Biomedical subjects

R Tao

Publications and source records attributed to R Tao.

At least 19 recordsLinked to original sources

PubMed2001

Transformation of Japanese persimmon (Diospyros kaki Thunb.) with apple cDNA encoding NADP-dependent sorbitol-6-phosphate dehydrogenase.

Japanese persimmon (Diospyros kaki Thunb. cv Jiro) was transformed with apple (Malus x domestica Borkh.) cDNA encoding NADP-dependent sorbitol-6-phosphate dehydrogenase (S6PDH) by an Agrobacterium-mediated leaf-disc transformation system. Integration and expression of the transgene were confirmed by genomic DNA blot and immunoblot analyses. Sorbitol accumulation in five of six transgenic plants obtained was confirmed by GC-MS. The amount of sorbitol in the leaves of transgenic plants varied from 14.5 to 61.5 µmol g(-1) fr wt(-1). Sorbitol was not found in leaves of non-transformed 'Jiro' or the line PS7 that produced S6PDH protein with no S6PDH activity. Eventually, two transformed lines producing high (PS1) and medium (PS6) amounts of sorbitol, one control transformed line (PS7), and non-transformed 'Jiro' were selected and evaluated for salt-stress tolerance. Under NaCl stress, the activity of photosystem II in leaves was determined in terms of the ratio of the variable (Fv) to the maximum (Fm) fluorescence of chlorophyll. The rate of decline in Fv/Fm under NaCl stress was lower in PS1 than the other three lines, suggesting that PS1 is more tolerant to NaCl stress than the other three lines. The factors that caused enhanced salt stress tolerance in PS1 are discussed in relation to sorbitol biosynthesis and its growth.

Journal Article↗

PubMed2001

Characterization of the S-locus region of almond (Prunus dulcis): analysis of a somaclonal mutant and a cosmid contig for an S haplotype.

Almond has a self-incompatibility system that is controlled by an S locus consisting of the S-RNase gene and an unidentified "pollen S gene." An almond cultivar "Jeffries," a somaclonal mutant of "Nonpareil" (S(c)S(d)), has a dysfunctional S(c) haplotype both in pistil and pollen. Immunoblot and genomic Southern blot analyses detected no S(c) haplotype-specific signal in Jeffries. Southern blot showed that Jeffries has an extra copy of the S(d) haplotype. These results indicate that at least two mutations had occurred to generate Jeffries: (1) deletion of the S(c) haplotype and (2) duplication of the S(d) haplotype. To analyze the extent of the deletion in Jeffries and gain insight into the physical limit of the S locus region, approximately 200 kbp of a cosmid contig for the S(c) haplotype was constructed. Genomic Southern blot analyses showed that the deletion in Jeffries extends beyond the region covered by the contig. Most cosmid end probes, except those near the S(c)-RNase gene, cross-hybridized with DNA fragments from different S haplotypes. This suggests that regions away from the S(c)-RNase gene can recombine between different S haplotypes, implying that the cosmid contig extends to the borders of the S locus.

Base Sequence↗

PubMed2000

Study on DNA strand breaks induced by sodium nitroprusside, a nitric oxide donor, in vivo and in vitro.

Nitric oxide (NO) as well as its donors has been shown to generate mutation and DNA damage in in vitro assays. The objective of this study was to identify that DNA single-strand breaks (SSBs) could be elicited by NO, not only in vitro but also in vivo. The alkaline single-cell gel electrophoresis (SCGE) was performed to examine the DNA damage in g12 cells and the cells isolated from the organs of mice exposed to sodium nitroprusside (SNP). A modified method, in which neither collagenase nor trypsin was necessary, was used to prepare the single-cell suspension isolated from organs of mice. Results showed that the exposure of g12 cells to 0.13-0.5 micromol/ml SNP with S9 for 1 h induced a concentration-dependent increase in DNA SSBs in g12 cells. The significant increase in DNA migration and comet frequency has appeared in the cells isolated from the spleen, thymus, and peritoneal macrophages of mice after injecting i.p. SNP in the dosage range of 0.67-6.0 mg/kg b.wt for 1 h. However, no obvious increase in DNA strand breaks was observed in the cells isolated from the liver, kidney, lung, brain and heart obtained from the same treated mice. These results suggested that DNA SSBs could be induced by NO in some cells both in vivo and in vitro. There were organ differences in sensitivity in the mice exposed to NO. Spleen, thymus, and macrophages might be the important targets of NO.

