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A peripheral dopamine marker undergoes seasonal changes
D12
9th Meeting
of the ESN
46
FREE AND STORED CENTRAL SEROTONlN IN STREPTOZOTOCIN(STZ)-tNCKtCED DUWETES. F.Mariin, J.Miguez, G.Atienza and MAldegunde. Dept. Physiology. Faculty of Biilogy. Univ. of Santiago de Compostela. 15706. Galicia. SPAIN. In previous studies we have reported that monoamines and their metaboliies in CSF (cerebrospinal fluid) provide an indirect indication of neurotransmitters state in the synaptic cleft Thus, contents in CSF and central intra/extracellular ratio (I/E; intracellular and extracellular = brain and CSF concentration, respectively) of neurotransmitters depend on their uptake, release and degradation in brain. ST&induced diabetes have been reported to be accompanied by changes in brain 5HlAA (5hydroxiindolacetic acid), and recently alteration in 5HT (serotonin) release was also found. The aim of the present work was to test the functiiallity of brain serotonergic system in STZ-induced diabetes. Therefore, 5HT and BHIAA contents in whole brain and CSF were determined. The treatment groups were: control, STZ-induced, STZinduced + insulin therapy, and insulin treated rats. Significant variations were only observed in diabetic group: brain SHIM decreased (-12% vs control). The alteration of brain 5HIAA, because of STZ treatment, were completely recovered after insulin therapy. 5HT and 5HlAA I/E ratios (1500 + 800 and 5 f 0.8, respectively) in control group were in agreement with those obtained by microdialysis.
W. Maruyamal), D. Nakahara2),A. Takahashil), T. Nagatsd), and M. Naoi4). 1) Department of Neurology, Nagoya University School of Medicine, Nagoya, Japan, 2) Nagoya University College of Medical Technology, Nagoya, Japan, 3) Division of Molecular Genetics (II) Neurochemistry, Institute for Comprehensive Medical Science, Fujita Health University, Toyoake, Japan, and 4) Department of Biosciences, Nagoya Institute of Teclmology, Nagoya, Japan. The effect of monoamine-derived 1,2,3,4-letrahydru isoquinolines ~Qs) on monoamine levels was studied by miff* dialysis in the 4 regions of the rat brains. Neurotransmitters such as monoamines and amino acids in microdialysis perfusate were quantitatively determined by high performance liquid chromatography with multi-electrochemical detector system. Perfusion of TIQs induced the release of dopamine, noradrenalkte, and serotonin, and inhibition of monoamine oxidase (MAO) was also observed in the striatum. The study on structure-activity relationship revealed that only TiQs with the catecbol structure, 6,7-dihydroxyiaw quindines (DHTIQs) released monoamines. But catecbol structure was not absolutely required for MAO inhibition. The affects of DHTIQs on monoamine neumns were similar to timae of dopaminergic neurotoxins, such as N-methyl-4-phenylpyridinium ion (MPP+)and amphetamine. In the substantia nigra, hippocampus, and hypothalamus, monoamine release and MAO inhibition were observed by DHTIQ perfusion, as in the striatum. DHTIQs, occurred in the mammalian brains, may be eudogenous compounds which perturb monoamine levels in the human brain.
9th Meeting
of the ESN
46
FREE AND STORED CENTRAL SEROTONlN IN STREPTOZOTOCIN(STZ)-tNCKtCED DUWETES. F.Mariin, J.Miguez, G.Atienza and MAldegunde. Dept. Physiology. Faculty of Biilogy. Univ. of Santiago de Compostela. 15706. Galicia. SPAIN. In previous studies we have reported that monoamines and their metaboliies in CSF (cerebrospinal fluid) provide an indirect indication of neurotransmitters state in the synaptic cleft Thus, contents in CSF and central intra/extracellular ratio (I/E; intracellular and extracellular = brain and CSF concentration, respectively) of neurotransmitters depend on their uptake, release and degradation in brain. ST&induced diabetes have been reported to be accompanied by changes in brain 5HlAA (5hydroxiindolacetic acid), and recently alteration in 5HT (serotonin) release was also found. The aim of the present work was to test the functiiallity of brain serotonergic system in STZ-induced diabetes. Therefore, 5HT and BHIAA contents in whole brain and CSF were determined. The treatment groups were: control, STZ-induced, STZinduced + insulin therapy, and insulin treated rats. Significant variations were only observed in diabetic group: brain SHIM decreased (-12% vs control). The alteration of brain 5HIAA, because of STZ treatment, were completely recovered after insulin therapy. 5HT and 5HlAA I/E ratios (1500 + 800 and 5 f 0.8, respectively) in control group were in agreement with those obtained by microdialysis.
W. Maruyamal), D. Nakahara2),A. Takahashil), T. Nagatsd), and M. Naoi4). 1) Department of Neurology, Nagoya University School of Medicine, Nagoya, Japan, 2) Nagoya University College of Medical Technology, Nagoya, Japan, 3) Division of Molecular Genetics (II) Neurochemistry, Institute for Comprehensive Medical Science, Fujita Health University, Toyoake, Japan, and 4) Department of Biosciences, Nagoya Institute of Teclmology, Nagoya, Japan. The effect of monoamine-derived 1,2,3,4-letrahydru isoquinolines ~Qs) on monoamine levels was studied by miff* dialysis in the 4 regions of the rat brains. Neurotransmitters such as monoamines and amino acids in microdialysis perfusate were quantitatively determined by high performance liquid chromatography with multi-electrochemical detector system. Perfusion of TIQs induced the release of dopamine, noradrenalkte, and serotonin, and inhibition of monoamine oxidase (MAO) was also observed in the striatum. The study on structure-activity relationship revealed that only TiQs with the catecbol structure, 6,7-dihydroxyiaw quindines (DHTIQs) released monoamines. But catecbol structure was not absolutely required for MAO inhibition. The affects of DHTIQs on monoamine neumns were similar to timae of dopaminergic neurotoxins, such as N-methyl-4-phenylpyridinium ion (MPP+)and amphetamine. In the substantia nigra, hippocampus, and hypothalamus, monoamine release and MAO inhibition were observed by DHTIQ perfusion, as in the striatum. DHTIQs, occurred in the mammalian brains, may be eudogenous compounds which perturb monoamine levels in the human brain.