analgesia. Few have investigated these same criteria for the less expensive alternative, fentanyl. In addition, the ventilatory effects of intrathecal fentanyl at clinically relevant doses are unclear. We performed this study to establish the dose-response relationship of intrathecal fentanyl for both analgesia and ventilatory depression. Ninety parturients in active early labor (< or = 5 cm dilation) received intrathecal fentanyl 5, 7.5, 10, 15, 20, or 25 micrograms in a double-blinded, randomized fashion (n = 15 patients in each group). Parturients were monitored for degree of pain (measured using a 100-mm visual analog pain scale), blood pressure, arterial oxygen saturation (SaO2), respiratory rate, ETCO2, and fetal heart rate 0, 1, 5, 10, 15, 20, 25, and 30 min after the administration of intrathecal fentanyl. An absolute visual analog pain scale score < or = 25 mm was defined a priori as analgesic success. The percentage of parturients who achieved analgesic success was used to construct quantal dose-response curves, from which the ED50 and ED95 values were derived for the total population (mixed parity) and the nulliparous and multiparous subpopulations separately. Overall ED50 and ED95 values (95% CI) were 5.5 (3.4-7.2) and 17.4 (13.8-27.1) micrograms, respectively. Nulliparous values were lower (5.3 and 15.9 micrograms, respectively) than multiparous values (6.9 and 26.0 micrograms, respectively) but were within the 95% CIs of the total population. Pruritus incidence in parturients with analgesic success displayed a dose-response relationship identical to that seen for analgesia. ETCO2 displayed a dose-related increase, particularly at doses > or = 15 micrograms, without concomitant changes in respiratory rate or SaO2, which suggests a decrease in tidal volume. Even in the absence of overt signs or symptoms of somnolence, intrathecal fentanyl at doses within the effective analgesic range induced a change in ventilation that may last longer than the 30-min period we studied. IMPLICATIONS: Intrathecal fentanyl induces rapid and satisfying dose-dependent analgesia in early labor; however, it also produces dose-related decreases in ventilation in the absence of overt somnolence.

Adult↗
PubMed1999

Apoptosis induced by propolis in human hepatocellular carcinoma cell line.

Propolis has been reported to exhibit a wide spectrum of activities including antibiotic, antiviral, anti-inflammatory, immunostimulatory and tumor carcinostatic properties. We showed propolis induced apoptosis in a human hepatoma cell line (SNU449) by FITC-Annexin V/PI staining. We also compared the apoptosis inducing effect between Korean and Commercial (Sigma # p-1010) propolis. There was no difference on apoptosis between them.

Annexin A5↗
PubMed1999

Altered renal expression of nitric oxide synthase isozymes in spontaneously hypertensive rats.

OBJECTIVES: The present study was aimed at exploring whether the pathogenesis of hypertension is related with an altered expression of nitric oxide synthase (NOS) isozymes, i.e., bNOS, iNOS and ecNOS. METHOD: By Western blot analysis, the expression of NOS isozymes were determined in the kidney isolated from spontaneously hypertensive rats (SHR) and their normotensive control, Wistar-Kyoto rats (WKY). The NOx (nitrite/nitrate) contents were also determined in the kidney and plasma. RESULTS: The plasma NOx was significantly increased in SHR compared with that in WKY. The basal level of NOx was higher in the medulla and cortex of the kidney in SHR compared with that in WKY rat. bNOS proteins were expressed higher in the outer medulla and cortex, and iNOS proteins were higher in the inner medulla, outer medulla and cortex in SHR. ecNOS expression did not significantly differ between the SHR and WKY. CONCLUSIONS: These results indicate that the NO generation may not be impaired, but rather increased. It is likely that the increased expression of NOS isozymes is a counter-reactive phenomenon secondary to the increased blood pressure in this model of hypertension.

Animals↗
PubMed1999

Role of nitric oxide in the pathogenesis of diabetic nephropathy in streptozotocin-induced diabetic rats.