Akathisia, Drug-Induced↗

PubMed2000

Association of the R485K polymorphism of the factor V gene with poor response to activated protein C and increased risk of coronary artery disease in the Chinese population.

Inherited predisposition to thrombosis contributes to the initiation and progression of coronary artery disease (CAD). The present study was designed to explore the relationship between genetic variation of coagulation factor V and occurrence of CAD. A total of 141 unrelated patients with CAD and 175 healthy controls were analyzed by polymerase chain reaction-denaturing gradient gel electrophoresis (PCR-DGGE) for variation detection in all 25 exons of the factor V gene. Among the study subjects, 55 CAD patients and 73 controls were evaluated at random for response to activated protein C (APC) by Coatest APC resistance test. Polymorphisms in exon 4, 10, 13 and 16 of factor V gene were documented [642G-->T(S156), 1628--> A(R485K), 4070A-->G(H1299R) and 5380G A(V1736M), respectively]. The study also identified a novel polymorphism 327A G in exon 2 which did not alter the amino acid residue. Leiden mutation (R506Q) was not detected in any of our 316 subjects. Among the five polymorphisms, the allele frequency of 1628G--> A was significantly different between the CAD patients and the controls (0.36 vs. 0.21, p < 0.05). Subjects homozygous or heterozygous for the A allele of 1628G-->A polymorphism had lower normalized APC ratios than those with the GG genotype in the CAD group (1.16+/-0.13 and 1.18+/-0.23 vs. 1.36+/-0.33, p <0.05) and in the controls, indicating that A(1628) allele was associated with a poor response to APC. We conclude that the 1628G-->A (R485K) polymorphism of factor V is associated with a poor response to APC and increased risk for CAD.

Activated Protein C Resistance↗

PubMed2000

Regulation of serotonin release by GABA and excitatory amino acids.

Regulation of serotonin release by gamma-aminobutyric acid (GABA) and glutamate was examined by microdialysis in unanaesthetized rats. The GABA(A) receptor agonist muscimol, or the glutamate receptor agonists kainate, alpha-amino-3-hydroxy-5-methyl-4-isoxazolaproprionate or N-methyl-D-aspartate were infused into the dorsal raphe nucleus (DRN) while extracellular serotonin was measured in the DRN and nucleus accumbens. Muscimol produced decreases, and the glutamate receptor agonists produced increases in serotonin. To determine if these receptors have a tonic influence on serotonergic neurons, glutamate or GABA(A) receptor antagonists were infused into the DRN. Kynurenate, a nonselective glutamate receptor blocker, produced a small, 30% decrease in serotonin. A similar decrease was obtained with combined infusion of AP-5 and DNQX into the DRN. The GABAA receptor blocker bicuculline produced an approximately three-fold increase in DRN serotonin. In conclusion, glutamate neurotransmitters have a weak tonic excitatory influence on serotonergic neurons in the rat DRN. However, the predominate influence is mediated by GABA(A) receptors.

Animals↗

PubMed2000

Differential effect of local infusion of serotonin reuptake inhibitors in the raphe versus forebrain and the role of depolarization-induced release in increased extracellular serotonin.

Systemic administration of selective serotonin reuptake inhibitors (SSRIs) elicits larger increases in serotonin (5-HT) in raphe than in forebrain sites. Because serotonergic neuronal activity is suppressed, the mechanism underlying SSRI-induced increases in extracellular 5-HT is unclear. This study determined whether local infusion of SSRIs also elicited regionally selective increases in extracellular 5-HT, and whether changes depended on serotonergic neuronal depolarization. Conventional microdialysis methods were used to measure 5-HT in dorsal raphe (DRN), median raphe, nucleus accumbens (NAcc), and frontal cortex of unanesthetized rats. During infusion of SSRIs into each site, the maximum response was an approximately 6- to 7-fold increase in 5-HT in NAcc and frontal cortex, and an approximately 20-fold increase in DRN and median raphe. The larger increase in 5-HT in raphe was confirmed using zero-net-flux microdialysis. In NAcc, baseline 5-HT was 0.7 nM, and levels increased to a maximum of 3.1 nM during infusion of the SSRI citalopram. Baseline 5-HT in DRN was greater, 1.3 nM, and increased to 12.4 nM in response to citalopram. Consistent with evidence that autoreceptor activation inhibits serotonergic neuronal discharge, SSRI infusion into DRN produced a moderate decrease in 5-HT in NAcc. However, increases in 5-HT in DRN elicited by SSRI infusion were attenuated by 8-hydroxydipropylaminotetralin and tetrodotoxin. These data indicate that depolarization-dependent 5-HT release was not fully inhibited during SSRI infusion into DRN. In summary, SSRIs produce larger increases in extracellular 5-HT in raphe than in forebrain sites. Increases depend in part on depolarization-induced release, which may be greater in raphe than in forebrain.

