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Biomedical subjects

Y Imai

Publications and source records attributed to Y Imai.

At least 181 records · Page 10Linked to original sources
PubMed2000

Association of osteopontin with ischemic axonal death in periventricular leukomalacia.

Osteopontin (OPN) is a bone matrix protein expressed my macrophages and related to the process of tissue calcification, and is also known to protect ischemic cells. To understand how OPN is involved in the process of ischemic axonal death in periventricular leukomalacia (PVL), we examined the immunoreactivity of OPN and ionized calcium binding adaptor molecule 1 (Iba1; microglia/macrophage marker) at various stages of PVL. OPN immunoreactivity paralleled the number of Iba1-positive foam cells; a finding which suggests the production of OPN protein by foam cells. OPN immunoreactivity was not found in either normal white matter or acute PVL lesions, but was detected at the subacute and chronic stages in swollen and calcified axons bordering the ischemic zone. These findings suggest that OPN is closely associated with death of swollen axons at the periphery of the ischemic zone, regulating the presence or absence of calcification.

Axons↗
PubMed2000

Sequential changes of cholinergic and dopaminergic receptors in brains after 6-hydroxydopamine lesions of the medial forebrain bundle in rats.

We studied sequential changes in muscarinic cholinergic receptors, high-affinity choline uptake sites and dopamine D2 receptors in the brain after 6-hydroxydopamine lesions of the medial forebrain bundle in rats. The animals were unilaterally lesioned in the medial forebrain bundle and the brains were analyzed at 1, 2, 4 and 8 weeks postlesion. [3H]Quinuclidinylbenzilate (QNB), [3H]hemicholinum-3 (HC-3) and [3H]raclopride were used to label muscarinic cholinergic receptors, high-affinity choline uptake sites and dopamine D2 receptors, respectively. The degeneration of nigrostriatal pathway produced a transient decrease in [3H]QNB binding in the parietal cortex of both ipsilateral and contralateral sides at 2 and 8 weeks postlesion. [3H]QNB binding also showed a mild but insignificant decrease in the ipsilateral striatum throughout the postlesion periods. No significant change was observed in the substantia nigra (SN) of both ipsilateral and contralateral sides throughout the postlesion periods. In contrast, [3H]HC-3 binding showed no significant change in the parietal cortex of both ipsilateral and contralateral sides during the postlesion. However, [3H]HC-3 binding was upregulated in the ipsilateral dorsolateral striatum throughout the postlesion periods. The ventromedial striatum also showed a significant increase in [3H]HC-3 binding at 1 week and 2 weeks postlesion. On the other hand, no significant change in [3H]raclopride binding was found in the parietal cortex of both ipsilateral and contralateral sides during the postlesion. [3H]Raclopride binding showed a conspicuous increase in the ipsilateral striatum (35-52% of the sham-operated values in the lateral part and 39-54% in the medial part) throughout the postlesion periods. In the contralateral side, a mild increase in [3H]raclopride binding was also found in the striatum (10-15% of the sham-operated values in the lateral part and 22% in the medial part) after lesioning. However, a significant decline in [3H]raclopride binding was observed in the ipsilateral SN and ventral tegmental area during the postlesion. The present study indicates that 6-hydroxydopamine injection of medial forebrain bundle in rats can cause functional changes in high-affinity choline uptake site in the striatum, as compared with muscarinic cholinergic receptors. Furthermore, our studies demonstrate an upregulation in dopamine D2 receptors in the striatum and a decrease in the receptors in the SN and ventral tegmental area after the 6-hydroxydopamine injection. Thus, these findings provide further support for neurodegeneration of the nigrostriatal pathway that occurs in Parkinson's disease.

Animals↗
PubMed2000

Cox-2 expression in retinoblastoma.

PURPOSE: Cox-2, a prostaglandin synthase, is overexpressed in colorectal cancers and is involved in angiogenesis as well as in tumorigenesis. In this study, we investigate the expression of Cox-2 in retinoblastoma. METHODS: Twenty-nine formalin-fixed retinoblastoma specimens were examined by the labeled-streptavidin-biotin method using anti-Cox-2 antibody. RESULTS: Cox-2 positive immunoreactions were observed in 28 (96%) of 29 retinoblastomas specimens. CONCLUSION: This preliminary study suggests the overexpression of Cox-2 in both differentiated and undifferentiated retinoblastoma and its possible role in tumorigenesis.

