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Parkinson Disease: HELP
Articles by Jaime Kaminer
Based on 2 articles published since 2010
(Why 2 articles?)

Between 2010 and 2020, Jaime Kaminer wrote the following 2 articles about Parkinson Disease.
+ Citations + Abstracts
1 Article Effects of subthalamic deep brain stimulation on blink abnormalities of 6-OHDA lesioned rats. 2015

Kaminer, Jaime / Thakur, Pratibha / Evinger, Craig. ·Program of Integrative Neuroscience, Department of Psychology, Stony Brook University, Stony Brook, New York; · Program in Neuroscience, Stony Brook University, Stony Brook, New York; · Department of Neurobiology and Behavior, Stony Brook University, Stony Brook, New York; and SUNY Eye Institute, Syracuse, New York leslie.evinger@stonybrook.edu. ·J Neurophysiol · Pubmed #25673748.

ABSTRACT: Parkinson's disease (PD) patients and the 6-hydroxydopamine (6-OHDA) lesioned rat model share blink abnormalities. In view of the evolutionarily conserved organization of blinking, characterization of blink reflex circuits in rodents may elucidate the neural mechanisms of PD reflex abnormalities. We examine the extent of this shared pattern of blink abnormalities by measuring blink reflex excitability, blink reflex plasticity, and spontaneous blinking in 6-OHDA lesioned rats. We also investigate whether 130-Hz subthalamic nucleus deep brain stimulation (STN DBS) affects blink abnormalities, as it does in PD patients. Like PD patients, 6-OHDA-lesioned rats exhibit reflex blink hyperexcitability, impaired blink plasticity, and a reduced spontaneous blink rate. At 130 Hz, but not 16 Hz, STN DBS eliminates reflex blink hyperexcitability and restores both short- and long-term blink plasticity. Replicating its lack of effect in PD patients, 130-Hz STN DBS does not reinstate a normal temporal pattern or rate to spontaneous blinking in 6-OHDA lesioned rats. These data show that the 6-OHDA lesioned rat is an ideal model system for investigating the neural bases of reflex abnormalities in PD and highlight the complexity of PD's effects on motor control, by showing that dopamine depletion does not affect all blink systems via the same neural mechanisms.

2 Article Frequency matters: beta-band subthalamic nucleus deep-brain stimulation induces Parkinsonian-like blink abnormalities in normal rats. 2014

Kaminer, Jaime / Thakur, Pratibha / Evinger, Craig. ·Program in Integrative Neuroscience, Department of Psychology, Stony Brook University, Stony Brook, NY, USA. ·Eur J Neurosci · Pubmed #25146113.

ABSTRACT: The synchronized beta-band oscillations in the basal ganglia-cortical networks in Parkinson's disease (PD) may be responsible for PD motor symptoms or an epiphenomenon of dopamine loss. We investigated the causal role of beta-band activity in PD motor symptoms by testing the effects of beta-frequency subthalamic nucleus deep-brain stimulation (STN DBS) on the blink reflex excitability, amplitude, and plasticity in normal rats. Delivering 16 Hz STN DBS produced the same increase in blink reflex excitability and impairment in blink reflex plasticity in normal rats as occurs in rats with 6-hydroxydopamine lesions and patients with PD. These deficits were not an artifact of STN DBS because, when these normal rats received 130 Hz STN DBS, their blink characteristics were the same as without STN DBS. To demonstrate that the blink reflex disturbances with 16 Hz STN DBS were frequency specific, we tested the same rats with 7 Hz STN DBS, a theta-band frequency typical of dystonia. In contrast to beta stimulation, 7 Hz STN DBS exaggerated the blink reflex plasticity as occurs in focal dystonia. Thus, without destroying dopamine neurons or blocking dopamine receptors, frequency-specific STN DBS can be used to create PD-like or dystonic-like symptoms in a normal rat.