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Results: 21 to 26 of 26

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Functional MRI of apomorphine activation of the basal ganglia in awake rhesus monkeys.
Zhang Z, Andersen AH, Avison MJ, Gerhardt GA, Gash DM
(2000) Brain Res 852: 290-6
MeSH Terms: Animals, Apomorphine, Arousal, Basal Ganglia, Cerebral Cortex, Corpus Callosum, Dopamine Agonists, Female, Macaca mulatta, Magnetic Resonance Imaging, Substantia Nigra, Video Recording
Show Abstract · Added December 10, 2013
Functional magnetic resonance imaging (fMRI) was used to analyze blood oxygen level-dependent (BOLD) responses in the nigrostriatal system (caudate nucleus, putamen and substantia nigra) of awake rhesus monkeys to systemic apomorphine administration. The study (1) measured BOLD responses as an index of neuronal activity in the three structures following injections of the mixed D1/D2 agonist, and (2) assessed the effects of isoflurane anesthesia on the fMRI responses. Compared to control saline injections, 0.1 mg/kg apomorphine significantly activated the caudate nucleus (P < or = 0.005), putamen (P < or = 0.001) and substantia nigra (P < or = 0.005). The responses were consistent with activation of GABAergic neurons in these three structures seen in other animal models. Isoflurane gas measurably blunted the response to apomorphine, so that a significant apomorphine activation was only seen in the substantia nigra of anesthetized animals. Even there, the mean MR signal change was reduced from 9.8% in awake monkeys to 2.3% in anesthetized animals. The data support the hypothesis that fMRI can be used to study the effects of drugs that alter basal ganglia activity in awake rhesus monkeys.
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12 MeSH Terms
Psychostimulant-induced Fos protein expression in the thalamic paraventricular nucleus.
Deutch AY, Bubser M, Young CD
(1998) J Neurosci 18: 10680-7
MeSH Terms: Amphetamine, Animals, Cocaine, Dopamine Agonists, Dopamine Antagonists, Dose-Response Relationship, Drug, Gene Expression, Male, Neural Pathways, Nucleus Accumbens, Oncogene Proteins v-fos, Psychotropic Drugs, Rats, Rats, Sprague-Dawley, Thalamic Nuclei, Time Factors, Tissue Distribution
Show Abstract · Added May 27, 2014
Lesions of glutamatergic afferents to the nucleus accumbens have been reported to block psychostimulant-induced behavioral sensitization. However, thalamic glutamatergic projections to the nucleus accumbens have received little attention in the context of psychostimulant actions. We examined the effects of acute amphetamine and cocaine administration on expression of Fos protein in the thalamic paraventricular nucleus (PVT), which provides glutamatergic inputs to the nucleus accumbens and also receives dopaminergic afferents. Immunoblot and immunohistochemical studies revealed that both psychostimulants dose-dependently increased PVT Fos expression. PVT neurons retrogradely labeled from the nucleus accumbens were among the PVT cells that showed a Fos response to amphetamine. D2 family dopamine agonists, including low doses of the D3-preferring agonist 7-OH-DPAT, increased the numbers of Fos-like-immunoreactive neurons in the PVT. Conversely, the effects of cocaine and amphetamine on PVT Fos expression were blocked by pretreatment with the dopamine D2/3 antagonist raclopride. Because PVT neurons express D3 but not other dopamine receptor transcripts, it appears that psychostimulants induce Fos in PVT neurons through a D3 dopamine receptor. We suggest that the PVT may be an important part of an extended circuit subserving both the arousing properties and reinforcing aspects of psychostimulants.
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17 MeSH Terms
Molecular components of striatal plasticity: the various routes of cyclic AMP pathways.
Rajadhyaksha A, Leveque J, MacĂ­as W, Barczak A, Konradi C
(1998) Dev Neurosci 20: 204-15
MeSH Terms: Animals, Benzazepines, Calcium, Colforsin, Corpus Striatum, Culture Techniques, Cyclic AMP, Cyclic AMP Response Element-Binding Protein, Dizocilpine Maleate, Dopamine, Dopamine Agonists, Excitatory Amino Acid Antagonists, Neuronal Plasticity, Phosphorylation, Rats, Rats, Sprague-Dawley, Receptors, N-Methyl-D-Aspartate
Show Abstract · Added May 27, 2014
Neuroplasticity serves an important role for normal striatal function and in disease states. One route to neuroplasticity involves activation of the transcription factor cyclic 3', 5'-adenosine monophosphate (cyclic AMP) response element binding protein (CREB) by phosphorylation of the amino acid 133Ser. Dopamine and glutamate, the two predominant neurotransmitters in the striatum, induce CREB phosphorylation in primary cultures of rat striatum through cyclic AMP and Ca2+ pathways. Here we present the role of N-methyl-D-aspartate receptors and Ca2+ in cyclic AMP-mediated CREB phosphorylation.
