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Norton H Neff - One of the best experts on this subject based on the ideXlab platform.
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tyrosine hydroxylase aromatic l amino acid decarboxylase and Dopamine Metabolism after chronic treatment with Dopaminergic drugs
Brain Research, 1999Co-Authors: Seongeun Cho, Norton H Neff, Annemarie Duchemin, Maria HadjiconstantinouAbstract:Mice were treated with Dopamine (DA) receptor agonist and antagonist drugs: Agonists: (+/-)-SKF 38393 ((+/-)-1-phenyl-2,3,4, 5-tetrahydro-(1H)-3-benzazepine-7,8-diol) [DA D1-like]; bromocriptine, [DA D2 selective]; quinpirole, [DA D2/D3 preferring]; (+/-)-7-hydroxy-dipropylamino-tetralin (7-OH-DPAT), [DA D3/D2 preferring], Antagonists: R(+)-SCH 23390 (R(+)-7-chloro-8-hydroxy-3-methyl-1-phenyl-2,3,4, 5-tetrahydro-1H-3-benzazepine), [DA D1-like]; and haloperidol, [DA D2-like]. All drugs were administered intraperitoneally, two injections daily 8 h apart for 30 days. Aromatic L-amino acid decarboxylase (AAAD) and tyrosine hydroxylase (TH) activity, protein and mRNA, as well as DA Metabolism were followed with time thereafter in the nigrostriatal neurons. We observed that chronic administration of D1-like agonists had no effect on TH or AAAD activity, while D2-like agonists decreased AAAD, but not TH activity. Additionally, chronic blockade of DA D2-like receptors resulted in prolonged induction of TH and AAAD, while chronic blockade of DA D1-like receptors induced changes of AAAD only. Compared to TH the induction of AAAD was longer lasting. DA Metabolism was altered by chronic administration of drugs acting on DA D2-like, but not DA D1-like receptors, and in general the patterns of change did not follow those for TH or AAAD. When studied 48 h after the last dose of the chronic haloperidol schedule TH displayed tolerance to acute drug challenge. At the same time interval, there was tolerance to the enhancing effects of haloperidol and SCH 23390 on DA Metabolism. The induction of AAAD by haloperidol or SCH 23990 did not appear to develop tolerance after chronic administration. These observations complement existing knowledge, and provide novel information about AAAD that may have practical importance for Parkinson's patients on L-DOPA therapy.
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dizocilpine enhances striatal tyrosine hydroxylase and aromatic l amino acid decarboxylase activity
European Journal of Pharmacology, 1995Co-Authors: Maria Hadjiconstantinou, Zvani Rossetti, T A Wemlinger, Norton H NeffAbstract:Dizocilpine administration enhances Dopamine Metabolism in the rat striatum, nucleus accumbens, olfactory tubercle, and prefrontal cortex. Concomitant with increased Metabolism is enhanced tyrosine hydroxylase and aromatic L-amino acid decarboxylase activities in the striatum and increased mRNA for the two enzymes in the midbrain. Activation of Dopaminergic neurons may, in part, explain increased locomotor activity in normal animals and the ability of dizocilpine to potentiate the antiparkinsonian action of L-3,4-dihydroxyphenylalanine in an animal model.
Maria Hadjiconstantinou - One of the best experts on this subject based on the ideXlab platform.