Child, Preschool↗
PubMed2000

High prevalence of herpes simplex virus type 2 in acute retinal necrosis syndrome associated with herpes simplex virus in Japan.

PURPOSE: To determine the type of herpes simplex virus in acute retinal necrosis syndrome associated with herpes simplex virus. METHODS: Herpes simplex virus type 1, herpes simplex virus type 2, varicella-zoster virus, Epstein-Barr virus, and cytomegalovirus were examined by polymerase chain reaction in intraocular specimens from 16 patients with acute retinal necrosis syndrome. Anti-herpes simplex virus type 1 and anti-herpes simplex virus type 2 type-specific antibodies in serum from the patients were detected by enzyme immunoassay. RESULTS: Of 16 patients with acute retinal necrosis syndrome, seven were polymerase chain reaction positive for herpes simplex virus type 2 and nine were positive for varicella-zoster virus. Anti-herpes simplex virus type 2 antibody was positive and anti-herpes simplex virus type 1 antibody was negative in the sera of the seven patients with herpes simplex virus type 2 DNA-positive acute retinal necrosis syndrome. In contrast, anti-herpes simplex virus type 2 antibody was absent in all nine varicella-zoster virus DNA-positive acute retinal necrosis syndrome patients. CONCLUSION: Herpes simplex virus type 2 has been demonstrated to be the major causative agent in acute retinal necrosis syndrome associated with herpes simplex virus by molecular biological and serological methods. Negative preexisting anti-herpes simplex virus type 1 antibody may play an important role in acute retinal necrosis syndrome associated with herpes simplex virus type 2.

Adolescent↗
PubMed2000

Anatomic biventricular correction by taking down bicaval Glenn shunt.

A 7-year-old boy underwent ventricular and atrial septal defect patch closures, pulmonary valvulotomy, left pulmonary artery dilatation, and bicaval Glenn shunt, which maintained good patency between the superior vena cava and right atrium, because of a reduced right ventricular end-diastolic volume (RVEDV). The RVEDV had increased at 15 years of age; therefore, we performed an anatomic biventricular correction by removing the bicaval Glenn shunt. We found that anatomic biventricular correction becomes possible if RVEDV increases postoperatively.

Adolescent↗
PubMed2000

Free hemoglobin impairs cardiac function in neonatal rabbit hearts.

BACKGROUND: Hemolysis caused by cardiopulmonary bypass causes renal dysfunction and other organ failure presumably by superoxide production catalyzed by iron derived from free hemoglobin (f-Hb). It might also impair cardiac function by the same mechanism, especially in the ischemia-reperfusion period and in neonates where serum antioxidant activity is lower than adults. METHODS: We evaluated effects of f-Hb on cardiac function with or without ischemia and reperfusion using a newborn (7 days old) rabbit crystalloid-perfused Langendorff model. After baseline measurements, the hearts were divided into the following four groups (8 hearts per group): (1) those perfused with regular Krebs-Henseleit bicarbonate buffer, (2) those perfused 30 minutes with KH buffer containing 1 mg/mL of f-Hb obtained from osmotic hemolysis, (3) those subjected to 180 minutes of cold global ischemia with infusion of crystalloid cardioplegia and reperfused with Krebs-Henseleit buffer, and (4) those subjected to the same ischemia and reperfused with Krebs-Henseleit buffer containing 1 mg/mL of f-Hb. The left ventricular function (using conductance catheter and isovolumic balloon) and coronary flow were measured. RESULTS: Free hemoglobin significantly impaired not only left ventricular function but also coronary flow even without ischemia (p < 0.05). When ischemia and reperfusion were involved, the group reperfused with f-Hb showed the worst left ventricular function and coronary flow among the groups. CONCLUSIONS: This study shows that f-Hb directly impaired cardiac function and coronary flow in neonatal hearts especially in ischemia and reperfusion.

Animals↗
PubMed2000

Impaired distensibility of neoaorta after arterial switch procedure.