OBJECTIVES: Several reports suggest that enhanced generation or actions of nitric oxide (NO) have been implicated in the pathogenesis of glomerular hyperfiltration and hyperperfusion that occurs in early diabetes. However, the precise role of altered NO generation in the pathogenesis of diabetic nephropathy is unclear. The present study was aimed at investigating the role of nitric oxide in the pathogenesis of glomerular hyperfiltration and hyperperfusion in streptozotocin-induced diabetic rats. METHODS: To evaluate the role of NO in diabetic hyperfiltration, we measured plasma and urine concentrations of NO2-/NO3-, stable metabolic products of NO and protein expressions of three isoforms of nitric oxide synthase (NOS) in streptozotocin-induced diabetic rats. We also investigated renal hemodynamic changes, such as glomerular filtration rate (GFR) and renal plasma flow (RPF), in responses to acute and chronic administration of NO synthesis inhibitor, nitro-L-arginine methyl ester (L-NAME), in diabetic and control rats. RESULTS: Diabetic rats exhibited significantly elevated plasma and urinary NO2-/NO3- levels at 28 days after streptozotocin injection, and total excretion of NO2-/NO3- was approximately five-fold higher in diabetic rats than controls. Insulin and L-NAME treatment prevented the increases in plasma and urinary NO2-/NO3- concentrations in diabetic rats, respectively. The three isoforms of NOS (bNOS, iNOS, and ecNOS) were all increased in the renal cortex, whereas they remained unaltered in the renal medulla at day 28. GFR and RPF were significantly elevated in diabetic rats, and acute and chronic inhibition of NO synthesis by L-NAME attenuated the renal hemodynamic changes (increases in GFR and RPF) in diabetic rats, respectively. CONCLUSIONS: NO synthesis was increased due to enhanced NOS expression in diabetic rats, and chronic NO blockade attenuated renal hyperfiltration and hyperperfusion in diabetic rats. In addition, diabetic rats exhibited enhanced renal hemodynamic responses to acute NO inhibition and excreted increased urinary NO2-/NO3-. These results suggest that excessive NO production may contribute to renal hyperfiltration and hyperperfusion in early diabetes.

Animals↗
PubMed1998

p21 expression and mutation in gastric carcinoma: analysis by immunohistochemistry and PCR-SSCP.

p21 protein has been reported to be a critical downstream effector of p53 and a potent inhibitor of cyclin-dependent kinases. Thus, the p21 gene is thought to play a central role in tumor suppression. In this study we investigated p21 protein expression and mutation in gastric adenocarcinoma. A total of 76 primary gastric carcinoma specimens were immunohistochemically stained for p21 protein expression and evaluated the correlations between p21 expression and clinicopathologic features. In a proportion of them (20 cases), we also analyzed the possible presence of p21 gene mutations using PCR-SSCP method. Fourty seven out of 76 cases (61.8%) were p21-negative, and the remaining twenty nine cases (38.2%) were p21 -positive on immunostains. There was a correlation between the expression of p21, and the depth of tumor invasion and lymph node metastasis (p<0.05). No mutation of the p21 gene was detected in all of 20 tumor tissues. These results suggest that the status of p21 expression may have prognostic value in gastric adenocarcinoma.

Adenocarcinoma↗
PubMed1998

Nitric oxide is a marker of peritonitis in patients on continuous ambulatory peritoneal dialysis.

The aim of this study was to determine whether nitric oxide (NO) production is altered during peritonitis in patients receiving continuous ambulatory peritoneal dialysis (CAPD), and if so, whether there is an association between this alteration and the severity and prognosis of CAPD-induced peritonitis. The study population comprised 30 patients with 30 episodes of peritonitis. Thirteen patients without peritonitis were used as CAPD-control, and eighteen patients with normal renal function were used as normal-control. Total NO metabolites (NOx; nitrite + nitrate) were measured by the Griess method to reflect nitric oxide production. Peritoneal dialysate effluent and plasma were collected from 30 patients during episodes of peritonitis every day for the first 3 days, and then every 3 days for 2 weeks or until the patients were discharged. Plasma NOx levels in the control, CAPD-control, and CAPD-peritonitis groups were 87.0 +/- 11.5, 163.0 +/- 30.7 and 146.3 +/- 18.1 microM, respectively. Dialysate NOx levels in the CAPD-control and CAPD-peritonitis groups were 91.8 +/- 13.1 and 103.8 +/- 14.1 microM, respectively, and dialysate NOx levels did not differ between the two groups. The peak dialysate/plasma (D/P) ratios during the acute phase exceeded 1.0 in 46.7% of the patients of the CAPD-peritonitis group. The D/P ratios of NOx levels before and after treatment were 1.03 +/- 0.07 and 0.56 +/- 0.05, respectively. On the contrary, NOx levels in dialysate after treatment were not decreased, but those in plasma were increased after effective treatment. The peak D/P ratio increased 2.1-fold in the bacterial peritonitis group and 2.3-fold in the fungal peritonitis group, compared with the CAPD-control group. The lowest D/P ratios after treatment were similar to those in the CAPD-control group in patients with effective treatment, but remained 1.5-fold higher in patients for whom treatment was ineffective. In the evolutional study, the D/P ratios of NOx levels gradually declined to CAPD-control group levels (6.6 +/- 2.5 days) after effective antibiotic treatment, but it took longer for leukocyte counts in the peritoneal dialysate effluents (3.8 +/- 1.2 days) to normalize. In 5 patients with refractory peritonitis (Candida infection in three, Staphylococcus aureus infection in two), the D/P ratios of NOx levels remained elevated by 1.5-fold despite treatment, and the catheters were removed. These results suggest that dialysate NOx may be influenced not only by local NO production, but also by plasma NO or NOx diffusion. Therefore, we can suppose that the D/P ratio of NOx levels provides more clinical significance than dialysate NOx levels only. In conclusion, the D/P ratios of NOx levels may serve as a marker to assess the severity of peritoneal inflammation, treatment efficacy, and progression of refractory peritonitis in CAPD patients with peritonitis.