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tyrosine hydroxylase aromatic l amino acid decarboxylase and Dopamine Metabolism after chronic treatment with Dopaminergic drugs
Brain Research, 1999Co-Authors: Seongeun Cho, Norton H Neff, Annemarie Duchemin, Maria HadjiconstantinouAbstract:Mice were treated with Dopamine (DA) receptor agonist and antagonist drugs: Agonists: (+/-)-SKF 38393 ((+/-)-1-phenyl-2,3,4, 5-tetrahydro-(1H)-3-benzazepine-7,8-diol) [DA D1-like]; bromocriptine, [DA D2 selective]; quinpirole, [DA D2/D3 preferring]; (+/-)-7-hydroxy-dipropylamino-tetralin (7-OH-DPAT), [DA D3/D2 preferring], Antagonists: R(+)-SCH 23390 (R(+)-7-chloro-8-hydroxy-3-methyl-1-phenyl-2,3,4, 5-tetrahydro-1H-3-benzazepine), [DA D1-like]; and haloperidol, [DA D2-like]. All drugs were administered intraperitoneally, two injections daily 8 h apart for 30 days. Aromatic L-amino acid decarboxylase (AAAD) and tyrosine hydroxylase (TH) activity, protein and mRNA, as well as DA Metabolism were followed with time thereafter in the nigrostriatal neurons. We observed that chronic administration of D1-like agonists had no effect on TH or AAAD activity, while D2-like agonists decreased AAAD, but not TH activity. Additionally, chronic blockade of DA D2-like receptors resulted in prolonged induction of TH and AAAD, while chronic blockade of DA D1-like receptors induced changes of AAAD only. Compared to TH the induction of AAAD was longer lasting. DA Metabolism was altered by chronic administration of drugs acting on DA D2-like, but not DA D1-like receptors, and in general the patterns of change did not follow those for TH or AAAD. When studied 48 h after the last dose of the chronic haloperidol schedule TH displayed tolerance to acute drug challenge. At the same time interval, there was tolerance to the enhancing effects of haloperidol and SCH 23390 on DA Metabolism. The induction of AAAD by haloperidol or SCH 23990 did not appear to develop tolerance after chronic administration. These observations complement existing knowledge, and provide novel information about AAAD that may have practical importance for Parkinson's patients on L-DOPA therapy.
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dizocilpine enhances striatal tyrosine hydroxylase and aromatic l amino acid decarboxylase activity
European Journal of Pharmacology, 1995Co-Authors: Maria Hadjiconstantinou, Zvani Rossetti, T A Wemlinger, Norton H NeffAbstract:Dizocilpine administration enhances Dopamine Metabolism in the rat striatum, nucleus accumbens, olfactory tubercle, and prefrontal cortex. Concomitant with increased Metabolism is enhanced tyrosine hydroxylase and aromatic L-amino acid decarboxylase activities in the striatum and increased mRNA for the two enzymes in the midbrain. Activation of Dopaminergic neurons may, in part, explain increased locomotor activity in normal animals and the ability of dizocilpine to potentiate the antiparkinsonian action of L-3,4-dihydroxyphenylalanine in an animal model.
David Wirtshafter - One of the best experts on this subject based on the ideXlab platform.
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studies on the behavioral activation produced by stimulation of gabab receptors in the median raphe nucleus
Behavioural Brain Research, 1993Co-Authors: David Wirtshafter, Thomas R. Stratford, Mark R PitzerAbstract:Abstract Injections of the GABA B agonist baclofen into the median raphe nucleus (MR) resulted in marked hyperactivity and in increases in food and water intake by non-deprived animals. The locomotor effects of baclofen were stereospecific and could be antagonized by coinjection of the GABA B antagonist 2-hydroxysaclofen. Hyperactivity was produced by lower doses of baclofen, at shorter latencies, when the drug was injected into the MR than when it applied to the dorsal raphe nucleus (DR) or the ventral tegmental area (VTA). The locomotor response to intra-MR baclofen was unaltered in animals pretreated with the serotonin synthesis inhibitor p -chlorophenylalanine. Finally, intra-MR injections of baclofen produced a large increase in Dopamine Metabolism in the nucleus accumbens and striatum but failed to alter hippocampal or striatal serotonin Metabolism. These findings suggest that baclofen may produce increases in activity and ingestive behavior as a result of an action on non-serotonergic cells in the MR.
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nonserotonergic control of nucleus accumbens Dopamine Metabolism by the median raphe nucleus
Pharmacology Biochemistry and Behavior, 1992Co-Authors: David Wirtshafter, Radmila TrifunovicAbstract:Abstract Injections of the GABA agonist muscimol into the median raphe nucleus (MR) have been shown to result in an acceleration of Dopamine Metabolism within the nucleus accumbens. To examine whether serotonergic mechanisms play a role in this effect, muscimol or its vehicle was injected into the MR of either control subjects or of rats that had received prior injections of the serotonin-depleting agent p -chlorophenylalanine (PCPA). Although PCPA treatments produced massive depletions of forebrain serotonin, they failed to alter the effect of muscimol infusions on Dopamine Metabolism. This finding suggests that the effects of intra-MR injections of muscinol on accumbens Dopamine turnover do not result entirely from an interaction between serotonergic and Dopaminergic systems.
Radmila Trifunovic - One of the best experts on this subject based on the ideXlab platform.
