Affiliation: New Jersey
- Delayed caffeine treatment prevents nigral dopamine neuron loss in a progressive rat model of Parkinson's diseasePatricia K Sonsalla
Department of Neurology, UMDNJ Robert Wood Johnson Medical School, Piscataway, NJ 08854, USA
Exp Neurol 234:482-7. 2012..Importantly, neuroprotection was still apparent when caffeine was introduced after the onset of the neurodegenerative process. These results add to the clinical relevance for adenosine receptors as a disease-modifying drug target for PD...
- The antiepileptic drug zonisamide inhibits MAO-B and attenuates MPTP toxicity in mice: clinical relevancePatricia K Sonsalla
Department of Neurology, UMDNJ Robert Wood Johnson Medical School, 675 Hoes Lane, Piscataway, NJ 08854, USA
Exp Neurol 221:329-34. 2010..The results also suggest that caution in its use may be necessary, especially when administered with other drugs, in the treatment of epilepsy or PD...
- Chronic intraventricular administration of 1-methyl-4-phenylpyridinium as a progressive model of Parkinson's diseasePatricia K Sonsalla
Department of Neurology, Robert Wood Johnson Medical School UMDNJ, 675 Hoes Lane, Piscataway, NJ 08854, USA
Parkinsonism Relat Disord 14:S116-8. 2008..We review features of this model that include loss of nigral DA neurons, swollen and abnormal mitochondria, striatal inclusion-like bodies and microgliosis. Advantages as well as limitations of the model are addressed...
- Protection of malonate-induced GABA but not dopamine loss by GABA transporter blockade in rat striatumGail D Zeevalk
Department of Neurology, University of Medicine and Dentistry of New Jersey, Piscataway, New Jersey 08854, USA
Exp Neurol 176:193-202. 2002..These findings also point to fundamental differences between immature and adult neurons in the downstream involvement of GABA receptors during metabolic insult...
- Mitochondrial stress-induced dopamine efflux and neuronal damage by malonate involves the dopamine transporterLily Y Moy
Department of Neurology, University of Medicine and Dentistry of New Jersey, Robert Wood Johnson Medical School, Piscataway, NJ 08854, USA
J Pharmacol Exp Ther 320:747-56. 2007....
- Adenosinergic protection of dopaminergic and GABAergic neurons against mitochondrial inhibition through receptors located in the substantia nigra and striatum, respectivelyPeter D Alfinito
Levine Neuroscience Laboratory, Department of Neurology, University of Medicine and Dentistry of New Jersey Robert Wood Johnson Medical School, Piscataway, New Jersey 08854, USA
J Neurosci 23:10982-7. 2003..Interestingly, these effects are mediated by A1 and A2a receptors located in the substantia nigra for DAergic neurons and in the striatum for GABAergic neurons...
- Na(+)/H(+) exchanger inhibition modifies dopamine neurotransmission during normal and metabolic stress conditionsMarcelo A Rocha
Department of Neurology, UMDNJ Robert Wood Johnson Medical School, Piscataway, New Jersey 08854, USA
J Neurochem 106:231-43. 2008..The absence of NHE1 co-location on DAergic neurons suggests that the effects of HOE-642 on striatal DA overflow are either mediated via NHE1 located on other cell types or that HOE-642 is acting through multiple NHE isoforms...
- Adenosine A2A receptors and brain injury: broad spectrum of neuroprotection, multifaceted actions and "fine tuning" modulationJiang Fan Chen
Department of Neurology, Boston University School of Medicine, 715 Albany Street, C329, Boston, MA 02118, USA
Prog Neurobiol 83:310-31. 2007....
- 8-(3-Chlorostyryl)caffeine may attenuate MPTP neurotoxicity through dual actions of monoamine oxidase inhibition and A2A receptor antagonismJiang Fan Chen
Department of Neurology, Molecular Neurobiology Laboratory, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02129, USA
J Biol Chem 277:36040-4. 2002..Together, these data indicate that CSC possesses dual actions of MAO-B inhibition and A(2A) receptor antagonism, a unique combination suggesting a new class of compounds with the potential for enhanced neuroprotective properties...
- Dopamine depletion causes fragmented clustering of neurons in the sensorimotor striatum: evidence of lasting reorganization of corticostriatal inputJeiwon Cho
Department of Psychology, Rutgers University, New Brunswick, New Jersey 08903, USA
J Comp Neurol 452:24-37. 2002..Switched signals could partially explain parkinsonian deficits in motor functions involving somatosensory guidance and their intractability to L-DOPA therapy-particularly if the switching involves sprouting...