Adult↗
PubMed1997

Renal angiomyolipoma: selective arterial embolization--effectiveness and changes in angiomyogenic components in long-term follow-up.

PURPOSE: To evaluate the efficacy of selective arterial embolization in symptomatic renal angiomyolipoma (AML) and the change in angiomyogenic components during long-term follow-up after embolization. MATERIALS AND METHODS: Fourteen adult patients with symptomatic AMLs underwent 16 selective arterial embolizations. The embolic materials used were absolute alcohol with (n = 5) or without (n = 3) iodized oil, Gianturco coils (n = 4), and polyvinyl alcohol foam powder with gelatin sponge (n = 2). Follow-up ultrasonography and computed tomography (CT) were performed in six and 14 patients, respectively. The effectiveness of selective arterial embolization was evaluated on the basis of the area of the angiomyogenic components in the AML on initial and follow-up images and clinical improvement. RESULTS: All patients showed devascularization of the tumor on the postembolization angiograms. In 13 patients, clinical symptoms disappeared. The follow-up period was 7-72 months (mean, 33 months). One patient underwent nephrectomy at 7 months after embolization because of a large cystic lesion found at 1 month. In long-term CT follow-up (> or =12 months) in 12 patients, nearly all angiomyogenic components disappeared, but fatty components partially shrank with liquefactive necrosis in tumors. CONCLUSION: Selective arterial embolization is an effective and safe treatment of AML. The angiomyomatous components crucial for the prevention of bleeding were very sensitive to the embolization.

Adult↗
PubMed1997

Effects of altered body fluid balance and high blood pressure on the plasma brain natriuretic peptide in rats.

The present study was aimed to investigate the regulatory mechanisms of BNP release. Effects of acute and chronic perturbations in body fluid balance, changes in BP, and regulatory roles of NO and endothelin systems on BNP release were examined in rats. Although acute extracellular volume expansion did not have significant effects on plasma BNP, prolonged high-salt intake increased plasma BNP levels. Plasma BNP levels were also higher in 2K1C rats compared with the control. Although infusion of L-NAME increased the plasma BNP in control, it did not further affect the plasma BNP in rats with high-salt intake. Although L-arginine (20 mg.kg-1 per min) per se did not have significant effects on plasma BNP, it blocked the stimulatory effect of L-NAME (200 micrograms.kg-1 per min). Plasma BNP was severalfold increased following a single injection of endothelin (0.3 micrograms/kg) in normal and high-salt intake groups, the magnitude of which was not significantly affected by the high-salt intake. Although indomethacin did not have significant effects on plasma BNP in normal rats, it blocked the stimulatory effect of 2K1C hypertension. It is concluded that BNP is regulated by chronic changes in body fluid balance and blood pressure. It is also suggested that endothelin and NO systems may directly regulate the secretion of BNP in vivo. An endogenous prostaglandin synthesis may be involved in the stimulated release of BNP in hypertension.

Animals↗
PubMed1997

Transforming growth factor beta 1 expression in gastric carcinoma.

Many types of human malignant tumor have been reported to amplify transforming growth factor-beta 1 (TGF-beta 1) gene and overexpress its protein. However, little work has been done about the content of TGF-beta 1 protein in tissue and blood of patients with malignant tumors. TGF-beta 1 protein of tissue (n = 29) and serum TGF-beta 1 levels in patients with gastric carcinoma (n = 62) were compared with those in normal subjects (n = 10) using a TGF-beta 1 enzyme-linked immunosorbent assay. Also, expression of TGF-beta 1 mRNA (n = 20) and immunohistochemical distribution of the protein (n = 70) in gastric carcinoma tissues were studied. The immunohistochemical expression of TGF-beta 1 protein was significantly correlated with the tissue TGF-beta 1 content (r = 0.45 : p < 0.05). The content of TGF-beta 1 was 311 +/- 212 ng/g wet carcinoma tissue. TGF-beta 1 mRNA was expressed in gastric carcinoma cells. However, unexpectedly serum TGF-beta 1 levels in patients with gastric carcinoma were lower (97.1 +/- 29.4 ng/ml) than those in normal subjects (140.3 +/- 85.7 ng/ml, P < 0.05). Our results support that the tumor cells directly produce TGF-beta 1 and that semiquantitative immunohistochemical staining method for TGF-beta 1 protein is a validative method for TGF-beta 1 protein quantitation.

