Changes in the central dopaminergic systems in the streptozotocin-induced diabetic rats
Tóm tắt
The behavioral response, dopamine metabolism, and characteristics of dopamine subtypes after developing the hyperglycemia were studied in the striata of rats. In animals developed hyperglycemia, the on-set and duration of cataleptic behavior responded to SCH 23390 injection was delayed and shortened, respectively. However, the cataleptic responses to spiperone occurred significantly earlier in on-set and prolonged in duration. Dopamine metabolites, dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA), were significantly reduced in the striata of hyperglycemic rats. However, level of DA was significantly increased. It is noted that the ratios of DOPAC and HVA to DA were decreased, suggesting decreased turnover of DA. The affinity of striatal D-1 receptors was significantly increased without changes in the number of binding sites, while the maximum binding number of D-2 receptors was significantly increased without affecting its affinity in the diabetic rats. These results indicate that the dopaminergic activity in the striata was altered in hyperglycemic rats. Furthermore, it suggests that the upregulation of dopamine receptors might be due to the decreased dopamine metabolism.
Tài liệu tham khảo
Barone, P., Tucci, I., Parashos, S. A. and Chase, T. N., Supersensitivity to a D-1 dopamine receptor agonist and subsensitivity to a D-2 receptor agonist following chronic D-1 receptor blockade.Eur. J. Pharmacol., 149, 225–232 (1988).
Bitar, M. S. and DeSouza, E. B., Diabetes-releated changes in brain beta adrenoreceptors in rats as assessed by quantitative autoradiography: Relationship to hypothalamic norepinephrine metabolism and pituitary-gonadal hormone secretion.J. Pharmacol. Exp. Ther., 254, 781–785 (1990).
Bitar, M. S., Koulu, M., Rapoport, S. I. and Linnoila, M., Diabetes-induced alterations in brain monoamine metabolism in rats.J. Pharmacol. Exp. Ther., 236, 432–437 (1986).
Brodde, O.-E. and Michel, M. C., Disease states can modify both receptor number and signal transduction pathways.Trends Pharmacol. Sci., 10, 383–384 (1989).
Carboni, E., Memo, M., Tanda, G. L., Carruba, M. O. and Spano, P. F., Effect of temperature and ionic environment on the specific binding of [3H]sulpiride to membranes from different rat brain regions.Neurochem. Int., 7, 279–284 (1985).
Carrier, O. and Aronstam, R. S., Increased muscarinic responsiveness and decreased muscarinic receptor content in ileal smooth muscle in diabetes.J. Pharmacol. Exp. Ther., 254, 445–449 (1990).
Chu, P. C., Lin, M. T. and Leu, S. Y., Alterations in physiologic functions in brain monoamine content in streptozotocin-diabetic rats.Diabetes., 35, 481–485 (1986).
Consolo, S., Girotti, P., Russi, G. and Di Chiara, G., Endogenous dopamine facilitates striatalin vivo acetylcholine release by acting on D1 receptors localized in the striatum.J. Neurochem., 59, 1555–1557 (1992).
Costall, B. and Naylor, R. J., Neuroleptic and non-neuroleptic catalepsy.Arznein-Forsch., 23, 674–683. (1973).
Dunstan, R., Broekkamp, C. L. and Lloyd, K. G., Involvement of caudate nucleus, amygdala or reticular formation in neuroleptic and narcotic catalepsy.Pharmacol. Biochem. Behav., 14, 169–174 (1981).
Emy, R. E., Berezo, M. W. and Perlman, R. L., Activation of tyrosine 3-monooxygenase in pheochromocytoma cells by adenosine.J. Biol. Chem., 256, 1335–1339 (1981).
Glowinski, J. and Iversen, L. L., Regional studies of catecholamine in the rat brain-I. The disposition of3H-norepinephrine, 3H-dopamine and 3H-DOPA in various regions of the rat.J. Neurochem., 13, 655–669 (1966).
Hoffman, D. C. and Beninger, R. J., The D1 receptor antagonist SCH23390 reduces locomotor activity and rearing in rats.Pharmacol. Biochem. Behav., 22, 341–342 (1985).
Horwitz, J. and Perlman, R. L., Activation of tyrosine hydroxylase in the superior cervical ganglion by nicotinic and muscarinic agonists.J. Neurochem., 43, 546–552 (1984).
Hoskins, B., and Scott, J. M., Evidence for a direct action of insulin to increase renal reabsorption of calcium and for an irreversible defect in renal ability to conserve calcium due to prolonged absence of insulin.Diabetes., 33, 991–994 (1984).
Hyttel, J., SCH 23390-the first selective dopamine D-1 antagonist.Eur. J. Pharmacol., 91, 153–154 (1983).