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nonserotonergic control of nucleus accumbens Dopamine Metabolism by the median raphe nucleus
Pharmacology Biochemistry and Behavior, 1992Co-Authors: David Wirtshafter, Radmila TrifunovicAbstract:Abstract Injections of the GABA agonist muscimol into the median raphe nucleus (MR) have been shown to result in an acceleration of Dopamine Metabolism within the nucleus accumbens. To examine whether serotonergic mechanisms play a role in this effect, muscimol or its vehicle was injected into the MR of either control subjects or of rats that had received prior injections of the serotonin-depleting agent p -chlorophenylalanine (PCPA). Although PCPA treatments produced massive depletions of forebrain serotonin, they failed to alter the effect of muscimol infusions on Dopamine Metabolism. This finding suggests that the effects of intra-MR injections of muscinol on accumbens Dopamine turnover do not result entirely from an interaction between serotonergic and Dopaminergic systems.
Robert H. Roth - One of the best experts on this subject based on the ideXlab platform.
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The predator odor, TMT, displays a unique, stress-like pattern of Dopaminergic and endocrinological activation in the rat
Brain research, 2000Co-Authors: Bret A. Morrow, Robert H. Roth, Andy J. Redmond, John D. ElsworthAbstract:Abstract Predator odors may provide a species relevant aversive stimuli to study the central effects of stress in rats and may have several benefits over currently applied models. Here, we examined one such odor, TMT, isolated from the fox, a predator of the rat, on fear-induced behaviors, serum corticosterone, and central Dopamine Metabolism. Habituated rats were exposed to TMT, or a control odor, butyric acid, in an open field. For comparison, other rats were subjected to a model of conditioned fear — a traditional fear model. Several similarities between the two stresses were observed including increased serum corticosterone and increased Dopamine Metabolism in the medial prefrontal cortex. Differences were also observed. TMT, but not conditioned fear, activated Dopamine Metabolism in the amygdala, but not the nucleus accumbens core and shell. Rats exposed to conditioned fear, but not TMT odor, demonstrated altered behaviors associated with fear, including locomotion, grooming and immobility. Finally, rats reexposed to TMT after a 24-h delay did not demonstrate any of the changes observed with acute exposure to TMT. These data indicate acute exposure to a predator odor, TMT, can result in a unique pattern of biochemical activation that is similar, but not identical, to conditioned fear. The differences may indicate unique features of a central ‘fear arousal’ pathway that responds to innate, unlearned stressful stimuli, such as predator odors.
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stress activation of mesocorticolimbic Dopamine neurons effects of a glycine nmda receptor antagonist
European Journal of Pharmacology, 1993Co-Authors: Bret A. Morrow, William A Clark, Robert H. RothAbstract:Restraint of brief duration causes a metabolic activation of mesocortical and some mesolimbic Dopaminergic systems with little effect on the nigrostriatal system. We have examined the ability of an antagonist of the allosteric glycine site of the N-methyl-D-aspartate receptor complex to block the stress-induced response in Dopamine utilization. Thirty minutes of restraint stress elevated Dopamine Metabolism, as measured by the ratio between 3,4-dihydroxyphenylacetic acid (DOPAC) and Dopamine, in both the medial prefrontal cortex and nucleus accumbens. An antagonist for the glycine/N-methyl-D-aspartate receptor complex, 1-hydroxy-3-aminopyrrolidone-2 ((+)-HA-966), given systemically or injected into the ventral tegmental area, prevents the stress-induced increase in Dopamine Metabolism in the prefrontal cortex without altering the response in the nucleus accumbens. Similarly, systemic administration of the non-competitive antagonist for the N-methyl-D-aspartate receptor, dizocilpine ((+)-MK-801), blocked the stress-induced rise in Dopamine Metabolism in the medial prefrontal cortex but not the nucleus accumbens. The negative enantiomer of HA-966 did not produce a selective antagonism of the stress-induced Dopamine Metabolism in the medial prefrontal cortex. These results support previous work which suggest the mesocortical and mesoaccumbens Dopamine neurons respond to excitatory input through different glutamate receptor mechanisms. Additionally, the specific blockade of the stress-induced change in Dopamine Metabolism in the medial prefrontal cortex by a glycine antagonist implies a role for such an antagonist in treatment of disease states which may involve disruptions of N-methyl-D-aspartate receptor function.