Adult↗
PubMed1997

Relationship of transforming growth factor beta 1 to angiogenesis in gastric carcinoma.

Transforming growth factor-beta (TGF-beta) comprises a group of multifunctional regulatory proteins, whose effects include angiogenesis. The expression of TGF-beta 1 in gastric carcinomas (70 cases) has been determined and related to pathological features and microvessel count by immunohistochemical staining for TGF-beta 1 and Factor VIII related antigen. Prominent reactivity for TGF-beta 1 was associated with the depth of invasion (r = 0.2; p < 0.05) and increased microvessel count (r = 0.5; p < 0.05). Also, the microvessel count had a significant correlation with invasiveness (r = 0.34; p < 0.05) and lymph node metastasis (r = 0.28; p < 0.05). These findings indicate that TGF-beta 1 may have a role in tumor invasion and angiogenesis.

Adult↗
PubMed1997

Attenuated central pressor response to nitric oxide synthesis inhibition in chronic renal failure rats.

OBJECTIVES: Central and peripheral roles of nitric oxide (NO) in blood pressure regulation have been suggested. The present study was aimed at examining if the role of NO in blood pressure regulation is altered in chronic renal failure. METHODS: Blood pressure responses to acute inhibition of NO were examined in 5/6 nephrectomized rats. Three weeks after the renal ablation, under thiopental (50 mg/kg, i.p.) anesthesia, an intracerebroventricular cannula was placed in the left lateral ventricle and the femoral vein was cannulated to serve as an infusion route. The arterial blood pressure was measured in the right femoral artery. NG-nito-L-arginine methyl ester (L-NAME) was infused (100 microgram/kg per min for 60 min either intracerebroventricularly or intravenously. RESULTS: Chronic renal failure rats showed a significantly higher arterial pressure than the control rats (147 +/- 14 mmHg vs. 122 +/- 13 mmHg). Intracerebroventricular L-NAME did not affect the arterial pressure in chronic renal failure rats (0.5 +/- 4 mmHg increase from the basal), while it significantly increased the arterial pressure in normal rats (22 +/- 3 mmHg increases from the basal). Intravenous L-NAME increased the arterial pressure, the magnitude of which did not differ between the normal and chronic renal failure rats (24 +/- 3 vs. 16 +/- 3 mmHg increases from the basal). CONCLUSION: These results indicate that the central role of NO in the regulation of blood pressure is altered in chronic renal failure.

Analysis of Variance↗
PubMed1997

Changes of the plasma endothelin in adaptation to increased salt intake in rats.

OBJECTIVES: Roles for vascular endothelial hormones in body fluid balance have been variously suggested. The present study was aimed at investigating whether the plasma endothelin is altered in responses to acute and chronic perturbations in body fluid balance. METHODS: Effects of intravenous infusion of MG-nitro-L-arginine methyl ester (L-NAME), a competitive inhibitor of endothelium-derived nitric oxide (NO) synthesis, on urinary excretion, blood pressure and plasma levels of endothelin were examined in rats kept on either normal or high-salt diet for two weeks. The plasma endothelin levels in response to an acute extracellular volume expansion (VE) were also determined in normal and 2-kidney, 1 clip (2K1C) hypertensive rats. RESULTS: L-NAME (20 and 200 micrograms.kg(-1) per min) elicited diuretic and natriuretic effects in association with increased blood pressure both in normal and high-salt rats. In high-salt rats, however, the urinary response to L-NAME was attenuated and the pressor response was augmented compared with the control. High-salt intake per se caused a small, but significant, increase of the plasma endothelin. L-NAME (200 micrograms(-1) per min) markedly increased the plasma endothelin was also marginally increased following VE, the magnitude of which did not differ between the normal and 2K1C rats. CONCLUSION: These results suggest that the endothelin system takes part in adaptation to increased salt-intake. Another evidence indicating a negative modulation of NO on the release of endothelin is also provided.

