Atlas of nerve cells, by M. Allen Starr. With the cooperation of Oliver S. Strong and Edward Leaming.

Leaming, Edward; Starr, Mark; Strong, Oliver S.

doi:10.5962/bhl.title.28486

Cited by 14 publications

(22 citation statements)

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“…The evaluation of locomotor activity induced by dopamine receptor agonists in reserpinized mice is a very useful in vivo model to study the function of striatal postsynaptic D 1 -like and D 2 -like receptors localized in GABAergic dynorphinergic and GABAergic enkephalinergic neurons without the influence of endogenous dopamine (24,37,38). In the present study we found that the D 3 receptor agonist PD 128907 potentiates the D 1 -mediated locomotor activation and that the effect of PD 128907 was counteracted by a specific In addition to the intramembrane receptor-receptor interaction, D 1 -D 3 receptor heteromerization can potentially modify D 1 receptor signaling and internalization as it has been shown for other receptor heteromers (25,26).…”

Section: Discussionmentioning

confidence: 99%

Identification of Dopamine D1–D3 Receptor Heteromers

Marcellino

Ferré

Casadó

et al. 2008

Journal of Biological Chemistry

216

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(GABAergic) 2 dynorphinergic neuron, which also expresses substance P (SP), and the GABAergic enkephalinergic neuron (4, 5). In fact, results obtained with in vivo techniques indicate that dopamine exerts differential effects on the two types of GABAergic efferent neurons, by acting on stimulatory D 1 receptors localized in the GABAergic SP-dynorphinergic neurons and inhibitory D 2 receptors localized in the GABAergic enkephalinergic neurons (6 -8). However, functional D 1 -like and D 2 -like receptors, as well as significant levels of D 1 and D 2 receptor mRNA expression, were detected in acutely dissociated striatonigral neurons (9). A more detailed and extensive analysis of the mRNA expression of the different receptor subtypes indicated that there is a limited subset of striatal neurons (ϳ15% of all GABAergic efferent neurons) with a mixed phenotype of GABAergic SP-dynorphinergic and GABAergic enkephalinergic neurons, with D 1 and D 2 receptors (10). This co-expression of D 1 and D 2 receptors has been confirmed in neostriatal neurons at the confocal microscopy level (11,12). George and coworkers (12, 13) have also found evidence for D 1 -D 2 receptor heteromerization (by co-immunoprecipitation) and for the generation of a unique pharmacology of the D 1 -D 2 receptor heteromer, with binding to selective ligands

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Section: Discussionmentioning

confidence: 99%

Identification of Dopamine D1–D3 Receptor Heteromers

Marcellino

Ferré

Casadó

et al. 2008

Journal of Biological Chemistry

216

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“…Where appropriate, data are expressed as the mean Ϯ SEM. Means, compared by using by an observer who did not know the genotypes of the animals, and the severity of seizures was rated by using published criteria (22,(34)(35)(36). Mice experiencing seizures induced by pilocarpine were assigned a rating for the entire 45-min period according to the following scale: 1, head bobbing; 2, single body or head jerks; 3, multiple clonic jerks; 4, one tonic-clonic seizure; 5, two tonic-clonic seizures; 6, three seizures.…”

Section: Construction Of the M1 Targetingmentioning

confidence: 99%

Disruption of the m1 receptor gene ablates muscarinic receptor-dependent M current regulation and seizure activity in mice

Hamilton

Loose

et al. 1997

Proc. Natl. Acad. Sci. U.S.A.

331

267

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Muscarinic acetylcholine receptors are members of the G protein-coupled receptor superfamily expressed in neurons, cardiomyocytes, smooth muscle, and a variety of epithelia. Five subtypes of muscarinic acetylcholine receptors have been discovered by molecular cloning, but their pharmacological similarities and frequent colocalization make it difficult to assign functional roles for individual subtypes in specific neuronal responses. We have used gene targeting by homologous recombination in embryonic stem cells to produce mice lacking the m1 receptor. These mice show no obvious behavioral or histological defects, and the m2, m3, and m4 receptors continue to be expressed in brain with no evidence of compensatory induction. However, the robust suppression of the M-current potassium channel activity evoked by muscarinic agonists in sympathetic ganglion neurons is completely lost in m1 mutant mice. In addition, both homozygous and heterozygous mutant mice are highly resistant to the seizures produced by systemic administration of the muscarinic agonist pilocarpine. Thus, the m1 receptor subtype mediates M current modulation in sympathetic neurons and induction of seizure activity in the pilocarpine model of epilepsy.

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“…(ii) The degeneracy of dopamine neurons accounts for an increase in the functional activity of the cholinergic system and is accompanied by the stimulating action of hyperactive glutamate on the NMDA receptors of cholinergic neurons [22,23].…”

Section: Antagonists Of Nmda Receptorsmentioning

confidence: 99%

“…It was suggested that it is the blocking of NR2B-containing NMDA receptors that leads to a decrease in muscle rigidity and a significant increase in locomotor activity [1,23,30]. In addition, it is possible to separate a group of agents preventing the release of glutamate [26].…”

Section: Antagonists Of Nmda Receptorsmentioning

confidence: 99%

“…The group of agents capable of blocking the open channels of NMDA receptors includes the following compounds: (+)-10,11-dihydro-5-methyl-5H-dibenzo[a,d]dicyclohepten-5,10-imine maleate (MK-801, dizocilpine maleate, XXVIII) [17, 23, 32]; 1-(1-phenylcyclohexyl)piperidine hydrochloride (phencyclidine, XXIX) [23,32]; (+)-cis-1,3,4,9,10,10a-hexahydro-6-methoxy-11-methyl-2H-10,4a-iminoethanophe nanthrene or 3-methoxy-17-methyl-19a,13a,14a-morphinan, dextromethorphan, DXM, XXX) [30]; 1-amino-3,5-dimethyladamantane hydrochloride (memantine, XXXI) [26,31,32,60]; and N-(1-naphthyl)-N¢-(4-ethylphenyl)-N¢-methylguanidine hydrochloride (aptiganel, cerestat, CNS-1102, XXXII) [61]. This ability allows these compounds to be considered potential antiparkinsonian and antiepileptic agents.…”

Section: Antagonists Of Nmda Receptorsmentioning

confidence: 99%

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Neurotoxins and medicinals for the treatment of Parkinson’s disease. Part 3: Drugs indirectly influencing the dopaminergic system (a review)

2005

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In recent years, much attention has been given to antiparkinsonian drugs which do not directly influence dopamine and its receptors but nevertheless produce a positive therapeutic action. This part of the review summarizes recent findings and discusses hypotheses concerning the role of antioxidants and inhibitors of adenosine and glutamate NMDA receptors in the treatment of Parkinson's disease. Promising approaches are provided by operative methods and gene therapy. The development of Parkinson's disease genetics will probably provide a key to the next generation of antiparkinsonian drugs.

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Atlas of nerve cells, by M. Allen Starr. With the cooperation of Oliver S. Strong and Edward Leaming.

Cited by 14 publications

References 0 publications

Identification of Dopamine D1–D3 Receptor Heteromers

Identification of Dopamine D1–D3 Receptor Heteromers

Disruption of the m1 receptor gene ablates muscarinic receptor-dependent M current regulation and seizure activity in mice

Neurotoxins and medicinals for the treatment of Parkinson’s disease. Part 3: Drugs indirectly influencing the dopaminergic system (a review)

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