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About: Dopaminergic is a(n) research topic. Over the lifetime, 29033 publication(s) have been published within this topic receiving 1408301 citation(s). The topic is also known as: Dopaminergic drugs & Dopaminergic Agents. more


Open accessJournal ArticleDOI: 10.1073/PNAS.85.14.5274
G. Di Chiara1, Assunta ImperatoInstitutions (1)
Abstract: The effect of various drugs on the extracellular concentration of dopamine in two terminal dopaminergic areas, the nucleus accumbens septi (a limbic area) and the dorsal caudate nucleus (a subcortical motor area), was studied in freely moving rats by using brain dialysis. Drugs abused by humans (e.g., opiates, ethanol, nicotine, amphetamine, and cocaine) increased extracellular dopamine concentrations in both areas, but especially in the accumbens, and elicited hypermotility at low doses. On the other hand, drugs with aversive properties (e.g., agonists of kappa opioid receptors, U-50,488, tifluadom, and bremazocine) reduced dopamine release in the accumbens and in the caudate and elicited hypomotility. Haloperidol, a neuroleptic drug, increased extracellular dopamine concentrations, but this effect was not preferential for the accumbens and was associated with hypomotility and sedation. Drugs not abused by humans [e.g., imipramine (an antidepressant), atropine (an antimuscarinic drug), and diphenhydramine (an antihistamine)] failed to modify synaptic dopamine concentrations. These results provide biochemical evidence for the hypothesis that stimulation of dopamine transmission in the limbic system might be a fundamental property of drugs that are abused. more

Topics: Dopamine receptor (63%), Mesolimbic pathway (62%), Dopaminergic (62%) more

4,392 Citations

Open accessJournal ArticleDOI: 10.1016/S0896-6273(03)00568-3
William T. Dauer1, Serge Przedborski1Institutions (1)
11 Sep 2003-Neuron
Abstract: Parkinson's disease (PD) results primarily from the death of dopaminergic neurons in the substantia nigra. Current PD medications treat symptoms; none halt or retard dopaminergic neuron degeneration. The main obstacle to developing neuroprotective therapies is a limited understanding of the key molecular events that provoke neurodegeneration. The discovery of PD genes has led to the hypothesis that misfolding of proteins and dysfunction of the ubiquitin-proteasome pathway are pivotal to PD pathogenesis. Previously implicated culprits in PD neurodegeneration, mitochondrial dysfunction and oxidative stress, may also act in part by causing the accumulation of misfolded proteins, in addition to producing other deleterious events in dopaminergic neurons. Neurotoxin-based models (particularly MPTP) have been important in elucidating the molecular cascade of cell death in dopaminergic neurons. PD models based on the manipulation of PD genes should prove valuable in elucidating important aspects of the disease, such as selective vulnerability of substantia nigra dopaminergic neurons to the degenerative process. more

Topics: Substantia nigra (59%), MPTP (58%), Neurodegeneration (57%) more

4,390 Citations

Journal ArticleDOI: 10.1038/277093A0
John W. Kebabian1, Donald B. Calne1Institutions (1)
11 Jan 1979-Nature
Abstract: Pharmacological and biochemical criteria can be used to separate those dopamine receptors which are linked to the enzyme adenylyl cyclase and those which are not. more

Topics: Dopamine binding (67%), Dopamine receptor D3 (65%), Dopamine receptor binding (65%) more

3,712 Citations

Journal ArticleDOI: 10.1126/SCIENCE.8493557
21 May 1993-Science
Abstract: A potent neurotrophic factor that enhances survival of midbrain dopaminergic neurons was purified and cloned. Glial cell line-derived neurotrophic factor (GDNF) is a glycosylated, disulfide-bonded homodimer that is a distantly related member of the transforming growth factor-beta superfamily. In embryonic midbrain cultures, recombinant human GDNF promoted the survival and morphological differentiation of dopaminergic neurons and increased their high-affinity dopamine uptake. These effects were relatively specific; GDNF did not increase total neuron or astrocyte numbers nor did it increase transmitter uptake by gamma-aminobutyric-containing and serotonergic neurons. GDNF may have utility in the treatment of Parkinson's disease, which is marked by progressive degeneration of midbrain dopaminergic neurons. more

3,168 Citations

Journal ArticleDOI: 10.1126/SCIENCE.2147780
07 Dec 1990-Science
Abstract: The striatum, which is the major component of the basal ganglia in the brain, is regulated in part by dopaminergic input from the substantia nigra. Severe movement disorders result from the loss of striatal dopamine in patients with Parkinson's disease. Rats with lesions of the nigrostriatal dopamine pathway caused by 6-hydroxydopamine (6-OHDA) serve as a model for Parkinson's disease and show alterations in gene expression in the two major output systems of the striatum to the globus pallidus and substantia nigra. Striatopallidal neurons show a 6-OHDA-induced elevation in their specific expression of messenger RNAs (mRNAs) encoding the D2 dopamine receptor and enkephalin, which is reversed by subsequent continuous treatment with the D2 agonist quinpirole. Conversely, striatonigral neurons show a 6-OHDA-induced reduction in their specific expression of mRNAs encoding the D1 dopamine receptor and substance P, which is reversed by subsequent daily injections of the D1 agonist SKF-38393. This treatment also increases dynorphin mRNA in striatonigral neurons. Thus, the differential effects of dopamine on striatonigral and striatopallidal neurons are mediated by their specific expression of D1 and D2 dopamine receptor subtypes, respectively. more

Topics: Dopamine receptor D3 (65%), Dopamine receptor D2 (65%), Dopaminergic (64%) more

2,794 Citations

No. of papers in the topic in previous years

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Topic's top 5 most impactful authors

Jacques Glowinski

121 papers, 10.3K citations

Kenneth E. Moore

82 papers, 3K citations

Robert H. Roth

81 papers, 7.8K citations

Nicola Biagio Mercuri

50 papers, 2.4K citations

Anders Björklund

45 papers, 5.6K citations

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