Adaptation, Physiological↗
PubMed1997

A case of carpal tunnel syndrome due to dialysis-related amyloidosis in a patient undergoing long-term hemodialysis.

Carpal tunnel syndrome (CTS) is characterized by burning pain, numbness and tingling sensation in the thumb, index and middle fingers and the lateral half of the palm and progressive atrophy of the thenar muscles by compression of the median nerve within the carpal tunnel due to a variety of etiologic factors. Surgical intervention usually successfully relieves symptoms of CTS. Recently CTS has been regarded as one of the major clinical manifestations of dialysis-related amyloidosis due to beta 2-microglobulin deposition and recognized with increasing frequency in patients undergoing long-term hemodialysis. We report a case of carpal tunnel syndrome due to dialysis-related amyloidosis in patients undergoing long-term hemodialysis, confirmed by electromyography and biopsy in transverse carpal ligament and median nerve.

Amyloid Neuropathies↗
PubMed1997

Fluoxetine selectively alters 5-hydroxytryptamine1A and gamma-aminobutyric acidB receptor-mediated hyperpolarization in area CA1, but not area CA3, hippocampal pyramidal cells.

Fluoxetine is a 5-hydroxytryptamine (5-HT, serotonin)-selective reuptake inhibitor (SSRI) and is one of the main drugs used for the treatment of depression. Because it takes 2 to 3 weeks of treatment before clinical efficacy is manifest, the acute actions of fluoxetine cannot account for the clinical actions of the drug. The chronic effects of fluoxetine have not been completely delineated. The experiments detailed here investigate the chronic effects of fluoxetine on 5-HT and gamma-aminobutyric acid (GABA) receptor-mediated actions using intracellular recording techniques in hippocampal brain slices. Rats were treated with fluoxetine for 3 weeks via osmotic minipumps implanted s.c. Fluoxetine and norfluoxetine plasma levels were determined. The hippocampal pyramidal cell characteristics and the 5-HT1A and GABA(B) receptor-mediated hyperpolarization were measured in the CA1 and the CA3 subfields. The 5-HT4 receptor-mediated decrease in the slow afterhyperpolarization amplitude was also recorded in area CA1. The time constant, magnitude of the change in resistance during 300-ms hyperpolarizing current pulses and half-decay time of the sAHP were altered by chronic fluoxetine treatment in area CA1 pyramidal cells. No changes were seen in any of the active or passive membrane properties of the CA3 hippocampal pyramidal cells. Fluoxetine treatment increased the potency of 5-HT for the 5-HT1A receptor-mediated hyperpolarization in area CA1, but not area CA3, and decreased the potency of baclofen for the GABA(B) receptor-mediated hyperpolarization in area CA1, but not area CA3. The characteristics of the concentration-response curve for the 5-HT-mediated decrease in sAHP amplitude in area CA1 were not altered by fluoxetine treatment. Chronic fluoxetine selectively and differentially altered the cell characteristics and the 5-HT1A and GABA(B) receptor-mediated responses in area CA1 of the hippocampus, which forms the final common output of the hippocampus.

Animals↗
PubMed1996

Corticosterone alters 5-HT1A receptor-mediated hyperpolarization in area CA1 hippocampal pyramidal neurons.

The 5-hydroxytryptamine1A (5-HT1A) receptor in the CA1 region of the hippocampus is linked through a G protein to an inwardly rectifying potassium conductance. Activation of the 5-HT1A receptor results in a membrane hyperpolarization and decreases neuronal firing rate. The hippocampus contains a high concentration of the mineralocorticoid (MR) and glucocorticoid (GR) corticosterone (CT) receptor subtypes. Some laboratories have reported that CT modulates 5-HT1A receptor binding density and mRNA levels in area CA1 of the hippocampus; however, others have reported no change. Previous electrophysiological studies have demonstrated that acute (1 to 4 hour) MR activation in slices from adrenalectomized (ADX) rats attenuates the 5-HT1A receptor-mediated hyperpolarization, while acute MR+ GR or GR activation alone did not alter the 5-HT1A response. Our results confirm that the 5-HT1A response was attenuated 2 to 8 hours following MR activation. However, we found that GR activation alone decreased the potency, but not the maximal response to 5-HT. Chronic (2-week) treatment with basal levels of CT did not alter the 5-HT1A response. Administration of high concentrations of CT in vitro to neurons from chronically treated ADX rats decreased the magnitude of the 5-HT1A receptor-mediated hyperpolarization. We conclude that the 5-HT1A receptor-effector system in CA1 hippocampal pyramidal neurons is modulated by CT in a dose- and time-dependent manner.

Analysis of Variance↗