BACKGROUND: Although the arterial switch operation has become the standard surgical procedure for treatment of complete transposition, postoperative problems have not been fully appreciated. One such problem may be the postoperative function of great arteries that are manipulated radically. METHODS: The diameters at four levels of the aorta were measured in 36 patients who had undergone arterial switch operation and the distensibilities were calculated. The data were compared with that of age-matched controls. RESULTS: At the level of the Valsalva sinus, aortic diameters after one-staged and two-staged operations were 137.0% +/- 21.3%N and 152.4% +/- 17.7%N of the normal aorta, respectively. The distensibilities at the Valsalva sinus in patients after one-staged and two-staged operations were 1.2 +/- 0.7 and 1.5 +/- 0.8 cm2 x dyn(-1) x 10(-6), and at the supraaortic ridge were 2.5 +/- 1.5 and 1.9 +/- 1.5 cm2 x dyn(-1) x 10(-6), respectively. CONCLUSIONS: In patients after arterial switch procedure, the distensibility of the base of aorta is decreased. Long-term follow-up is necessary to clarify the influence of the "stiffness" of the base of aorta.

Aortography↗
PubMed2000

Effect of hemofiltrated whole blood pump priming on hemodynamics and respiratory function after the arterial switch operation in neonates.

BACKGROUND: Primed blood might have some deleterious effects on neonates during cardiopulmonary bypass (CPB) due to unbalanced electrolytes and inflammatory mediators. We hemofiltrated pump-primed blood before CPB to reduce inflammatory mediators and to adjust pH and the concentrations of electrolytes. The current study investigated the effects of hemofiltrated whole blood priming on hemodynamics and respiratory function after CPB in neonates. METHODS: Patients who underwent the arterial switch operation in the neonatal period for transposition of the great arteries with intact ventricular septum were chosen for this study. Seventeen patients underwent CPB with hemofiltrated blood priming (group HF) and 23 patients underwent CPB with nonhemofiltrated blood priming (group N). The concentrations of electrolytes and bradykinin and high molecular weight kininogen of the primed blood before and after hemofiltration were measured. At 4 hours after completion of CPB, the left ventricular percent fractional shortening, and the relation between the mean velocity of shortening and the end-systolic wall stress (stress velocity index), were measured by echocardiogram in 7 patients in group HF and 6 patients in group N. Alveolar--arterial oxygen tension difference (AaDO2) and respiratory index (AaDO2 divided by arterial oxygen tension) were measured at several points for 48 hours after CPB in all patients. RESULTS: Hemofiltration of the primed blood maintained electrolytes within a physiologic level and significantly reduced the concentrations of bradykinin (5,649 +/- 1,353 pg/mL versus 510 +/- 35 pg/mL, p < 0.05) and high molecular weight kininogen (52.7% +/- 3.2% versus 40.1% +/- 3.0% of normal plasma value, p < 0.05). The percent of fractional shortening at 4 hours after completion of CPB was significantly higher in group HF (n = 7) than in group N (n = 6) (22.0% +/- 0.7% versus 16.0% +/- 0.4%, p < 0.01). There was also a trend toward better stress velocity index in group HF than in group N (0.81 +/- 0.81 versus -2.17 +/- 0.45, p = 0.09). AaDO2 and respiratory index were significantly lower in group HF than in group N for 48 hours after CPB, respectively (p < 0.05). CONCLUSIONS: Hemofiltrated fresh whole blood used for CPB priming attenuated cardiac impairment at early reperfusion periods and reduced pulmonary dysfunction in neonates with transposition of the great arteries with intact ventricular septum. This therapeutic strategy may have an advantage in preventing lung and heart dysfunction in pediatric patients who need CPB priming with blood.

Cardiopulmonary Bypass↗
PubMed2000

A novel type of ATP block on a Ca(2+)-activated K(+) channel from bullfrog erythrocytes.

Using the patch-clamp technique, we have identified an intermediate conductance Ca(2+)-activated K(+) channel from bullfrog (Rana catesbeiana) erythrocytes and have investigated the regulation of channel activity by cytosolic ATP. The channel was highly selective for K(+) over Na(+), gave a linear I-V relationship with symmetrical 117.5 mM K(+) solutions and had a single-channel conductance of 60 pS. Channel activity was dependent on Ca(2+) concentration (K(1/2) = 600 nM) but voltage-independent. These basic characteristics are similar to those of human and frog erythrocyte Ca(2+)-activated K(+) (Gardos) channels previously reported. However, cytoplasmic application of ATP reduced channel activity with block exhibiting a novel bell-shaped concentration dependence. The channel was inhibited most by approximately 10 microM ATP (P(0) reduced to 5% of control) but less blocked by lower and higher concentrations of ATP. Moreover, the novel type of ATP block did not require Mg(2+), was independent of PKA or PKC, and was mimicked by a nonhydrolyzable ATP analog, AMP-PNP. This suggests that ATP exerts its effect by direct binding to sites on the channel or associated regulatory proteins, but not by phosphorylation of either of these components.