8-Hydroxy-2-(di-n-propylamino)tetralin↗

PubMed2000

[Recent trends in the standardization of laboratory automation].

Laboratory automation systems have been introduced to many clinical laboratories since early 1990s. Meanwhile, it was found that the difference in the specimen tube dimensions, specimen identification formats, specimen carrier transportation equipment architecture, electromechanical interfaces between the analyzers and the automation systems was preventing the systems from being introduced to a wider extent. To standardize the different interfaces and reduce the cost necessary for the laboratory automation, NCCLS and JCCLS started establishing standards for the laboratory automation in 1996 and 1997 respectively. NCCLS has published five proposed standards which that are expected to be approved by the end of 2000.

Automation↗

PubMed2000

[Standardization of operation monitoring and control of the clinical laboratory automation system].

Laboratory automation systems showed up in the 1980s and have been introduced to many clinical laboratories since early 1990s. Meanwhile, it was found that the difference in the specimen tube dimensions, specimen identification formats, specimen carrier transportation equipment architecture, electromechanical interfaces between the analyzers and the automation systems was preventing the systems from being introduced to a wider extent. To standardize the different interfaces and reduce the cost of laboratory automation, NCCLS and JCCLS started establishing standards for laboratory automation in 1996 and 1997 respectively. Operation monitoring and control of the laboratory automation system have been included in their activities, resulting in the publication of an NCCLS proposed standard in 1999.

Automation↗

PubMed1999

Glial cell responses, complement and apolipoprotein J expression following axon injury in the neonatal rat.

Immature motoneurons are highly susceptible to degeneration following axon injury. The response of perineuronal glia to axon injury may significantly influence neuronal survival and axon regeneration. We have examined the central reactions to neonatal facial nerve transection with emphasis on the expression of complement component C3 (C3) and the multifunctional apolipoprotein J (ApoJ). Axotomy was performed on one-day-old rats. Animals were perfused from eight hours to two weeks after the lesion. The astroglial marker, glial fibrillary acidic protein (GFAP) was increased from one day and the microglial marker OX-42 from two days after injury. ApoJ immunoreactivity was increased in axotomized neuronal perikarya and astroglial cells from one day postaxotomy, but no C3 immunoreactive profiles were found at any postoperative survival time. Cell proliferation as judged by bromodeoxyuridine labeling and immunoreactivity for the cyclin Ki-67 antigen (antibody MIB5) occurred only at two days after injury. Double immunostaining revealed that the vast majority of proliferating cells were microglia, although occasional cells double labeled astrocytes were found as well. Our results indicate that the non-neuronal response in neonatal animals differ from that of adult ones as follows: 1) microglia transform rapidly into phagocytes in parallel with the degeneration of axotomized neurons, 2) despite the presence of neuronal degeneration, no expression of C3 was found, and the upregulation of the expression of the complement C3 receptor (CR3) is delayed, 3) ApoJ is strongly upregulated in perineuronal astrocytes as well as in the axotomized motoneurons. The marked upregulation of ApoJ in both instances suggests a general role of this protein in the neuronal response to axotomy.

Aging↗

PubMed1999

Human growth hormone increases apo(a) expression in transgenic mice.

