Decreased intracranial self-stimulation after neuroleptics or 6-hydroxydopamine: Evidence for mediation by motor deficits rather than by reduced reward

1976 ◽  
Vol 47 (1) ◽  
pp. 21-27 ◽  
Author(s):  
H. C. Fibiger ◽  
D. A. Carter ◽  
A. G. Phillips
Keyword(s):  
Motor Deficits ◽  
6 Hydroxydopamine ◽  
Self Stimulation

scholarly journals In vivo electrophysiology of nigral and thalamic neurons in alpha-synuclein-overexpressing mice highlights differences from toxin-based models of parkinsonism

2013 ◽  
Vol 110 (12) ◽  
pp. 2792-2805 ◽  
Author(s):  
C. J. Lobb ◽  
A. K. Zaheer ◽  
Y. Smith ◽  
D. Jaeger
Keyword(s):  
Primary Motor Cortex ◽  
Alpha Synuclein ◽  
Motor Dysfunction ◽  
Motor Deficits ◽  
Dopamine Depletion ◽  
Wild Type ◽  
Beta Oscillations ◽  
Nigrostriatal Dopamine ◽  
6 Hydroxydopamine

Numerous studies have suggested that alpha-synuclein plays a prominent role in both familial and idiopathic Parkinson's disease (PD). Mice in which human alpha-synuclein is overexpressed (ASO) display progressive motor deficits and many nonmotor features of PD. However, it is unclear what in vivo pathophysiological mechanisms drive these motor deficits. It is also unknown whether previously proposed pathophysiological features (i.e., increased beta oscillations, bursting, and synchronization) described in toxin-based, nigrostriatal dopamine-depletion models are also present in ASO mice. To address these issues, we first confirmed that 5- to 6-mo-old ASO mice have robust motor dysfunction, despite the absence of significant nigrostriatal dopamine degeneration. In the same animals, we then recorded simultaneous single units and local field potentials (LFPs) in the substantia nigra pars reticulata (SNpr), the main basal ganglia output nucleus, and one of its main thalamic targets, the ventromedial nucleus, as well as LFPs in the primary motor cortex in anesthetized ASO mice and their age-matched, wild-type littermates. Neural activity was examined during slow wave activity and desynchronized cortical states, as previously described in 6-hydroxydopamine-lesioned rats. In contrast to toxin-based models, we found a small decrease, rather than an increase, in beta oscillations in the desynchronized state. Similarly, synchronized burst firing of nigral neurons observed in toxin-based models was not observed in ASO mice. Instead, we found more subtle changes in pauses of SNpr firing compared with wild-type control mice. Our results suggest that the pathophysiology underlying motor dysfunction in ASO mice is distinctly different from striatal dopamine-depletion models of parkinsonism.

Effect of subthalamic nucleus lesions in a 6-hydroxydopamine–induced rat parkinsonian model: behavioral and biochemical studies

2006 ◽  
Vol 105 (2) ◽  
pp. 284-287 ◽  
Author(s):  
Yong Sup Hwang ◽  
Insop Shim ◽  
Bom Bee Lee ◽  
Jin Woo Chang
Keyword(s):  
Kainic Acid ◽  
Subthalamic Nucleus ◽  
Behavioral Changes ◽  
Motor Deficits ◽  
Biochemical Studies ◽  
Tissue Dissection ◽  
Neurochemical Changes ◽  
6 Hydroxydopamine ◽  
Behavioral Improvement ◽  
Globus Pallidus Externus

Object The purpose of this study was to determine whether subthalamic nucleus (STN) ablation caused by kainic acid can restore dopaminergic neurotransmission and improve motor deficits in a 6-hydroxydopamine (6-OHDA)–induced hemiparkinsonian model. Methods The authors investigated behavioral changes in rats displaying parkinsonian symptoms (6-OHDA–lesioned rats) after an STN lesion was created using kainic acid. They also measured levels of dopamine and its metabolites following tissue dissection. The results of this study showed that STN ablation led to behavioral improvement in parkinsonian motor deficits. Increased levels of dopamine were also observed in the striatum and globus pallidus externus (GPE). Conclusions The results indicate that creation of an STN lesion in this hemiparkinsonian rat model may counteract some of the neurochemical changes within the striatum and GPE caused by the 6-OHDA, and influence striatal dopaminergic metabolism.

Silymarin recovers 6-hydroxydopamine-induced motor deficits in mice

2018 ◽  
Vol 118 ◽  
pp. 549-556 ◽  
Author(s):  
Catiuscia Molz de Freitas ◽  
Bárbara Nunes Krum ◽  
Ana Paula Chiapinotto Ceretta ◽  
Larissa Finger Schaffer ◽  
Elizete de Moraes Reis ◽  
...  
Keyword(s):  
Motor Deficits ◽  
6 Hydroxydopamine
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