Adenosine Diphosphate↗
PubMed2000

Evidence for association between paraoxonase gene polymorphisms and atherosclerotic diseases.

Paraoxonase 1 (PON1) is proposed to have an anti-atherogenic action. Two polymorphisms at the PON1 (M/L55 and Q/R192) have been shown to be associated with coronary artery disease (CAD). This conclusion is not drawn universally, however, and specific ethnic characteristics may be important determinants in this association. Recently two homologues of PON1 - PON2 and PON3 - were identified and Sanghera et al. demonstrated C/S311 polymorphism at PON2 was associated with the risk of CAD. Within that context, we investigated the association between the aforementioned three polymorphisms and CAD and ischemic stroke in a Japanese population. The study population included 431 control subjects, 210 CAD patients, and 235 ischemic stroke patients. Genotype distributions and allele frequencies of M/L55 and C/S311 were similar among the control and patient groups, whereas the R192 allele frequency was significantly higher (P<0.001) in CAD (75%) and ischemic stroke (76%) patients than in control subjects (65%). When confounding influences of other risk factors were controlled for by multivariate analysis, R192 remained an independent risk determinant (additive model: OR (95% CI), P value CAD: 2.01 (1.45-2.79), 0.0001; ischemic stroke: 1.84 (1.34-2.52), 0.0002 (three genotypes into calculation)). Taken together, our data indicate that the Q/R192 is principally associated with both CAD and ischemic stroke in Japanese.

Aged↗
PubMed2000

Human G-protein beta3 subunit variant is associated with serum potassium and total cholesterol levels but not with blood pressure.

The activity of a sodium-proton exchanger is enhanced in the patients with essential hypertension and regulated via G-protein, which is a signal transducer between receptors and intracellular effectors. A recent study has revealed that a novel variant (C825T) in exon 10 of the gene encoding the beta3 subunit of heterotrimetric G proteins (GNB3) is a genetic factor predisposing to hypertension in Caucasians. We examined the association between GNB3/ C825T and blood pressure, lipids, electrolytes, and other parameters in a Japanese population. Subjects (n = 352) were selected from the Ohasama Study, the population of which is regarded as from a rural community in Japan. To obtain precise clinical measurements, 24-h ambulatory blood pressure monitoring (ABPM), brain magnetic resonance imaging (MRI), and carotid ultrasonography (CUS) were conducted in this population. In addition, we recruited 762 subjects from outpatients at the Osaka University Medical School to carry out the association study between hypertension and GNB3. The GNB3 genotype distribution did not differ significantly between normotensives and hypertensives in either of the two studies. The T825 allele of GNB3 was not associated with the presence of hypertension, blood pressure level, the number of brain lacunae or carotid wall thickness. However, the serum potassium and total cholesterol levels were significantly higher in subjects with the T allele (P < .005). The T825 allele of GNB3 is associated with increased serum potassium and total cholesterol levels but not with blood pressure in a Japanese population.

Adult↗
PubMed2000

Gene polymorphism of the renin-angiotensin system associates with risk for lacunar infarction. The Ohasama study.

The polymorphism of the angiotensin-converting enzyme gene is considered to be associated with increased risk for stroke, but there is a diversity in the results obtained. The genetic involvement of the renin-angiotensin system in stroke also remains unclear. To predict the genetic risk of lacunar infarction, we conducted an association study in an Ohasama population, which is the cohort in a rural region of northern Japan. A total of 134 subjects without major neurological, cardiovascular, or metabolic disorders were recruited. Using brain magnetic resonance imaging, the number of lacunae in each of four brain regions were calculated, and periventricular hyperintensity was classified into five grades. We used the following four candidate gene polymorphisms: angiotensin converting enzyme (ACE)/Insertion(I)-Deletion(D), angiotensinogen (AGT)/M235T, angiotensin II type 1 receptor (AT1)/ A1166C, type 2 receptor (AT2)/C3123A, to examine the association between polymorphisms and the severity of lacunar infarction. AGT/M235T was significantly associated with the number of lacunae in the brain stem, the basal ganglia (P < .05), and whole brain (P < .005) regions. The AT1 polymorphism was also significantly associated with the number of lacunae in the basal ganglia and whole brain regions (P < .05), and with periventricular hyperintensity grade (P < .005) in the younger population. However, ACE and AT2 polymorphisms failed to show an association with either the number of lacunae or the PVH grade. We concluded that AGT and AT1 polymorphisms are independent genetic risk factors for lacunar infarction.

