The Effects of Destructive Lesions and Stimulation of the Basal Ganglia on Speech Mechanisms

1966 ◽  
Vol 27 (1-3) ◽  
pp. 197-207 ◽  
Author(s):  
K. Hermann ◽  
J.W. Turner ◽  
F.J. Gillingham ◽  
R.M. Gaze
Keyword(s):  
Basal Ganglia ◽  
Stimulation Of

scholarly journals Corticostriatal Plastic Changes in Experimental L-DOPA-Induced Dyskinesia

2012 ◽  
Vol 2012 ◽  
pp. 1-10 ◽  
Author(s):  
Veronica Ghiglieri ◽  
Vincenza Bagetta ◽  
Valentina Pendolino ◽  
Barbara Picconi ◽  
Paolo Calabresi
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Basal Ganglia ◽  
Experimental Models ◽  
Striatal Neurons ◽  
Da Receptors ◽  
Electrophysiological Studies ◽  
Plastic Changes ◽  
Stimulation Of

In Parkinson’s disease (PD), alteration of dopamine- (DA-) dependent striatal functions and pulsatile stimulation of DA receptors caused by the discontinuous administration of levodopa (L-DOPA) lead to a complex cascade of events affecting the postsynaptic striatal neurons that might account for the appearance of L-DOPA-induced dyskinesia (LID). Experimental models of LID have been widely used and extensively characterized in rodents and electrophysiological studies provided remarkable insights into the inner mechanisms underlying L-DOPA-induced corticostriatal plastic changes. Here we provide an overview of recent findings that represent a further step into the comprehension of mechanisms underlying maladaptive changes of basal ganglia functions in response to L-DOPA and associated to development of LID.

Effect of electrical stimulation of the cerebral cortex on the expression of the fos protein in the basal ganglia

Neuroscience ◽  
1997 ◽  
Vol 81 (1) ◽  
pp. 93-112 ◽  
Author(s):  
V Sgambato ◽  
V Abo ◽  
M Rogard ◽  
M.J Besson ◽  
J.M Deniau
Keyword(s):  
Cerebral Cortex ◽  
Electrical Stimulation ◽  
Basal Ganglia ◽  
Fos Protein ◽  
Stimulation Of

SYMPOSIUM: BEHAVIOR MODIFICATION BY DRUGS

PEDIATRICS ◽  
1972 ◽  
Vol 49 (5) ◽  
pp. 694-701
Author(s):  
Ross J. Baldessarini
Keyword(s):  
Basal Ganglia ◽  
Synaptic Transmission ◽  
Tissue Distribution ◽  
Behavior Modification ◽  
Nerve Terminals ◽  
Median Forebrain Bundle ◽  
Stereotyped Behaviors ◽  
Synaptic Receptors ◽  
Oxidative Processes ◽  
Stimulation Of

The pharmacology of the amphetamines has been studied for several decades. There is now a great deal of information about their tissue distribution and catabolism, largely by enzymatic oxidative processes. The most clearly characterized actions of the amphetamines occur at catecholamineconaining nerve terminals and tend to enhance the availability of the transmitter to post-synaptic receptors. The actions of the drugs in the CNS include stimulation of the ascending reticular formation of the brainstem, and probably enhancement of the activity of a behavior reinforcement system mediated by the median forebrain bundle. Toxic effects of amphetamine include apparent interactions at the basal ganglia to produce stereotyped behaviors in animals and man. All of these actions might involve catecholaminergic synaptic transmission systems. Under careful, controlled medical supervision the amphetamines are remarkably safe, although in excessive doses they can produce severe toxic, sympathomimetic and psychotic effects and can be lethal. They are subject to gross abuses, and to habituation. Tolerance develops to some of their actions, but usually not to their legitimate and rational uses in narcolepsy and hyperkinesis. Withdrawal symptoms are relatively minor.

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