Levels of Lp(a), an atherogenic lipoprotein that circulates in human plasma, are increased by the administration of growth hormone (GH). Many of the physiological effects of GH are mediated through insulin-like growth factor-1 (IGF-1), but ironically, IGF-1 treatment of humans is associated with a fall in plasma Lp(a) levels. To glean insight into the mechanism responsible for the GH-associated increase in plasma levels of Lp(a), we administered recombinant human GH (rhGH) to mice expressing a 370-kb human genomic fragment containing the apo(a) gene, 40 kb of 5'-, and 200 kb of 3'-flanking sequence [YAC-apo(a) transgenic mice]. The plasma levels of apo(a) and hepatic levels of apo(a) mRNA rose dramatically in the post-pubertal male mice in response to rhGH treatment. To determine whether the increase in plasma apo(a) was mediated by IGF-1, we treated castrated and noncastrated YAC-apo(a) transgenic mice with a continuous infusion of IGF-1 (100 microg/d) for 2 weeks, and plasma levels of apo(a) fell by approximately 50%. Thus the effects of rhGH and IGF-1 administration on plasma levels of apo(a) in the YAC-apo(a) transgenic mice simulate those seen in humans. The coordinate changes in apo(a) mRNA and plasma levels of apo(a) in response to rhGH and IGF-1 strongly suggest that these 2 hormones have independent effects on the transcription of the apo(a) gene.

Animals↗

PubMed1999

Transgenic mice expressing a human apolipoprotein[a] allele.

The most important determinant of plasma levels of Lp[a] are sequence differences at the highly polymorphic apolipoprotein[a] (apo[a]) locus. To define the sequences that mediate the regulation of apo[a] expression, we cloned a 370 kb DNA fragment that included a 130 kb apo[a] gene, and 40 kb 5'- and 200 kb 3'-flanking region from an individual with high plasma levels of Lp[a] using a YAC vector. This genomic clone was used to generate transgenic mice. In the YAC-apo[a] transgenic mouse, apo[a] was only expressed in the liver, as it is in humans. The mean serum level of apo[a] in 4-week-old YAC-apo[a] transgenic mice was 20 mg/dl. In the female mice the levels of apo[a] varied over a 1.5-fold range during the 4-day estrus cycle and the levels correlated directly with serum progesterone levels. The serum levels of apo[a] decreased to almost undetectable level in male mice after puberty and this decrease was reversed by castration. Ingestion of a high-fat diet resulted in a approximately 100-fold fall in hepatic apo[a] mRNA levels and >60-fold decrease in serum apo[a] levels. To delimit the control elements that mediate tissue-specific and sex hormone-responsive apo[a] transcription, we derived a reporter YAC in which 40 kb of 5' flanking sequences from the cloned apo[a] allele were linked to a luciferase reporter gene. Analysis of four independent transgenic lines revealed no hepatic luciferase expression, suggesting that important cis -acting elements located outside the apo[a] 5'-flanking region are necessary for in vivo expression of apo[a].

Alleles↗

PubMed1999

Hereditary absence of complement C5 in adult mice influences Wallerian degeneration, but not retrograde responses, following injury to peripheral nerve.

We have examined the role of complement component 5 (C5) in peripheral nerve fiber degeneration and regeneration, as well as in glial and neuronal cell responses in the central nervous system (CNS). Adult congenic mice lacking C5 (C5(-)) and the corresponding normal strain (C5(+)) were used. Macrophage recruitment as well as axonal and myelin sheath elimination were delayed from 1 to 21 days postinjury in C5(-) mice compared to the C5(+) group after sciatic nerve crush. Despite this, recovery of motor function was not delayed. In the CNS, microglial cells and astrocytes responded in the same way from 3 to 21 days after sciatic nerve injury in C5(-) and C5(+) mice, and the extent of neuron death following hypoglossal nerve avulsion was the same in both groups. These findings suggest that C5 and/or its derivatives play an important role in initiating the recruitment of macrophages to the injured nerve and, probably indirectly, in early remyelination of regenerating axons, but does not influence the longterm functional restoration or axotomy-induced nerve cell death. C5-derived molecules do not appear to participate in central glial cell responses to peripheral nerve injury. These findings elucidate new aspects on the functional role of the complement system in the peripheral nervous system following peripheral nerve injury.

Animals↗

PubMed1998

Low density lipoprotein receptor-negative mice expressing human apolipoprotein B-100 develop complex atherosclerotic lesions on a chow diet: no accentuation by apolipoprotein(a).