Aged↗
PubMed2000

Temporal changes of dopaminergic and glutamatergic receptors in 6-hydroxydopamine-treated rat brain.

Quantitative receptor autoradiography was used to examine the sequential patterns of changes in dopaminergic and glutamatergic receptors in the brain of rats lesioned with 6-hydroxydopamine. The animals were unilaterally lesioned in the medial forebrain bundle and the brains were analyzed at 1, 2, 4 and 8 weeks of postlesion. Degeneration of the nigrostriatal pathway caused a significant increase in dopamine D(2) receptors in the ipsilateral striatum from 1 to 8 weeks of postlesion. In the ipsilateral substantia nigra (SN), a significant decrease in dopamine D(2) receptors was also observed from 1 to 8 weeks of postlesion. On the other hand, dopamine D(1) receptors were increased in the ipsilateral ventromedial striatum from 2 to 4 weeks of postlesion. In the ipsilateral SN, a transient increase in dopamine D(1) receptors was observed only 1 week after lesioning. However, other regions in both ipsilateral and contralateral sides showed no significant change in dopamine D(1) and D(2) receptors during postlesion except for a transient change in a few regions. N-Methyl-D-aspartate (NMDA) receptors showed no significant changes in all brain regions studied during the postlesion. In contrast, a transient increase in excitatory amino acid transport sites was observed only in the frontal cortex and ventromedial striatum of the ipsilateral side at 2 weeks of postlesion. However, glycine receptors showed a significant change in any brain areas of both ipsilateral and contralateral sides after lesioning. The change in the brain areas of contralateral side was more pronounced than that of ipsilateral side for glycine receptors. In addition, dopamine uptake sites showed a severe damage in the ipsilateral striatum from 1 to 8 weeks after lesioning. In the contralateral side, in contrast, no significant change in dopamine uptake sites was found in the striatum during the postlesion. These results indicate that unilateral injection of 6-hydroxydopamine in the medial forebrain bundle can cause a significant increase in dopamine D(1) and D(2) receptors in the striatum. The increase in dopamine D(2) receptors was more pronounced than that in dopamine D(1) receptors in the striatum after 6-hydroxydopamine treatment. In contrast, dopamine uptake sites showed a severe damage in the striatum during the postlesion. Furthermore, our results support the existence of dopamine D(2) receptors on the neurons of SN, but not dopamine D(1) receptors. For glutamatergic receptor system, the present study suggests that the changes in glycine receptors may be more susceptible to degeneration of nigrostriatal pathway than NMDA receptors and excitatory amino acid transport sites. Thus, our findings are of interest in relation of degeneration of the nigrostriatal pathway that occurs in Parkinson's disease

Animals↗
PubMed2000

Changes in serum hepatic fibrosis markers in biochemical responders to interferon therapy for chronic hepatitis C.

Serum hepatic fibrosis markers (7s domain of type IV collagen, N-terminal peptide of type III procollagen, and hyaluronate) were determined during and after a 6-month interferon treatment of patients with chronic hepatitis C. Changes in these markers were compared among the patients who showed a sustained normalization of serum alanine transaminase (ALT) levels with and without eradication of serum hepatitis C virus RNA (complete responders and biochemical responders) and nonresponders. In the case of complete responders, the serum 7s domain of type IV collagen and the N-terminal peptide of type III procollagen levels decreased at the end and 24 weeks after the end of the treatment. Hyaluronate levels were significantly decreased 24 weeks after the end of the treatment, as compared with those prior to the treatment. During and after interferon treatment, changes in these markers in the case of biochemical responders were nearly the same as those in the complete responders. These results suggest that serum hepatic fibrosis markers decrease in patients with chronic hepatitis C who show a sustained normalization of ALT after interferon treatment, even if serum hepatitis C virus RNA fails to be eradicated.

Journal Article↗
PubMed2000

Molecular cloning and characterization of mouse testis poly(A) binding protein II encoded by the Pabp3 gene, which transcomplements meiotic mutant sme2 of S. pombe.