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17 MeSH Terms
Dopaminergic regulation of extracellular gamma-aminobutyric acid levels in the prefrontal cortex of the rat.
Grobin AC, Deutch AY
(1998) J Pharmacol Exp Ther 285: 350-7
MeSH Terms: Animals, Apomorphine, Benzazepines, Dopamine Agonists, Dopamine Antagonists, Male, Prefrontal Cortex, Rats, Rats, Sprague-Dawley, Time Factors, gamma-Aminobutyric Acid
Show Abstract · Added May 27, 2014
Dopaminergic axons in the prefrontal cortex synapse with interneurons as well as pyramidal cells. Electrophysiological data suggest that dopamine depolarizes certain gamma-aminobutyric acid (GABA)-containing interneurons in the cortex. We investigated the dopaminergic regulation of extracellular GABA levels in the prefrontal cortex using in vivo microdialysis. Systemic administration of the mixed D1/D2 dopamine receptor agonist apomorphine increased extracellular GABA levels in the prefrontal cortex, but did not increase levels of glycine; the apomorphine-elicited increase in GABA levels was blocked by tetrodotoxin infusion into the prefrontal cortex. Local administration of the D2 agonist quinpirole into the cortex via the dialysis probe resulted in a dose-dependent increase in extracellular GABA levels. In contrast, administration of the D1 agonist SKF 38393 did not alter GABA levels. The ability of systemic apomorphine to increase extracellular GABA levels in the prefrontal cortex was blocked by local administration of the D2-like antagonist sulpiride to the cortex, but was not attenuated significantly by local perfusion of the D1 antagonist SCH 23390. Similarly, the ability of local infusion of the D2 agonist quinpirole to enhance extracellular GABA levels was blocked by sulpiride but not by SCH 23390. These data suggest that dopamine agonists increase the release of GABA in the prefrontal cortex through a D2-like receptor. In view of posited changes in prefrontal cortical dopamine and GABA systems in schizophrenia, it is possible that changes in GABAergic function in the cortex in schizophrenia are secondary to changes in cortical dopamine function.
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11 MeSH Terms
The molecular basis of dopamine and glutamate interactions in the striatum.
Konradi C
(1998) Adv Pharmacol 42: 729-33
MeSH Terms: Animals, Cells, Cultured, Colforsin, Corpus Striatum, Cyclic AMP, Cyclic AMP Response Element-Binding Protein, Dizocilpine Maleate, Dopamine, Dopamine Agonists, Excitatory Amino Acid Antagonists, Glutamic Acid, Neurons, Proto-Oncogene Proteins c-fos, Receptors, Dopamine D1, Receptors, N-Methyl-D-Aspartate, Second Messenger Systems, Transcription, Genetic
Added May 27, 2014
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17 MeSH Terms
Dopamine regulation of transcription factor-target interactions in rat striatum.
Hyman SE, Cole RL, Konradi C, Kosofsky BE
(1995) Chem Senses 20: 257-60
MeSH Terms: Animals, Corpus Striatum, Dopamine, Dopamine Agonists, Dopamine Antagonists, Gene Expression Regulation, Rats, Transcription Factors
Show Abstract · Added May 27, 2014
Transcriptional regulation is an important mechanism by which neurons adapt to environmental stimuli. The indirect dopamine agonists, amphetamine and cocaine have been shown to induce expression of immediate early genes, such as c-fos, and neuropeptide genes, such as prodynorphin in the rat striatum. Here we show that phosphorylation of transcription factor CREB is a critical early event coupling dopamine stimulation to gene regulation. CREB interacts with functional regulatory elements in both the c-fos and prodynorphin genes, and is phosphorylated in response to dopamine in a D1 dopamine receptor-dependent manner. In addition, we show by intra-striatal injection of antisense oligonucleotides directed against CREB mRNA, that CREB protein is required for c-fos induction by amphetamine.
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8 MeSH Terms