We have generated mice with markedly elevated plasma levels of human low density lipoprotein (LDL) and reduced plasma levels of high density lipoprotein. These mice have no functional LDL receptors [LDLR-/-] and express a human apolipoprotein B-100 (apoB) transgene [Tg(apoB+/+)] with or without an apo(a) transgene [Tg(apoa+/-)]. Twenty animals (10 males and 10 females) of each of the following four genotypes were maintained on a chow diet: (i) LDLR-/-, (ii) LDLR-/-;Tg(apoa+/-), (iii) LDLR-/-;Tg(apoB+/+), and (iv)LDLR-/-;Tg(apoB+/+);Tg(apo+/-). The mice were killed at 6 mo, and the percent area of the aortic intimal surface that stained positive for neutral lipid was quantified. Mean percent areas of lipid staining were not significantly different between the LDLR-/- and LDLR-/-;Tg(apoa+/-) mice (1.0 +/- 0.2% vs. 1.4 +/- 0.3%). However, the LDLR-/-;Tg(apoB+/+) mice had approximately 15-fold greater mean lesion area than the LDLR-/- mice. No significant difference was found in percent lesion area in the LDLR-/-;Tg(apoB+/+) mice whether or not they expressed apo(a) [18.5 +/- 2.5%, without lipoprotein(a), Lp(a), vs. 16.0 +/- 1.7%, with Lp(a)]. Histochemical analyses of the sections from the proximal aorta of LDLR-/-;Tg(apoB+/+) mice revealed large, complex, lipid-laden atherosclerotic lesions that stained intensely with human apoB-100 antibodies. In mice expressing Lp(a), large amounts of apo(a) protein colocalized with apoB-100 in the lesions. We conclude that LDLR-/-; Tg(apoB+/+) mice exhibit accelerated atherosclerosis on a chow diet and thus provide an excellent animal model in which to study atherosclerosis. We found no evidence that apo(a) increased atherosclerosis in this animal model.

Animal Feed↗

PubMed1998

Cloning and characterization of cDNAs encoding S-RNases from almond (Prunus dulcis): primary structural features and sequence diversity of the S-RNases in Rosaceae.

cDNAs encoding three S-RNases of almond (Prunus dulcis), which belongs to the family Rosaceae, were cloned and sequenced. The comparison of amino acid sequences between the S-RNases of almond and those of other rosaceous species showed that the amino acid sequences of the rosaceous S-RNases are highly divergent, and intra-subfamilial similarities are higher than inter-subfamilial similarities. Twelve amino acid sequences of the rosaceous S-RNases were aligned to characterize their primary structural features. In spite of their high level of diversification, the rosaceous S-RNases were found to have five conserved regions, C1, C2, C3, C5, and RC4 which is Rosaceae-specific conserved region. Many variable sites fall into one region, named RHV. RHV is located at a similar position to that of the hypervariable region a (HVa) of the solanaceous S-RNases, and is assumed to be involved in recognizing S-specificity of pollen. On the other hand, the region corresponding to another solanaceous hypervariable region (HVb) was not variable in the rosaceous S-RNases. In the phylogenetic tree of the T2/S type RNase, the rosaceous S-RNase fall into two subfamily-specific groups (Amygdaloideae and Maloideae). The results of sequence comparisons and phylogenetic analysis imply that the present S-RNases of Rosaceae have diverged again relatively recently, after the divergence of subfamilies.

Amino Acid Sequence↗

PubMed1998

Clinical and bacteriologic study of eighty-six patients with systemic lupus erythematosus complicated by infections.

OBJECTIVE: To investigate the clinical and bacteriologic features of patients with systemic lupus erythematosus (SLE) complicated by bacterial and/or fungal infections. METHODS: Statistical analysis was made on basis of the clinical and bacteriologic data of 86 patients with SLE complicated by bacterial and/or fungal infections. RESULTS: One hundred and thirty-three episodes of infections occurred in 86 patients with SLE, in which 51.13% were nosocomial infections and 76.69% occurred in the blood system, respiratory tract, lungs and urinary tract. Gram-negative bacilli, gram-positive cocci, fungal and other bacterial infections accounted for 39.85%, 31.58%, 18.80% and 9.77%, respectively. In the bacterial infections, 18.52% were caused by L-form bacteria and more than 60% of the patients had no apparent toxic manifestations. The odds ratio (OR) of infection increased significantly in patients with damaged functions of the heart, lungs and kidneys, and in those who received high-dosage steroids. CONCLUSIONS: Patients with SLE tend to develop nosocomial infections with gram-negative bacilli which are the most common pathogens. The clinical manifestations of the infection are atypical. Careful inspection and monitoring, timely collecting the specimens for L-form bacterial culture can reduce misdiagnosis and missed diagnosis of the infection.