Lozovsky, D., Saller, C. F. and Kopin, I., Dopamine receptor binding is increased in diabetic rats.Science, 214, 1031–1033 (1981).
Lowry, O. H., Rosebrough, N. J., Farr, A. L. and Randall, R. J., Protein measurement with the Folin phenol reagent.J. Biol. Chem., 193, 265–275 (1951).
Marshall, J. F., Friedman, M. I. and Heffner, T. G., Reduced anorexic and locomotor-stimulant action of D-amphetamine in alloxan-diabetic rats.Brain Res., 111, 428–432 (1976).
Mayer, G. S. and Shoup, R. E., Simultaneous multiple electrode liquid chromatographical assay for catecholamines, indoleamines and metabolites in brain tissue.J. Chromatography, 255, 533–544 (1983).
Meller, E., Kuga, S., Friedhoff, A. J. and Goldstein, M., Selective D2 dopamine receptor agonists prevent calepsy induced by SCH-23390, a selective D1 antagonist.Life Sci., 36, 1857–1864 (1985).
Munson, P. J. and Rodbard, D., A versatile computerized approach for the characterization of ligand binding systems.Anal. Biochem., 107, 220–239 (1980).
Porceddu, M. L., Giorgi, O., Ongini, E., Mele, S. and Biggio, G.,3H-23390 binding sites in the rat substantia nigra: Evidence for a presynaptic localization and innervation by dopamine.Life Sci., 39, 321–328 (1986).
Quimet, C. C., Miller, P. E., Hemmings, H. C., Walaas, S. I. and Greengard, P., DARPP-32, a dopamine- and adenosine 3,5-monophosphate-regulated phosphoprotein enriched in dopamine innervated brain regions.J. Neurosci., 4, 111–124 (1984).
Robertson, G. S. and Robertson, H. A., D1 and D2 agonist synergism: seperate sites of action?Trends Pharmacol. Sci., 8, 295–299 (1987).
Ryall, R. W., Drugs used in schizophrenia. In Ryall, R. W. ed. Mechanisms of drug action on the nervous system. Cambridge Univ. Press, N.Y. 1989 pp. 171–192.
Salkovic, M. and Lackovic, Z., Brain D1 dopamine receptor in alloxan-induced diabetes.Diabetes, 41, 1119–1121 (1992).
Saller, C. F., Dopaminergic activity is reduced in diabetic rats.Neurosci. Letter, 99, 301–306 (1984).
Saller, C. F. and Chiodo, L. A., Glucose suppresses basal firing and haloperidol-induced increases in the firing rate of central dopaminergic neurons.Science, 210, 1269–1271 (1980).
Saller, C. F. and Salama, A. I., D-1 and D-2 dopamine receptor blockade: Interactive effectsin vitro andin vivo.J. Pharmacol. Exp. Ther., 236, 714–720 (1986).
Scatton, B., Worms, P., Lloyd, K. G. and Bartholini, G., Cortical modulation of striatal function.Brain Res., 232, 331–343 (1982).
Seeman, P., Brain dopamine receptors.Pharmacol. Rev., 32, 229–313 (1980).
Shimomura, Y., Shimizu, H., Takahashi, M., Sato, N., Uehara, Y., Suwa, K., Kobayashi, I., Tadokoro, S. and Kobayashi, S., Changes in ambulatory activity and dopamine turnover in streptozotocin-induced diabetic rats.Endocrinol., 123, 2621–2625 (1988).
Shimomura, Y., Shimizu, H., Takahashi, M., Uehara, Y., Kobayashi, I. and Kobayashi, S., Ambulatory activity and dopamine turnover in streptozotocin-induced rats.Exp. Clin. Endocrinol., 95, 385–388 (1990).
Stoof, J. C., Drukarch, B., De Boer, P., Westerink, B. H. C. and Groenewegen, H. J., Regulation of the activity of striatal cholinergic neurons by dopamine.Neuroscience, 47, 755–770 (1992).
Stoof, J. C. and Kebabian, J., Two dopamine receptors: Biochemistry, physiology and pharmacology.Life Sci., 35, 2281–2296 (1984).
Watkins, J. B. and Sherman, S. E., Long-term diabetes alters the hepatobiliary clearance of acetaminophen, bilirubin and digoxin.J. Pharmacol. Exp. Ther., 260, 1337–1343 (1992).
Westerink, N. H. C. and Korf, J., Turnover of acid dopamine metabolites in striatal and mesolimbic tissue of the rat brain.Eur. J. Pharmacol., 37, 249–255 (1976).
Zukins, S. R., Young, A. E. and Snyder, S. H., Gamma-aminobutyric acid binding to receptro sites in rat central nerve system.Proc. Natl. Acad. Sci. U.S.A. 71, 4802–4807 (1974).