A cDNA clone from a mouse testis cDNA library was isolated by the transcomplementation method using a Schizosaccharomyces pombe meiotic mutant (sme2) that is defective in meiosis I. The cDNA clone isolated has an open reading frame encoding 302 amino acids constituting a protein with a strong similarity to mouse poly(A) binding protein II (mPABII) and bovine poly(A) binding protein II (PABII). PABII is known to bind to the growing poly(A) tail and stimulates poly(A) polymerase, which catalyzes the polymerization of the mRNA poly(A) tail. Northern blot analysis of the cDNA clone identified as mPABII revealed a single transcript of 1.2 kb. This was detectable exclusively in adult testis. Immunohistochemical analysis using a polyclonal antibody demonstrated that mPABII protein was expressed in the nucleus at specific stages from late pachytene spermatocytes to round spermatids. Genetic mapping showed the Pabp3 gene encoding mPABII to be located near position 19.5 on mouse chromosome 14. These results suggest that mPABII might be involved in specific spermatogenetic cell differentiation.

Animals↗
PubMed2000

Long-term responders without eradication of hepatitis C virus after interferon therapy: characterization of clinical profiles and incidence of hepatocellular carcinoma.

AIMS/BACKGROUND: The aim of this study was to determine the characteristics of patients with chronic hepatitis C showing long-term normalization of alanine aminotransferase (ALT) without eradication of HCV RNA, as well as to investigate the incidence of hepatocellular carcinoma (HCC) in such patients. METHODS: Four hundred and nineteen patients with histologically-proven chronic hepatitis C who had received interferon (IFN) therapy were studied. Complete response (CR) was defined as persistent normalization of ALT levels with eradication of serum HCV RNA (n= 126). Long-term biochemical response with positive HCV RNA (HCV-positive BR) was defined as a normal ALT level at 6 months after IFN therapy with further persistent normalization of ALT levels for 2 or more years without eradication of serum HCV RNA (n=49). All other patterns were classified as non-response (NR, n=244). RESULTS: Mean follow-up periods of CR, HCV-positive BR and NR groups were 4.9, 5.2 and 4.9 years, respectively. The HCV-positive BR group had significantly higher serum HCV RNA levels and a higher rate of HCV serological group 1 classification than the CR group. The other characteristics of the HCV-positive BR group were lower histologic activity, lower ALT levels, and a higher rate of females when compared with both the CR and NR groups. Histologic staging in the HCV-positive BR group was significantly lower than that in the NR group. Cumulative incidences of HCC estimated by the Kaplan-Meier method in both the CR and HCV-positive BR groups were significantly lower than those in the NR group (log-rank test, CR vs NR p<0.001, HCV-positive BR vs NR p=0.026). CONCLUSION: The patients with HCV-positive BR were virologically different from those with CR, and had lower ALT levels and histologic activity when compared to those with CR and NR.

Alanine Transaminase↗
PubMed2000

Sequential changes of [H]forskolin, [H]cyclohexyladenosine and [H]PN200-110 binding sites in the brain of 6-hydroxydopamine-lesioned rats.

Receptor autoradiographic technique was studied to investigate sequential changes in adenylyl cyclase, adenosine A1 receptors and L-type calcium channels in the striatum and substantia nigra 1-8 weeks after unilateral 6-hydroxydopamine injection of the medial forebrain bundle in rats. [3H]Forskolin, [3H]cyclohexyladenosine (CHA) and [3H]PN200-110 were used to label adenylyl cyclase, adenosine A1 receptors and L-type calcium channels, respectively. The degeneration of the nigrostriatal pathway caused a significant increase in [3H]forskolin binding in the striatum of both the ipsilateral and contralateral sides from 2 to 4 weeks post-lesion. The ipsilateral substantia nigra showed a transient increase in [3H]forskolin binding 4 weeks post-lesion. In contrast, [3H]CHA binding showed no significant change in most brain areas after lesioning. On the other hand, a conspicuous decrease in [3H]PN200-110 binding was observed in the dorsolateral striatum of ipsilateral side 4 weeks post-lesion. Thereafter, the striatum of both the ipsilateral and contralateral sides showed a significant decrease in [3H]PN200-110 binding 8 weeks post-lesion. These results demonstrate that unilateral 6-hydroxydopamine into the medial forebrain bundle of rats can experimentally cause a significant increase in adenylyl cyclase binding sites in the striatum and substantia nigra, whereas no conspicuous change in adenosine A1 receptors is observed in these areas during post-lesion. In contrast, L-type calcium channels were progressively damaged in the striatum after unilateral 6-hydroxydopamine treatment. These findings suggest that adenylyl cyclase and calcium system may contribute to the degeneration processes of the dopaminergic neurones.

Adenosine↗