title: Information in pallidal neurons increases with parkinsonian severity.
abstract: BACKGROUND
  The motor symptoms of Parkinson's disease (PD) present with pathological neuronal activity in the basal ganglia. Although neuronal firing rate changes in the globus pallidus internus (GPi) and externus (GPe) are reported to underlie the development of PD motor signs, firing rates change inconsistently, vary confoundingly with some therapies, and are poor indicators of symptom severity.
  
  
  METHODS
  We explored the relationship between parkinsonian symptom severity and the effectiveness with which pallidal neurons transmit information. We quantify neuronal entropy and information - alternatives to firing rate and correlations respectively - in and between GPe and GPi neurons using a progressive, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine, non-human primate model of PD.
  
  
  RESULTS
  Neuronal entropy and symptom severity were not linearly correlated: in both pallidal segments, entropy increased from naive to moderate parkinsonism, but decreased with further progression to the severely parkinsonian condition. In contrast, information transmitted from GPe to GPi increased consistently with symptom severity. Furthermore, antidromic information from GPi to GPe increased substantially with symptom severity. Together, these findings suggest that as parkinsonian severity increases, more and more information enters GPe and GPi from common sources, diminishing the relative importance of the orthodromic GPe to GPi connection.
  
  
  CONCLUSIONS
  With parkinsonian progression, the direct and indirect pathways lose their independence and start to convey redundant information. We hypothesize that a loss of parallel processing impairs the ability of the network to select and implement motor commands, thus promoting the hypokinetic symptoms of PD.
authors.affiliation: Department of Bioengineering, University of Utah, Salt Lake City, UT, USA. Electronic address: chuck.dorval@utah.edu.
authors.forename: Alan D
authors.initials: AD
authors.lastname: Dorval
authors.affiliation: Department of Neurology, University of Minnesota, Minneapolis, MN, USA.
authors.forename: Abirami
authors.initials: A
authors.lastname: Muralidharan
authors.affiliation: Department of Neurology, University of Minnesota, Minneapolis, MN, USA.
authors.forename: Alicia L
authors.initials: AL
authors.lastname: Jensen
authors.affiliation: Department of Neurology, University of Minnesota, Minneapolis, MN, USA.
authors.forename: Kenneth B
authors.initials: KB
authors.lastname: Baker
authors.affiliation: Department of Neurology, University of Minnesota, Minneapolis, MN, USA.
authors.forename: Jerrold L
authors.initials: JL
authors.lastname: Vitek
mesh_terms: D000818:Animals; D004195:Disease Models, Animal; D055724:Electrophysiological Phenomena; D019277:Entropy; D005260:Female; D005917:Globus Pallidus / Q000503:physiopathology*; D008253:Macaca mulatta; D008297:Male; D009474:Neurons / Q000502:physiology*; D010300:Parkinson Disease / Q000503:physiopathology*; D012720:Severity of Illness Index
keywords: Basal ganglia; Globus pallidus; Neural information; Parkinson's disease