Adolescent↗

PubMed1998

[Expression of interleukin-8 and its receptor in acute promyelocytic leukemia under all-trans retinoic acid treatment].

OBJECTIVE: To evaluate the clinical significance of expression of interleukin-(IL-8) and its type A receptor(IL-8RA) in acute promyelocytic leukemia(APL) patients under all trans-retinoic acid(ATRA) induction. METHODS: Serum IL-8 level of 18 APL patients were dynamically studied(ELISA). Fresh APL cells from 3 patients were cultured with ATRA(10(-6) mmol/L). Supernatant IL-8 level and IL-8RA expression on APL cells were measured by FACS. RESULTS: In vitro, IL-8 concentrations decreased 72 hours after incubation, while IL-8RA increased. In vivo, IL-8 increased more rapidly and markedly than temperature and WBC counts did before retinoic acid syndrome(RA-S) occurred. Serum IL-6 and IL-8 levels significantly increased when the patients suffered infection, and IL-8 increased even before fever. Both IL-8 and D-dimer increased while DIC progressed. CONCLUSION: ATRA inhibited IL-8 secretion of APL cells while increased the expression of IL-8RA. Monitoring serum IL-8 concentrations could predict the development of RA-S and infection. Increase of both IL-8 and D-dimer concentrations suggested DIC progression.

Adolescent↗

PubMed1998

Alteration in regulation of serotonin release in rat dorsal raphe nucleus after prolonged exposure to morphine.

Regulation of serotonin (5-HT) release may be altered during the development of opioid tolerance and dependency. To test this hypothesis, changes in extracellular 5-HT during prolonged administration of morphine were determined by microdialysis in the dorsal raphe nucleus (DRN) of freely behaving rats. Morphine or placebo pellets were implanted s.c. As compared to placebo, morphine pellets induced a sustained, approximately 50% increase in DRN 5-HT and a significant elevation in hot plate latency during the 12-hr period after implantation. One week later DRN 5-HT had returned to control levels, and implanting additional morphine pellets had no effect on 5-HT or hot plate latency. One day after removing the pellets from rats exposed to morphine for 2 wk, acute challenge with morphine (20 mg/kg, s.c.) had a significantly smaller effect on 5-HT in the DRN as compared to the placebo treatment group. Administration of naltrexone to rats implanted with morphine pellets for 2 wk induced signs of withdrawal and a significant decrease in DRN 5-HT. These results suggest that the regulation of 5-HT release is altered during the development of tolerance to morphine. Thus, DRN 5-HT may be one of the factors involved in the changes in physiology and behavioral state during opioid withdrawal.

Animals↗

PubMed1997

Influence of AMPA/kainate receptors on extracellular 5-hydroxytryptamine in rat midbrain raphe and forebrain.

1. The regulation of 5-hydroxytryptamine (5-HT) release by excitatory amino acid (EAA) receptors was examined by use of microdialysis in the CNS of freely behaving rats. Extracellular 5-HT was measured in the dorsal raphe nucleus (DRN), median raphe nucleus (MRN), nucleus accumbens, hypothalamus, frontal cortex, dorsal and ventral hippocampus. 2. Local infusion of kainate produced increases in extracellular 5-HT in the DRN and MRN. Kainate infusion into forebrain sites had a less potent effect. 3. In further studies of the DRN and nucleus accumbens, kainate-induced increases in extracellular 5-HT were blocked by the EAA receptor antagonists, kynurenate and 6,7-dinitroquinoxaline-2,3-dione (DNQX). 4. The effect of infusing kainate into the DRN or nucleus accumbens was attenuated or abolished by tetrodotoxin (TTX), suggesting that the increase in extracellular 5-HT is dependent on 5-HT neuronal activity. In contrast, ibotenate-induced lesion of intrinsic neurones did not attenuate the effect of infusing kainate into the nucleus accumbens. Thus, the effect of kainate in the nucleus accumbens does not depend on intrinsic neurones. 5. Infusion of alpha-amino-3-hydroxy-5-methyl-4-isoxazolaproprionate (AMPA) into the DRN and nucleus accumbens induced nonsignificant changes in extracellular 5-HT. Cyclothiazide and diazoxide, which attenuate receptor desensitization, greatly enhanced the effect of AMPA on 5-HT in the DRN, but not in the nucleus accumbens. 6. In conclusion, AMPA/kainate receptors regulate 5-HT in the raphe and in forebrain sites.

Animals↗